The Experts below are selected from a list of 270 Experts worldwide ranked by ideXlab platform
Yoshiki Shiba - One of the best experts on this subject based on the ideXlab platform.
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irsogladine maleate counters the interleukin 1β induced suppression in gap junctional intercellular communication but does not affect the interleukin 1β induced Zonula Occludens Protein 1 levels in human gingival epithelial cells
Journal of Periodontal Research, 2007Co-Authors: T Fujita, Arata Ashikaga, Hideki Shiba, Mikihito Kajiya, Akiyoshi Kishimoto, Reika Hirata, Noriko Tsunekuni, Chikara Hirono, Hiroyuki Kawaguchi, Yoshiki ShibaAbstract:Background and Objective: Irsogladine maleate counters gap junctional intercellular communication reduction induced by interleukin-8 or Actinobacillus actinomycetemcomitans in cultured human gingival epithelial cells. Interleukin-1β is involved in periodontal disease. Little is known, however, about the effect of interleukin-1β on intercellular junctional complexes in human gingival epithelial cells. Furthermore, irsogladine maleate may affect the actions of interleukin-1β. In this study, we examined how interleukin-1β affected gap junctional intercellular communication, connexin 43 and Zonula Occludens Protein-1, and how irsogladine maleate modulated the interleukin-1β-induced changes in the intercellular junctional complexes in human gingival epithelial cells. Material and Methods: Human gingival epithelial cells were exposed to interleukin-1β, with or without irsogladine maleate. Connexin 43 and Zonula Occludens Protein-1 were examined at mRNA and Protein levels by real-time polymerase chain reaction and western blotting, respectively. Gap junctional intercellular communication was determined using the dye transfer method. The expression of Zonula Occludens Protein-1 was also confirmed by immunofluorescence. Results: Interleukin-1β decreased connexin 43 mRNA levels, but increased Zonula Occludens Protein-1 mRNA levels. Irsogladine maleate countered the interleukin-1β-induced reduction in gap junctional intercellular communication and connexin 43 levels. However, irsogladine maleate did not influence the increased Zonula Occludens Protein-1 levels. Conclusion: The effect of interleukin-1β on gap junctional intercellular communication and tight junctions of human gingival epithelial cells is different. The recovery of gap junctional intercellular communication by irsogladine maleate in the gingival epithelium may be a normal process in gingival epithelial homeostasis.
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Irsogladine maleate counters the interleukin‐1β‐induced suppression in gap‐junctional intercellular communication but does not affect the interleukin‐1β‐induced Zonula Occludens Protein‐1 levels in human gingival epithelial cells
Journal of Periodontal Research, 2007Co-Authors: T Fujita, Arata Ashikaga, Hideki Shiba, Mikihito Kajiya, Akiyoshi Kishimoto, Reika Hirata, Noriko Tsunekuni, Chikara Hirono, Hiroyuki Kawaguchi, Yoshiki ShibaAbstract:Background and Objective: Irsogladine maleate counters gap junctional intercellular communication reduction induced by interleukin-8 or Actinobacillus actinomycetemcomitans in cultured human gingival epithelial cells. Interleukin-1β is involved in periodontal disease. Little is known, however, about the effect of interleukin-1β on intercellular junctional complexes in human gingival epithelial cells. Furthermore, irsogladine maleate may affect the actions of interleukin-1β. In this study, we examined how interleukin-1β affected gap junctional intercellular communication, connexin 43 and Zonula Occludens Protein-1, and how irsogladine maleate modulated the interleukin-1β-induced changes in the intercellular junctional complexes in human gingival epithelial cells. Material and Methods: Human gingival epithelial cells were exposed to interleukin-1β, with or without irsogladine maleate. Connexin 43 and Zonula Occludens Protein-1 were examined at mRNA and Protein levels by real-time polymerase chain reaction and western blotting, respectively. Gap junctional intercellular communication was determined using the dye transfer method. The expression of Zonula Occludens Protein-1 was also confirmed by immunofluorescence. Results: Interleukin-1β decreased connexin 43 mRNA levels, but increased Zonula Occludens Protein-1 mRNA levels. Irsogladine maleate countered the interleukin-1β-induced reduction in gap junctional intercellular communication and connexin 43 levels. However, irsogladine maleate did not influence the increased Zonula Occludens Protein-1 levels. Conclusion: The effect of interleukin-1β on gap junctional intercellular communication and tight junctions of human gingival epithelial cells is different. The recovery of gap junctional intercellular communication by irsogladine maleate in the gingival epithelium may be a normal process in gingival epithelial homeostasis.
