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Gary J. Fisher - One of the best experts on this subject based on the ideXlab platform.
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Ultraviolet irradiation alters Transforming Growth Factor β/Smad pathway in human skin in vivo
Journal of Investigative Dermatology, 2002Co-Authors: Taihao Quan, Tianyuan He, Sewon Kang, John J Voorhees, Gary J. FisherAbstract:Solar ultraviolet irradiation damages human skin and causes premature skin aging and skin cancer. As Transforming Growth Factor β plays an important role in regulating cell Growth and extracellular matrix synthesis, we investigated expression of Transforming Growth Factor β isoforms, Transforming Growth Factor β receptors, and Transforming Growth Factor β regulated Smad transcription Factors following irradiation with an ultraviolet B source and solar-simulated ultraviolet irradiation of human skin in vivo . Full-thickness, sun-protected adult human skin expressed Transforming Growth Factor β1, β2, and β3 transcripts in a ratio of 1:5:3, as determined by quantitative real-time reverse transcription polymerase chain reaction. Northern analysis demonstrated that the ultraviolet irradiation (2 minimal erythema dose) caused moderate (2–3-fold) gradual increases of Transforming Growth Factor β1 and β3 mRNA expression during 3 d post exposure. In contrast, expression of Transforming Growth Factor β2 mRNA, the predominant form of Transforming Growth Factor β in human skin, decreased within 4 h after ultraviolet irradiation. In situ hybridization revealed Transforming Growth Factor β1, β2, and β3 mRNA expression in cells throughout the epidermis and the dermis in nonirradiated skin. Following ultraviolet or solar-simulated ultraviolet irradiation, Transforming Growth Factor β1 and β3 mRNA were increased and Transforming Growth Factor β2 mRNA was reduced throughout the epidermis and dermis. No significant changes were observed in Transforming Growth Factor β type I receptor mRNA expression after ultraviolet irradiation. In contrast, Transforming Growth Factor β type II receptor mRNA expression was reduced 60% within 4 h following ultraviolet exposure in human skin in vivo . Transforming Growth Factor β type II receptor mRNA levels remained reduced for 8 h and recovered by 24 h post ultraviolet. In situ hybridization revealed that ultraviolet or solar-simulated ultraviolet irradiation caused loss of Transforming Growth Factor β type II receptor mRNA in basal and suprabasal cells in the epidermis and dermal cells. In addition, no significant changes were observed in Smad2, Smad3, and Smad4 expression after ultraviolet irradiation. In contrast, ultraviolet and solar-simulated ultraviolet irradiation rapidly induced gene expression of Smad7, which antagonizes the actions of the Transforming Growth Factor β/Smad pathway. Smad7 mRNA induction occurred throughout the epidermis and dermal cells as determined by in situ hybridization. Ultraviolet irradiation also caused reduced DNA binding of Smad3/4 in human skin in vivo . Reduced Smad3/4 DNA binding was observed within 4 h following irradiation. Taken together, these results demonstrate that ultraviolet and solar-simulated ultraviolet irradiation alter the Transforming Growth Factor β/Smad pathway in human skin in vivo . Ultraviolet induction of Smad7 and reduction of Transforming Growth Factor β2 and Transforming Growth Factor β type II receptor should diminish Transforming Growth Factor β signaling, and probably contribute to the decrease of Transforming Growth Factor β regulated type I and type III procollagen gene expression observed in ultraviolet and solar-simulated ultraviolet irradiated human skin in vivo .
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Ultraviolet irradiation alters Transforming Growth Factor beta/smad pathway in human skin in vivo.