Patrick C Baer - One of the best experts on this subject based on the ideXlab platform.
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during epithelial differentiation of human adipose derived stromal stem cells expression of Zonula Occludens Protein 1 is induced by a combination of retinoic acid activin a and bone morphogenetic Protein 7
Cytotherapy, 2012Co-Authors: Nadine Griesche, Jurgen Bereiterhahn, Helmut Geiger, Ralf Schubert, Patrick C BaerAbstract:Background aims. Adipose-derived stromal/stem cells (ASC) possess a multilineage differentiation potential, can be used from an autologous origin, and are, therefore, attractive candidates for clinical applications to repair or regenerate damaged tissues and organs. Beside their well-known differentiation into cells of mesodermal origin, ASC are able to differentiate into cells of ecto- and endodermal origin. Methods . Previous studies have shown that all trans retinoic acid (ATRA) induces the expression of cytokeratin 18 (CK18), indicating the beginning of differentiation into the epithelial lineage. Nevertheless, ATRA does not induce the expression of other epithelial markers. Therefore, we tested the additional infl uence of two growth factors on the onset of epithelial differentiation of ASC. The cells were cultured with ATRA, Activin A (ActA) and bone morphogenetic Protein-7 (BMP-7), either alone or in combination. Differentiation into the epithelial lineage was assessed by the expression of the characteristic epithelial markers CK18 and Zonula Occludens Protein 1 (ZO-1) using Western blot, immunofl uorescence staining and polymerase chain reaction (PCR) analysis. Results . The mixture of all three factors induced epithelial differentiation of ASC without enhancing cell proliferation. Upon induction, the ASC showed phenotypic changes consistent with an epithelial phenotype. The addition of the growth factors ActA and BMP-7 enhanced the inductive effect of ATRA, as shown by the de novo expression of ZO-1 in addition to CK18 expression. Conclusions. Our study highlights the onset of the epithelial differentiation of ASC induced by culture with a combination of ATRA, ActA and BMP-7.
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During epithelial differentiation of human adipose-derived stromal/stem cells, expression of Zonula Occludens Protein-1 is induced by a combination of retinoic acid, activin-A and bone morphogenetic Protein-7
Cytotherapy, 2011Co-Authors: Nadine Griesche, Helmut Geiger, Ralf Schubert, Jürgen Bereiter-hahn, Patrick C BaerAbstract:Background aims. Adipose-derived stromal/stem cells (ASC) possess a multilineage differentiation potential, can be used from an autologous origin, and are, therefore, attractive candidates for clinical applications to repair or regenerate damaged tissues and organs. Beside their well-known differentiation into cells of mesodermal origin, ASC are able to differentiate into cells of ecto- and endodermal origin. Methods . Previous studies have shown that all trans retinoic acid (ATRA) induces the expression of cytokeratin 18 (CK18), indicating the beginning of differentiation into the epithelial lineage. Nevertheless, ATRA does not induce the expression of other epithelial markers. Therefore, we tested the additional infl uence of two growth factors on the onset of epithelial differentiation of ASC. The cells were cultured with ATRA, Activin A (ActA) and bone morphogenetic Protein-7 (BMP-7), either alone or in combination. Differentiation into the epithelial lineage was assessed by the expression of the characteristic epithelial markers CK18 and Zonula Occludens Protein 1 (ZO-1) using Western blot, immunofl uorescence staining and polymerase chain reaction (PCR) analysis. Results . The mixture of all three factors induced epithelial differentiation of ASC without enhancing cell proliferation. Upon induction, the ASC showed phenotypic changes consistent with an epithelial phenotype. The addition of the growth factors ActA and BMP-7 enhanced the inductive effect of ATRA, as shown by the de novo expression of ZO-1 in addition to CK18 expression. Conclusions. Our study highlights the onset of the epithelial differentiation of ASC induced by culture with a combination of ATRA, ActA and BMP-7.
T Fujita - One of the best experts on this subject based on the ideXlab platform.