The Journal of investigative dermatology, 2002Co-Authors: Taihao Quan, Tianyuan He, Sewon Kang, John J Voorhees, Gary J. FisherAbstract:Solar ultraviolet irradiation damages human skin and causes premature skin aging and skin cancer. As Transforming Growth Factor beta plays an important role in regulating cell Growth and extracellular matrix synthesis, we investigated expression of Transforming Growth Factor beta isoforms, Transforming Growth Factor beta receptors, and Transforming Growth Factor beta regulated Smad transcription Factors following irradiation with an ultraviolet B source and solar-simulated ultraviolet irradiation of human skin in vivo. Full-thickness, sun-protected adult human skin expressed Transforming Growth Factor beta1, beta2, and beta3 transcripts in a ratio of 1:5:3, as determined by quantitative real-time reverse transcription polymerase chain reaction. Northern analysis demonstrated that the ultraviolet irradiation (2 minimal erythema dose) caused moderate (2-3-fold) gradual increases of Transforming Growth Factor beta1 and beta3 mRNA expression during 3 d post exposure. In contrast, expression of Transforming Growth Factor beta2 mRNA, the predominant form of Transforming Growth Factor beta in human skin, decreased within 4 h after ultraviolet irradiation. In situ hybridization revealed Transforming Growth Factor beta1, beta2, and beta3 mRNA expression in cells throughout the epidermis and the dermis in nonirradiated skin. Following ultraviolet or solar-simulated ultraviolet irradiation, Transforming Growth Factor beta1 and beta3 mRNA were increased and Transforming Growth Factor beta2 mRNA was reduced throughout the epidermis and dermis. No significant changes were observed in Transforming Growth Factor beta type I receptor mRNA expression after ultraviolet irradiation. In contrast, Transforming Growth Factor beta type II receptor mRNA expression was reduced 60% within 4 h following ultraviolet exposure in human skin in vivo. Transforming Growth Factor beta type II receptor mRNA levels remained reduced for 8 h and recovered by 24 h post ultraviolet. In situ hybridization revealed that ultraviolet or solar-simulated ultraviolet irradiation caused loss of Transforming Growth Factor beta type II receptor mRNA in basal and suprabasal cells in the epidermis and dermal cells. In addition, no significant changes were observed in Smad2, Smad3, and Smad4 expression after ultraviolet irradiation. In contrast, ultraviolet and solar-simulated ultraviolet irradiation rapidly induced gene expression of Smad7, which antagonizes the actions of the Transforming Growth Factor beta/Smad pathway. Smad7 mRNA induction occurred throughout the epidermis and dermal cells as determined by in situ hybridization. Ultraviolet irradiation also caused reduced DNA binding of Smad3/4 in human skin in vivo. Reduced Smad3/4 DNA binding was observed within 4 h following irradiation. Taken together, these results demonstrate that ultraviolet and solar-simulated ultraviolet irradiation alter the Transforming Growth Factor beta/Smad pathway in human skin in vivo. Ultraviolet induction of Smad7 and reduction of Transforming Growth Factor beta2 and Transforming Growth Factor beta type II receptor should diminish Transforming Growth Factor beta signaling, and probably contribute to the decrease of Transforming Growth Factor beta regulated type I and type III procollagen gene expression observed in ultraviolet and solar-simulated ultraviolet irradiated human skin in vivo.
Ugo Ripamonti - One of the best experts on this subject based on the ideXlab platform.
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Induction of Bone Formation in Primates: The Transforming Growth Factor-beta 3 - Induction of Bone Formation in Primates : The Transforming Growth Factor-beta 3
2015Co-Authors: Ugo RipamontiAbstract:Introduction: The Discovery of Redundancy and the Bone Induction Prerogative of the Three Mammalian Transforming Growth Factor-ss Isoforms Ugo Ripamonti Induction of Bone Formation before Redundancy and the Discovery of the Induction of Bone Formation by the Mammalian Transforming Growth Factor-ss Isoforms Regenerative Medicine, the Induction of Bone Formation, Bone Tissue Engineering, and the Osteogenic Proteins of the Transforming Growth Factor-ss Supergene Family Ugo Ripamonti Regenerative Medicine and Bone: Formation by Autoinduction Induction of Bone Formation: Osteogenesis in Angiogenesis Homologous but Molecularly Different Pleiotropic Proteins of the TGF-ss Supergene Family Initiate Endochondral Bone Formation Rapid Induction of Bone Formation by the Transforming Growth Factor-ss3 Isoform Ugo Ripamonti Transforming Growth Factor-ss3 Isoform TGF-ss3 Isoform and the Induction of Bone Formation in Primates Coral-Derived Mascroporous Bioreactor as Delivery System for the Biological Activity of the Recombinant hTGF-ss3 Isoform hTGF-ss3 Master Gene and Gene Product: Transfiguration of Neoplastic Masses into Bone Induction of Bone Formation by the Mammalian Transforming Growth Factor-sss: Molecular and Morphological Insights Raquel Duarte, Kurt Lightfoot, and Ugo Ripamonti Introduction Role of TGF-ss in Differentiation of Osteoblasts Role of TGF-ss3 in Bone Formation: Lessons from the Nonhuman Primate Papio ursinus Perspectives Regeneration of Mandibular Defects in Nonhuman Primates by the Transforming Growth Factor-ss3 and Translational Research in Clinical Contexts Ugo Ripamonti and Carlo Ferretti Tissue Induction and Regeneration of Craniomandibulofacial Defects Rapid Induction of Bone Formation by the hTGF-ss3 Osteogenic Device in Mandibular Defects of the Chacma Baboon (P. ursinus) Synergistic Induction of Bone Formation by Relatively Low Doses of Transforming Growth Factor-ss1 and -ss3 in Binary Application with Recombinant Human Osteogenic Protein-1 Ugo Ripamonti Homologous but Molecularly Different Multiple Isoforms of the TGF-ss Supergene Family initiate the Induction of Bone Formation in Primate Species Tissue Morphogenesis and Synergistic Interaction by Interposed Homologous Recombinant Morphogens Synergistic Induction of Bone Formation Temporal Expression of Markers of Bone Differentiation by Induction: Mechanistic Insights into the Synergistic Induction of Bone Formation Synergistic Induction of Bone Formation in Full-Thickness Mandibular Defects of P. ursinus Induction of Periodontal Tissue Regeneration by Recombinant Human Transforming Growth Factor-ss3 with and without Myoblastic/Pericytic Stem Cells in Papio ursinus Jean-Claude Petit and Ugo Ripamonti Introduction Origins Periodontal Tissue Regeneration by the Osteogenic Proteins of the TGF-ss Supergene Family Periodontal Tissue Regeneration by Naturally Derived, Highly Purified and Recombinant Human Bone Morphogenetic Proteins Induction of Periodontal Tissue Regeneration by Recombinant Human TGF-ss3 in P. ursinus Challenges and Perspectives in Regenerative Medicine of the Periodontal Tissues by the hTGF-ss3 Isoform
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induction of cementogenesis and periodontal ligament regeneration by recombinant human Transforming Growth Factor β3 in matrigel with rectus abdominis responding cells
Journal of Periodontal Research, 2009Co-Authors: Ugo Ripamonti, R Parak, Jeanclaude PetitAbstract:Background and Objective: In primates and in primates only, the Transforming Growth Factor-β proteins induce endochondral bone formation. Transforming Growth Factor-β3 also induces periodontal tissue regeneration. Two regenerative treatments using human recombinant Transforming Growth Factor-β3 were examined after implantation in mandibular furcation defects of the nonhuman primate, Papio ursinus. Material and Methods: Class III furcation defects were surgically created bilaterally in the mandibular first and second molars of two adult Chacma baboons (P. ursinus). Different doses of recombinant Transforming Growth Factor-β3 reconstituted with Matrigel® matrix were implanted in the rectus abdominis muscle to induce heterotopic ossicles for subsequent transplantation to selected furcation defects. Twenty days after heterotopic implantation, periodontal defects were re-exposed, further debrided and implanted with minced fragments of induced heterotopic ossicles. Contralateral class III furcation defects were implanted directly with recombinant Transforming Growth Factor-β3 in Matrigel® matrix with the addition of minced fragments of autogenous rectus abdominis muscle. Treated quadrants were not subjected to oral hygiene procedures so as to study the effect of the direct application of the recombinant morphogen in Matrigel® on periodontal healing. Histomorphometric analyses on undecalcified sections cut from specimen blocks harvested on day 60 measured the area of newly formed alveolar bone and the coronal extension of the newly formed cementum along the exposed root surfaces. Results: Morphometric analyses showed greater alveolar bone regeneration and cementogenesis in furcation defects implanted directly with 75 μg of Transforming Growth Factor-β3 in Matrigel® matrix with the addition of minced muscle tissue. Conclusion: Matrigel® matrix is an optimal delivery system for the osteogenic proteins of the Transforming Growth Factor-β superfamily, including the mammalian Transforming Growth Factor-β3 isoform. The addition of minced fragments of rectus abdominis muscle provides responding stem cells for further tissue induction and morphogenesis by the Transforming Growth Factor-β3 protein.