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irsogladine maleate counters the interleukin 1β induced suppression in gap junctional intercellular communication but does not affect the interleukin 1β induced Zonula Occludens Protein 1 levels in human gingival epithelial cells
Journal of Periodontal Research, 2007Co-Authors: T Fujita, Arata Ashikaga, Hideki Shiba, Mikihito Kajiya, Akiyoshi Kishimoto, Reika Hirata, Noriko Tsunekuni, Chikara Hirono, Hiroyuki Kawaguchi, Yoshiki ShibaAbstract:Background and Objective: Irsogladine maleate counters gap junctional intercellular communication reduction induced by interleukin-8 or Actinobacillus actinomycetemcomitans in cultured human gingival epithelial cells. Interleukin-1β is involved in periodontal disease. Little is known, however, about the effect of interleukin-1β on intercellular junctional complexes in human gingival epithelial cells. Furthermore, irsogladine maleate may affect the actions of interleukin-1β. In this study, we examined how interleukin-1β affected gap junctional intercellular communication, connexin 43 and Zonula Occludens Protein-1, and how irsogladine maleate modulated the interleukin-1β-induced changes in the intercellular junctional complexes in human gingival epithelial cells. Material and Methods: Human gingival epithelial cells were exposed to interleukin-1β, with or without irsogladine maleate. Connexin 43 and Zonula Occludens Protein-1 were examined at mRNA and Protein levels by real-time polymerase chain reaction and western blotting, respectively. Gap junctional intercellular communication was determined using the dye transfer method. The expression of Zonula Occludens Protein-1 was also confirmed by immunofluorescence. Results: Interleukin-1β decreased connexin 43 mRNA levels, but increased Zonula Occludens Protein-1 mRNA levels. Irsogladine maleate countered the interleukin-1β-induced reduction in gap junctional intercellular communication and connexin 43 levels. However, irsogladine maleate did not influence the increased Zonula Occludens Protein-1 levels. Conclusion: The effect of interleukin-1β on gap junctional intercellular communication and tight junctions of human gingival epithelial cells is different. The recovery of gap junctional intercellular communication by irsogladine maleate in the gingival epithelium may be a normal process in gingival epithelial homeostasis.
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Irsogladine maleate counters the interleukin‐1β‐induced suppression in gap‐junctional intercellular communication but does not affect the interleukin‐1β‐induced Zonula Occludens Protein‐1 levels in human gingival epithelial cells
Journal of Periodontal Research, 2007Co-Authors: T Fujita, Arata Ashikaga, Hideki Shiba, Mikihito Kajiya, Akiyoshi Kishimoto, Reika Hirata, Noriko Tsunekuni, Chikara Hirono, Hiroyuki Kawaguchi, Yoshiki ShibaAbstract:Background and Objective: Irsogladine maleate counters gap junctional intercellular communication reduction induced by interleukin-8 or Actinobacillus actinomycetemcomitans in cultured human gingival epithelial cells. Interleukin-1β is involved in periodontal disease. Little is known, however, about the effect of interleukin-1β on intercellular junctional complexes in human gingival epithelial cells. Furthermore, irsogladine maleate may affect the actions of interleukin-1β. In this study, we examined how interleukin-1β affected gap junctional intercellular communication, connexin 43 and Zonula Occludens Protein-1, and how irsogladine maleate modulated the interleukin-1β-induced changes in the intercellular junctional complexes in human gingival epithelial cells. Material and Methods: Human gingival epithelial cells were exposed to interleukin-1β, with or without irsogladine maleate. Connexin 43 and Zonula Occludens Protein-1 were examined at mRNA and Protein levels by real-time polymerase chain reaction and western blotting, respectively. Gap junctional intercellular communication was determined using the dye transfer method. The expression of Zonula Occludens Protein-1 was also confirmed by immunofluorescence. Results: Interleukin-1β decreased connexin 43 mRNA levels, but increased Zonula Occludens Protein-1 mRNA levels. Irsogladine maleate countered the interleukin-1β-induced reduction in gap junctional intercellular communication and connexin 43 levels. However, irsogladine maleate did not influence the increased Zonula Occludens Protein-1 levels. Conclusion: The effect of interleukin-1β on gap junctional intercellular communication and tight junctions of human gingival epithelial cells is different. The recovery of gap junctional intercellular communication by irsogladine maleate in the gingival epithelium may be a normal process in gingival epithelial homeostasis.