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Induction of cementogenesis and periodontal ligament regeneration by recombinant human Transforming Growth Factor‐β3 in Matrigel with rectus abdominis responding cells
Journal of Periodontal Research, 2008Co-Authors: Ugo Ripamonti, R Parak, Jeanclaude PetitAbstract:Background and Objective: In primates and in primates only, the Transforming Growth Factor-β proteins induce endochondral bone formation. Transforming Growth Factor-β3 also induces periodontal tissue regeneration. Two regenerative treatments using human recombinant Transforming Growth Factor-β3 were examined after implantation in mandibular furcation defects of the nonhuman primate, Papio ursinus. Material and Methods: Class III furcation defects were surgically created bilaterally in the mandibular first and second molars of two adult Chacma baboons (P. ursinus). Different doses of recombinant Transforming Growth Factor-β3 reconstituted with Matrigel® matrix were implanted in the rectus abdominis muscle to induce heterotopic ossicles for subsequent transplantation to selected furcation defects. Twenty days after heterotopic implantation, periodontal defects were re-exposed, further debrided and implanted with minced fragments of induced heterotopic ossicles. Contralateral class III furcation defects were implanted directly with recombinant Transforming Growth Factor-β3 in Matrigel® matrix with the addition of minced fragments of autogenous rectus abdominis muscle. Treated quadrants were not subjected to oral hygiene procedures so as to study the effect of the direct application of the recombinant morphogen in Matrigel® on periodontal healing. Histomorphometric analyses on undecalcified sections cut from specimen blocks harvested on day 60 measured the area of newly formed alveolar bone and the coronal extension of the newly formed cementum along the exposed root surfaces. Results: Morphometric analyses showed greater alveolar bone regeneration and cementogenesis in furcation defects implanted directly with 75 μg of Transforming Growth Factor-β3 in Matrigel® matrix with the addition of minced muscle tissue. Conclusion: Matrigel® matrix is an optimal delivery system for the osteogenic proteins of the Transforming Growth Factor-β superfamily, including the mammalian Transforming Growth Factor-β3 isoform. The addition of minced fragments of rectus abdominis muscle provides responding stem cells for further tissue induction and morphogenesis by the Transforming Growth Factor-β3 protein.
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Periodontal tissue regeneration by recombinant human Transforming Growth Factor‐β3 in Papio ursinus
Journal of Periodontal Research, 2007Co-Authors: June Teare, Lentsha Nathaniel Ramoshebi, Ugo RipamontiAbstract:BACKGROUND AND OBJECTIVE: Osteogenic proteins of the Transforming Growth Factor-beta superfamily induce periodontal tissue regeneration in animal models, including primates. To our knowledge, no studies have been performed in periodontal regeneration using the Transforming Growth Factor-beta 3 isoform. In the present study, recombinant human Transforming Growth Factor-beta 3 was examined for its ability to induce periodontal tissue regeneration in the nonhuman primate, Papio ursinus. MATERIAL AND METHODS: Class II furcation defects were surgically created bilaterally in the maxillary and mandibular molars of four adult baboons. Heterotopic ossicles, for transplantation to selected furcation defects, were induced within the rectus abdominis muscle by recombinant human Transforming Growth Factor-beta 3. Forty days later, the periodontal defects were implanted with recombinant human Transforming Growth Factor-beta 3 in Matrigel as the delivery system, with recombinant human Transforming Growth Factor-beta 3 plus minced muscle tissue in Matrigel, or with the harvested recombinant human Transforming Growth Factor-beta 3-induced ossicles. Sixty days after periodontal implantation, the animals were killed and the specimens harvested. Histological analysis on undecalcified sections measured the area and volume of new alveolar bone and the coronal extension of newly formed alveolar bone and cementum. RESULTS: Morphometric analyses showed pronounced periodontal regeneration in experimental defects compared with controls. Substantial regeneration was observed in defects implanted with fragments of heterotopically induced ossicles and with recombinant human Transforming Growth Factor-beta 3 plus minced muscle tissue. CONCLUSION: Recombinant human Transforming Growth Factor-beta 3 in Matrigel significantly enhanced periodontal tissue regeneration in the nonhuman primate, P. ursinus.
Taihao Quan - One of the best experts on this subject based on the ideXlab platform.
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Ultraviolet irradiation alters Transforming Growth Factor β/Smad pathway in human skin in vivo
Journal of Investigative Dermatology, 2002Co-Authors: Taihao Quan, Tianyuan He, Sewon Kang, John J Voorhees, Gary J. FisherAbstract:Solar ultraviolet irradiation damages human skin and causes premature skin aging and skin cancer. As Transforming Growth Factor β plays an important role in regulating cell Growth and extracellular matrix synthesis, we investigated expression of Transforming Growth Factor β isoforms, Transforming Growth Factor β receptors, and Transforming Growth Factor β regulated Smad transcription Factors following irradiation with an ultraviolet B source and solar-simulated ultraviolet irradiation of human skin in vivo . Full-thickness, sun-protected adult human skin expressed Transforming Growth Factor β1, β2, and β3 transcripts in a ratio of 1:5:3, as determined by quantitative real-time reverse transcription polymerase chain reaction. Northern analysis demonstrated that the ultraviolet irradiation (2 minimal erythema dose) caused moderate (2–3-fold) gradual increases of Transforming Growth Factor β1 and β3 mRNA expression during 3 d post exposure. In contrast, expression of Transforming Growth Factor β2 mRNA, the predominant form of Transforming Growth Factor β in human skin, decreased within 4 h after ultraviolet irradiation. In situ hybridization revealed Transforming Growth Factor β1, β2, and β3 mRNA expression in cells throughout the epidermis and the dermis in nonirradiated skin. Following ultraviolet or solar-simulated ultraviolet irradiation, Transforming Growth Factor β1 and β3 mRNA were increased and Transforming Growth Factor β2 mRNA was reduced throughout the epidermis and dermis. No significant changes were observed in Transforming Growth Factor β type I receptor mRNA expression after ultraviolet irradiation. In contrast, Transforming Growth Factor β type II receptor mRNA expression was reduced 60% within 4 h following ultraviolet exposure in human skin in vivo . Transforming Growth Factor β type II receptor mRNA levels remained reduced for 8 h and recovered by 24 h post ultraviolet. In situ hybridization revealed that ultraviolet or solar-simulated ultraviolet irradiation caused loss of Transforming Growth Factor β type II receptor mRNA in basal and suprabasal cells in the epidermis and dermal cells. In addition, no significant changes were observed in Smad2, Smad3, and Smad4 expression after ultraviolet irradiation. In contrast, ultraviolet and solar-simulated ultraviolet irradiation rapidly induced gene expression of Smad7, which antagonizes the actions of the Transforming Growth Factor β/Smad pathway. Smad7 mRNA induction occurred throughout the epidermis and dermal cells as determined by in situ hybridization. Ultraviolet irradiation also caused reduced DNA binding of Smad3/4 in human skin in vivo . Reduced Smad3/4 DNA binding was observed within 4 h following irradiation. Taken together, these results demonstrate that ultraviolet and solar-simulated ultraviolet irradiation alter the Transforming Growth Factor β/Smad pathway in human skin in vivo . Ultraviolet induction of Smad7 and reduction of Transforming Growth Factor β2 and Transforming Growth Factor β type II receptor should diminish Transforming Growth Factor β signaling, and probably contribute to the decrease of Transforming Growth Factor β regulated type I and type III procollagen gene expression observed in ultraviolet and solar-simulated ultraviolet irradiated human skin in vivo .
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Ultraviolet irradiation alters Transforming Growth Factor beta/smad pathway in human skin in vivo.
The Journal of investigative dermatology, 2002Co-Authors: Taihao Quan, Tianyuan He, Sewon Kang, John J Voorhees, Gary J. FisherAbstract:Solar ultraviolet irradiation damages human skin and causes premature skin aging and skin cancer. As Transforming Growth Factor beta plays an important role in regulating cell Growth and extracellular matrix synthesis, we investigated expression of Transforming Growth Factor beta isoforms, Transforming Growth Factor beta receptors, and Transforming Growth Factor beta regulated Smad transcription Factors following irradiation with an ultraviolet B source and solar-simulated ultraviolet irradiation of human skin in vivo. Full-thickness, sun-protected adult human skin expressed Transforming Growth Factor beta1, beta2, and beta3 transcripts in a ratio of 1:5:3, as determined by quantitative real-time reverse transcription polymerase chain reaction. Northern analysis demonstrated that the ultraviolet irradiation (2 minimal erythema dose) caused moderate (2-3-fold) gradual increases of Transforming Growth Factor beta1 and beta3 mRNA expression during 3 d post exposure. In contrast, expression of Transforming Growth Factor beta2 mRNA, the predominant form of