Nadine Griesche - One of the best experts on this subject based on the ideXlab platform.
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during epithelial differentiation of human adipose derived stromal stem cells expression of Zonula Occludens Protein 1 is induced by a combination of retinoic acid activin a and bone morphogenetic Protein 7
Cytotherapy, 2012Co-Authors: Nadine Griesche, Jurgen Bereiterhahn, Helmut Geiger, Ralf Schubert, Patrick C BaerAbstract:Background aims. Adipose-derived stromal/stem cells (ASC) possess a multilineage differentiation potential, can be used from an autologous origin, and are, therefore, attractive candidates for clinical applications to repair or regenerate damaged tissues and organs. Beside their well-known differentiation into cells of mesodermal origin, ASC are able to differentiate into cells of ecto- and endodermal origin. Methods . Previous studies have shown that all trans retinoic acid (ATRA) induces the expression of cytokeratin 18 (CK18), indicating the beginning of differentiation into the epithelial lineage. Nevertheless, ATRA does not induce the expression of other epithelial markers. Therefore, we tested the additional infl uence of two growth factors on the onset of epithelial differentiation of ASC. The cells were cultured with ATRA, Activin A (ActA) and bone morphogenetic Protein-7 (BMP-7), either alone or in combination. Differentiation into the epithelial lineage was assessed by the expression of the characteristic epithelial markers CK18 and Zonula Occludens Protein 1 (ZO-1) using Western blot, immunofl uorescence staining and polymerase chain reaction (PCR) analysis. Results . The mixture of all three factors induced epithelial differentiation of ASC without enhancing cell proliferation. Upon induction, the ASC showed phenotypic changes consistent with an epithelial phenotype. The addition of the growth factors ActA and BMP-7 enhanced the inductive effect of ATRA, as shown by the de novo expression of ZO-1 in addition to CK18 expression. Conclusions. Our study highlights the onset of the epithelial differentiation of ASC induced by culture with a combination of ATRA, ActA and BMP-7.
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During epithelial differentiation of human adipose-derived stromal/stem cells, expression of Zonula Occludens Protein-1 is induced by a combination of retinoic acid, activin-A and bone morphogenetic Protein-7
Cytotherapy, 2011Co-Authors: Nadine Griesche, Helmut Geiger, Ralf Schubert, Jürgen Bereiter-hahn, Patrick C BaerAbstract:Background aims. Adipose-derived stromal/stem cells (ASC) possess a multilineage differentiation potential, can be used from an autologous origin, and are, therefore, attractive candidates for clinical applications to repair or regenerate damaged tissues and organs. Beside their well-known differentiation into cells of mesodermal origin, ASC are able to differentiate into cells of ecto- and endodermal origin. Methods . Previous studies have shown that all trans retinoic acid (ATRA) induces the expression of cytokeratin 18 (CK18), indicating the beginning of differentiation into the epithelial lineage. Nevertheless, ATRA does not induce the expression of other epithelial markers. Therefore, we tested the additional infl uence of two growth factors on the onset of epithelial differentiation of ASC. The cells were cultured with ATRA, Activin A (ActA) and bone morphogenetic Protein-7 (BMP-7), either alone or in combination. Differentiation into the epithelial lineage was assessed by the expression of the characteristic epithelial markers CK18 and Zonula Occludens Protein 1 (ZO-1) using Western blot, immunofl uorescence staining and polymerase chain reaction (PCR) analysis. Results . The mixture of all three factors induced epithelial differentiation of ASC without enhancing cell proliferation. Upon induction, the ASC showed phenotypic changes consistent with an epithelial phenotype. The addition of the growth factors ActA and BMP-7 enhanced the inductive effect of ATRA, as shown by the de novo expression of ZO-1 in addition to CK18 expression. Conclusions. Our study highlights the onset of the epithelial differentiation of ASC induced by culture with a combination of ATRA, ActA and BMP-7.
Hiroyuki Kawaguchi - One of the best experts on this subject based on the ideXlab platform.