Transforming Growth Factor beta in human skin, decreased within 4 h after ultraviolet irradiation. In situ hybridization revealed Transforming Growth Factor beta1, beta2, and beta3 mRNA expression in cells throughout the epidermis and the dermis in nonirradiated skin. Following ultraviolet or solar-simulated ultraviolet irradiation, Transforming Growth Factor beta1 and beta3 mRNA were increased and Transforming Growth Factor beta2 mRNA was reduced throughout the epidermis and dermis. No significant changes were observed in Transforming Growth Factor beta type I receptor mRNA expression after ultraviolet irradiation. In contrast, Transforming Growth Factor beta type II receptor mRNA expression was reduced 60% within 4 h following ultraviolet exposure in human skin in vivo. Transforming Growth Factor beta type II receptor mRNA levels remained reduced for 8 h and recovered by 24 h post ultraviolet. In situ hybridization revealed that ultraviolet or solar-simulated ultraviolet irradiation caused loss of Transforming Growth Factor beta type II receptor mRNA in basal and suprabasal cells in the epidermis and dermal cells. In addition, no significant changes were observed in Smad2, Smad3, and Smad4 expression after ultraviolet irradiation. In contrast, ultraviolet and solar-simulated ultraviolet irradiation rapidly induced gene expression of Smad7, which antagonizes the actions of the Transforming Growth Factor beta/Smad pathway. Smad7 mRNA induction occurred throughout the epidermis and dermal cells as determined by in situ hybridization. Ultraviolet irradiation also caused reduced DNA binding of Smad3/4 in human skin in vivo. Reduced Smad3/4 DNA binding was observed within 4 h following irradiation. Taken together, these results demonstrate that ultraviolet and solar-simulated ultraviolet irradiation alter the Transforming Growth Factor beta/Smad pathway in human skin in vivo. Ultraviolet induction of Smad7 and reduction of Transforming Growth Factor beta2 and Transforming Growth Factor beta type II receptor should diminish Transforming Growth Factor beta signaling, and probably contribute to the decrease of Transforming Growth Factor beta regulated type I and type III procollagen gene expression observed in ultraviolet and solar-simulated ultraviolet irradiated human skin in vivo.
Jeanclaude Petit - One of the best experts on this subject based on the ideXlab platform.
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induction of cementogenesis and periodontal ligament regeneration by recombinant human Transforming Growth Factor β3 in matrigel with rectus abdominis responding cells
Journal of Periodontal Research, 2009Co-Authors: Ugo Ripamonti, R Parak, Jeanclaude PetitAbstract:Background and Objective: In primates and in primates only, the Transforming Growth Factor-β proteins induce endochondral bone formation. Transforming Growth Factor-β3 also induces periodontal tissue regeneration. Two regenerative treatments using human recombinant Transforming Growth Factor-β3 were examined after implantation in mandibular furcation defects of the nonhuman primate, Papio ursinus. Material and Methods: Class III furcation defects were surgically created bilaterally in the mandibular first and second molars of two adult Chacma baboons (P. ursinus). Different doses of recombinant Transforming Growth Factor-β3 reconstituted with Matrigel® matrix were implanted in the rectus abdominis muscle to induce heterotopic ossicles for subsequent transplantation to selected furcation defects. Twenty days after heterotopic implantation, periodontal defects were re-exposed, further debrided and implanted with minced fragments of induced heterotopic ossicles. Contralateral class III furcation defects were implanted directly with recombinant Transforming Growth Factor-β3 in Matrigel® matrix with the addition of minced fragments of autogenous rectus abdominis muscle. Treated quadrants were not subjected to oral hygiene procedures so as to study the effect of the direct application of the recombinant morphogen in Matrigel® on periodontal healing. Histomorphometric analyses on undecalcified sections cut from specimen blocks harvested on day 60 measured the area of newly formed alveolar bone and the coronal extension of the newly formed cementum along the exposed root surfaces. Results: Morphometric analyses showed greater alveolar bone regeneration and cementogenesis in furcation defects implanted directly with 75 μg of Transforming Growth Factor-β3 in Matrigel® matrix with the addition of minced muscle tissue. Conclusion: Matrigel® matrix is an optimal delivery system for the osteogenic proteins of the Transforming Growth Factor-β superfamily, including the mammalian Transforming Growth Factor-β3 isoform. The addition of minced fragments of rectus abdominis muscle provides responding stem cells for further tissue induction and morphogenesis by the Transforming Growth Factor-β3 protein.
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Induction of cementogenesis and periodontal ligament regeneration by recombinant human Transforming Growth Factor‐β3 in Matrigel with rectus abdominis responding cells
Journal of Periodontal Research, 2008Co-Authors: Ugo Ripamonti, R Parak, Jeanclaude PetitAbstract:Background and Objective: In primates and in primates only, the Transforming Growth Factor-β proteins induce endochondral bone formation. Transforming Growth Factor-β3 also induces periodontal tissue regeneration. Two regenerative treatments using human recombinant Transforming Growth Factor-β3 were examined after implantation in mandibular furcation defects of the nonhuman primate, Papio ursinus. Material and Methods: Class III furcation defects were surgically created bilaterally in the mandibular first and second molars of two adult Chacma baboons (P. ursinus). Different doses of recombinant Transforming Growth Factor-β3 reconstituted with Matrigel® matrix were implanted in the rectus abdominis muscle to induce heterotopic ossicles for subsequent transplantation to selected furcation defects. Twenty days after heterotopic implantation, periodontal defects were re-exposed, further debrided and implanted with minced fragments of induced heterotopic ossicles. Contralateral class III furcation defects were implanted directly with recombinant Transforming Growth Factor-β3 in Matrigel® matrix with the addition of minced fragments of autogenous rectus abdominis muscle. Treated quadrants were not subjected to oral hygiene procedures so as to study the effect of the direct application of the recombinant morphogen in Matrigel® on periodontal healing. Histomorphometric analyses on undecalcified sections cut from specimen blocks harvested on day 60 measured the area of newly formed alveolar bone and the coronal extension of the newly formed cementum along the exposed root surfaces. Results: Morphometric analyses showed greater alveolar bone regeneration and cementogenesis in furcation defects implanted directly with 75 μg of Transforming Growth Factor-β3 in Matrigel® matrix with the addition of minced muscle tissue. Conclusion: Matrigel® matrix is an optimal delivery system for the osteogenic proteins of the Transforming Growth Factor-β superfamily, including the mammalian Transforming Growth Factor-β3 isoform. The addition of minced fragments of rectus abdominis muscle provides responding stem cells for further tissue induction and morphogenesis by the Transforming Growth Factor-β3 protein.
John J Voorhees - One of the best experts on this subject based on the ideXlab platform.
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Ultraviolet irradiation alters Transforming Growth Factor β/Smad pathway in human skin in vivo
Journal of Investigative Dermatology, 2002Co-Authors: Taihao Quan, Tianyuan He, Sewon Kang, John J Voorhees, Gary J. FisherAbstract:Solar ultraviolet irradiation damages human skin and causes premature skin aging and skin cancer. As Transforming Growth Factor β plays an important role in regulating cell Growth and extracellular matrix synthesis, we investigated expression of Transforming Growth Factor β isoforms, Transforming Growth Factor β receptors, and Transforming Growth Factor β regulated Smad transcription Factors following irradiation with an ultraviolet B source and solar-simulated ultraviolet irradiation of human skin in vivo . Full-thickness, sun-protected adult human skin expressed Transforming Growth Factor β1, β2, and β3 transcripts in a ratio of 1:5:3, as determined by quantitative real-time reverse transcription polymerase chain reaction. Northern analysis demonstrated that the ultraviolet irradiation (2 minimal erythema dose) caused moderate (2–3-fold) gradual increases of Transforming Growth Factor β1 and β3 mRNA expression during 3 d post exposure. In contrast, expression of Transforming Growth Factor β2 mRNA, the predominant form of Transforming Growth Factor β in human skin, decreased within 4 h after ultraviolet irradiation. In situ hybridization revealed Transforming Growth Factor β1, β2, and β3 mRNA expression in cells throughout the epidermis and the dermis in nonirradiated skin. Following ultraviolet or solar-simulated ultraviolet irradiation, Transforming Growth Factor β1 and β3 mRNA were increased and Transforming Growth Factor β2 mRNA was reduced throughout the epidermis and dermis. No significant changes were observed in Transforming Growth Factor β type I receptor mRNA expression after ultraviolet irradiation. In contrast, Transforming Growth Factor β type II receptor mRNA expression was reduced 60% within 4 h following ultraviolet exposure in human skin in vivo . Transforming Growth Factor β type II receptor mRNA levels remained reduced for 8 h and recovered by 24 h post ultraviolet. In situ hybridization revealed that ultraviolet or solar-simulated ultraviolet irradiation caused loss of Transforming Growth Factor β type II receptor mRNA in basal and suprabasal cells in the epidermis and dermal cells. In addition, no significant changes were observed in Smad2, Smad3, and Smad4 expression after ultraviolet irradiation. In contrast, ultraviolet and solar-simulated ultraviolet irradiation rapidly induced gene expression of Smad7, which antagonizes the actions of the Transforming Growth Factor β/Smad pathway. Smad7 mRNA induction occurred throughout the epidermis and dermal cells as determined by in situ hybridization. Ultraviolet irradiation also caused reduced DNA binding of Smad3/4 in human skin in vivo . Reduced Smad3/4 DNA binding was observed within 4 h following irradiation. Taken together, these results demonstrate that ultraviolet and solar-simulated ultraviolet irradiation alter the Transforming Growth Factor β/Smad pathway in human skin in vivo . Ultraviolet induction of Smad7 and reduction of Transforming Growth Factor β2 and Transforming Growth Factor β type II receptor should diminish Transforming Growth Factor β signaling, and probably contribute to the decrease of Transforming Growth Factor β regulated type I and type III procollagen gene expression observed in ultraviolet and solar-simulated ultraviolet irradiated human skin in vivo .