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irsogladine maleate counters the interleukin 1β induced suppression in gap junctional intercellular communication but does not affect the interleukin 1β induced Zonula Occludens Protein 1 levels in human gingival epithelial cells
Journal of Periodontal Research, 2007Co-Authors: T Fujita, Arata Ashikaga, Hideki Shiba, Mikihito Kajiya, Akiyoshi Kishimoto, Reika Hirata, Noriko Tsunekuni, Chikara Hirono, Hiroyuki Kawaguchi, Yoshiki ShibaAbstract:Background and Objective: Irsogladine maleate counters gap junctional intercellular communication reduction induced by interleukin-8 or Actinobacillus actinomycetemcomitans in cultured human gingival epithelial cells. Interleukin-1β is involved in periodontal disease. Little is known, however, about the effect of interleukin-1β on intercellular junctional complexes in human gingival epithelial cells. Furthermore, irsogladine maleate may affect the actions of interleukin-1β. In this study, we examined how interleukin-1β affected gap junctional intercellular communication, connexin 43 and Zonula Occludens Protein-1, and how irsogladine maleate modulated the interleukin-1β-induced changes in the intercellular junctional complexes in human gingival epithelial cells. Material and Methods: Human gingival epithelial cells were exposed to interleukin-1β, with or without irsogladine maleate. Connexin 43 and Zonula Occludens Protein-1 were examined at mRNA and Protein levels by real-time polymerase chain reaction and western blotting, respectively. Gap junctional intercellular communication was determined using the dye transfer method. The expression of Zonula Occludens Protein-1 was also confirmed by immunofluorescence. Results: Interleukin-1β decreased connexin 43 mRNA levels, but increased Zonula Occludens Protein-1 mRNA levels. Irsogladine maleate countered the interleukin-1β-induced reduction in gap junctional intercellular communication and connexin 43 levels. However, irsogladine maleate did not influence the increased Zonula Occludens Protein-1 levels. Conclusion: The effect of interleukin-1β on gap junctional intercellular communication and tight junctions of human gingival epithelial cells is different. The recovery of gap junctional intercellular communication by irsogladine maleate in the gingival epithelium may be a normal process in gingival epithelial homeostasis.
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Irsogladine maleate counters the interleukin‐1β‐induced suppression in gap‐junctional intercellular communication but does not affect the interleukin‐1β‐induced Zonula Occludens Protein‐1 levels in human gingival epithelial cells
Journal of Periodontal Research, 2007Co-Authors: T Fujita, Arata Ashikaga, Hideki Shiba, Mikihito Kajiya, Akiyoshi Kishimoto, Reika Hirata, Noriko Tsunekuni, Chikara Hirono, Hiroyuki Kawaguchi, Yoshiki ShibaAbstract:Background and Objective: Irsogladine maleate counters gap junctional intercellular communication reduction induced by interleukin-8 or Actinobacillus actinomycetemcomitans in cultured human gingival epithelial cells. Interleukin-1β is involved in periodontal disease. Little is known, however, about the effect of interleukin-1β on intercellular junctional complexes in human gingival epithelial cells. Furthermore, irsogladine maleate may affect the actions of interleukin-1β. In this study, we examined how interleukin-1β affected gap junctional intercellular communication, connexin 43 and Zonula Occludens Protein-1, and how irsogladine maleate modulated the interleukin-1β-induced changes in the intercellular junctional complexes in human gingival epithelial cells. Material and Methods: Human gingival epithelial cells were exposed to interleukin-1β, with or without irsogladine maleate. Connexin 43 and Zonula Occludens Protein-1 were examined at mRNA and Protein levels by real-time polymerase chain reaction and western blotting, respectively. Gap junctional intercellular communication was determined using the dye transfer method. The expression of Zonula Occludens Protein-1 was also confirmed by immunofluorescence. Results: Interleukin-1β decreased connexin 43 mRNA levels, but increased Zonula Occludens Protein-1 mRNA levels. Irsogladine maleate countered the interleukin-1β-induced reduction in gap junctional intercellular communication and connexin 43 levels. However, irsogladine maleate did not influence the increased Zonula Occludens Protein-1 levels. Conclusion: The effect of interleukin-1β on gap junctional intercellular communication and tight junctions of human gingival epithelial cells is different. The recovery of gap junctional intercellular communication by irsogladine maleate in the gingival epithelium may be a normal process in gingival epithelial homeostasis.