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Ultraviolet irradiation alters Transforming Growth Factor beta/smad pathway in human skin in vivo.
The Journal of investigative dermatology, 2002Co-Authors: Taihao Quan, Tianyuan He, Sewon Kang, John J Voorhees, Gary J. FisherAbstract:Solar ultraviolet irradiation damages human skin and causes premature skin aging and skin cancer. As Transforming Growth Factor beta plays an important role in regulating cell Growth and extracellular matrix synthesis, we investigated expression of Transforming Growth Factor beta isoforms, Transforming Growth Factor beta receptors, and Transforming Growth Factor beta regulated Smad transcription Factors following irradiation with an ultraviolet B source and solar-simulated ultraviolet irradiation of human skin in vivo. Full-thickness, sun-protected adult human skin expressed Transforming Growth Factor beta1, beta2, and beta3 transcripts in a ratio of 1:5:3, as determined by quantitative real-time reverse transcription polymerase chain reaction. Northern analysis demonstrated that the ultraviolet irradiation (2 minimal erythema dose) caused moderate (2-3-fold) gradual increases of Transforming Growth Factor beta1 and beta3 mRNA expression during 3 d post exposure. In contrast, expression of Transforming Growth Factor beta2 mRNA, the predominant form of Transforming Growth Factor beta in human skin, decreased within 4 h after ultraviolet irradiation. In situ hybridization revealed Transforming Growth Factor beta1, beta2, and beta3 mRNA expression in cells throughout the epidermis and the dermis in nonirradiated skin. Following ultraviolet or solar-simulated ultraviolet irradiation, Transforming Growth Factor beta1 and beta3 mRNA were increased and Transforming Growth Factor beta2 mRNA was reduced throughout the epidermis and dermis. No significant changes were observed in Transforming Growth Factor beta type I receptor mRNA expression after ultraviolet irradiation. In contrast, Transforming Growth Factor beta type II receptor mRNA expression was reduced 60% within 4 h following ultraviolet exposure in human skin in vivo. Transforming Growth Factor beta type II receptor mRNA levels remained reduced for 8 h and recovered by 24 h post ultraviolet. In situ hybridization revealed that ultraviolet or solar-simulated ultraviolet irradiation caused loss of Transforming Growth Factor beta type II receptor mRNA in basal and suprabasal cells in the epidermis and dermal cells. In addition, no significant changes were observed in Smad2, Smad3, and Smad4 expression after ultraviolet irradiation. In contrast, ultraviolet and solar-simulated ultraviolet irradiation rapidly induced gene expression of Smad7, which antagonizes the actions of the Transforming Growth Factor beta/Smad pathway. Smad7 mRNA induction occurred throughout the epidermis and dermal cells as determined by in situ hybridization. Ultraviolet irradiation also caused reduced DNA binding of Smad3/4 in human skin in vivo. Reduced Smad3/4 DNA binding was observed within 4 h following irradiation. Taken together, these results demonstrate that ultraviolet and solar-simulated ultraviolet irradiation alter the Transforming Growth Factor beta/Smad pathway in human skin in vivo. Ultraviolet induction of Smad7 and reduction of Transforming Growth Factor beta2 and Transforming Growth Factor beta type II receptor should diminish Transforming Growth Factor beta signaling, and probably contribute to the decrease of Transforming Growth Factor beta regulated type I and type III procollagen gene expression observed in ultraviolet and solar-simulated ultraviolet irradiated human skin in vivo.
