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Mary F Barbe - One of the best experts on this subject based on the ideXlab platform.
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exposure dependent increases in il 1β substance p ctgf and tendinosis in flexor digitorum tendons with upper extremity repetitive strain injury
2009Co-Authors: Jane M Fedorczyk, Ann E Barr, Shobha Rani, Mamta Amin, Shreya Amin, Judith Litvin, Mary F BarbeAbstract:Upper extremity tendinopathies are associated with performance of forceful repetitive tasks. We used our rat model of repetitive strain injury to study changes induced in forelimb flexor digitorum tendons. Rats were trained to perform a high repetition high force (HRHF) handle-pulling task (12 reaches/min at 60 ± 5 % maximum pulling force (MPF)), or a low repetition negligible force (LRNF) reaching and food retrieval task (3 reaches/min at 5 ± 5% MPF), for 2 hrs/day in 30 min sessions, 3 days/wk for 3–12 weeks. Forelimb grip strength was tested. Flexor digitorum tendons were examined at mid tendon at the level of the carpal tunnel for interleukin (IL)-1β; neutrophil and macrophage influx; Substance P, connective tissue growth factor (CTGF) and periostin like factor (PLF) immunoexpression; and histopathological changes. In HRHF rats, grip strength progressively decreased, while IL-1β levels progressively increased in the flexor digitorum peritendon (para- and epitendon combined) and endotendon with task performance. Macrophage invasion was evident in week 6 and 12 HRHF peritendon but not endotendon. Also in HRHF rats, Substance P immunoexpression increased in week 12 peritendon as did CTGF- and PLF-immunopositive fibroblasts, the increased fibroblasts contributing greatly to peritendon thickening. Endotendon collagen disorganization was evident in week 12 HRHF tendons. LRNF tendons did not differ from controls, even at 12 weeks. Thus, we observed exposure dependent changes in flexor digitorum tendons within the carpal tunnel, including increased inflammation, nociceptor-related neuropeptide immunoexpression, and fibrotic histopathology, changes associated with grip strength declines.
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exposure dependent increases in il 1β substance p ctgf and tendinosis in flexor digitorum tendons with upper extremity repetitive strain injury
2009Co-Authors: Jane M Fedorczyk, Ann E Barr, Shobha Rani, Mamta Amin, Shreya Amin, Judith Litvin, Mary F Barbe, Helen G L GaoAbstract:Upper extremity tendinopathies are associated with performance of forceful repetitive tasks. We used our rat model of repetitive strain injury to study changes induced in forelimb flexor digitorum tendons. Rats were trained to perform a high repetition high force (HRHF) handle-pulling task (12 reaches/min at 60 +/- 5% maximum pulling force [MPF]), or a low repetition negligible force (LRNF) reaching and food retrieval task (three reaches/min at 5 +/- 5% MPF), for 2 h/day in 30 min sessions, 3 days/week for 3-12 weeks. Forelimb grip strength was tested. Flexor digitorum tendons were examined at midtendon at the level of the carpal tunnel for interleukin (IL)-1beta, neutrophil, and macrophage influx, Substance P, connective tissue growth factor (CTGF), and periostin-like factor (PLF) immunoexpression, and histopathological changes. In HRHF rats, grip strength progressively decreased, while IL-1beta levels progressively increased in the flexor digitorum peritendon (para- and epitendon combined) and endotendon with task performance. Macrophage invasion was evident in week 6 and 12 HRHF peritendon but not endotendon. Also in HRHF rats, Substance P immunoexpression increased in week 12 peritendon as did CTGF- and PLF-immunopositive fibroblasts, the increased fibroblasts contributing greatly to peritendon thickening. Endotendon collagen disorganization was evident in week 12 HRHF tendons. LRNF tendons did not differ from controls, even at 12 weeks. Thus, we observed exposure-dependent changes in flexor digitorum tendons within the carpal tunnel, including increased inflammation, nociceptor-related neuropeptide immunoexpression, and fibrotic histopathology, changes associated with grip strength decline.
James Chang - One of the best experts on this subject based on the ideXlab platform.
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flexor tendon tissue engineering temporal distribution of donor tenocytes versus recipient cells
2009Co-Authors: Johan Thorfinn, Sepideh Saber, Ioannis K Angelidis, Andrew Y Zhang, Alphonsus K S Chong, Hung M Pham, Gordon K Lee, James ChangAbstract:Background: Tissue-engineered tendon material may address tendon shortages in mutilating hand injuries. Tenocytes from rabbit flexor tendon can be successfully seeded onto acellularized tendons that are used as tendon constructs. These constructs in vivo exhibit a population of tenocyte-like cells; however, it is not known to what extent these cells are of donor or recipient origin. Furthermore, the temporal distribution is also not known. Methods: Tenocytes from New Zealand male rabbits were cultured and seeded onto acellularized rabbit forepaw flexor tendons (n = 48). These tendon constructs were transplanted into female recipients. Tendons were examined after 3, 6, 12, and 30 weeks using fluorescent in situ hybridization to detect the Y chromosome in the male donor cells. One unseeded, acellularized allograft in each animal was used as a control. Results: The donor male tenocytes populate the epitenon and Endotenon of the grafts at greater numbers than the recipient female tenocytes at 3 and 6 weeks. The donor and recipient tenocytes are present jointly in the grafts until 12 weeks. At 30 weeks, nearly all cells are recipient tenocyte-like cells. Conclusions: Donor male cells survive in decreasing numbers over time until 30 weeks. The presence of cells in tissue-engineered tendon grafts has been shown in prior studies to add to the strength of the constructs in vitro. This study shows that recipient cells can migrate into and repopulate the tendon construct. Cell seeding onto tendon material may create stronger constructs that will allow the initiation of motion earlier. (Plast. Reconstr. Surg. 124: 2019, 2009.)
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mannose 6 phosphate an inhibitor of transforming growth factor β improves range of motion after flexor tendon repair
2006Co-Authors: Steven J Bates, Michael T. Longaker, Andrew Y Zhang, Hung Pham, Ellen Morrow, James ChangAbstract:Background: Adhesion formation between the flexor tendon and its surrounding fibro-osseous sheath results in a decreased postoperative range of motion in the hand. Transforming growth factor-beta (TGF-β) is a key cytokine in the pathogenesis of tissue fibrosis. In this study, the effects of two natural inhibitors of TGF-β, decorin and mannose-6-phosphate, were investigated in vitro and in vivo. Methods: In the in vitro investigation, primary cell cultures from rabbit flexor tendon sheath, epitenon, and Endotenon were established and each was supplemented with TGF-β along with increasing doses of decorin or mannose-6-phosphate. Collagen-I production was measured with enzyme-linked immunosorbent assay (ELISA). For the in vivo study, rabbit zone-II flexor tendons were transected and then immediately repaired. Single intraoperative graded doses of decorin, mannose-6-phosphate, or phosphate-buffered saline solution (control) were added to the repair sites, and the forepaws were tested for the range of motion and repair strength at eight weeks postoperatively. Results: Decorin and mannose-6-phosphate both reduced TGF-β upregulated collagen production. Intraoperative application of low-dose mannose-6-phosphate significantly improved the range of motion of the operatively treated digits. The effect on breaking strength of the tendon repair was inconclusive. Conclusions: Mannose-6-phosphate is effective in reducing TGF-β upregulated collagen production in an in vitro model. This finding correlated with our in vivo finding that a single intraoperative dose of mannose-6-phosphate improved the postoperative range of motion. Clinical Relevance: Mannose-6-phosphate is ubiquitous, nonimmunogenic, and easily produced, making it an ideal candidate for clinical application to reduce adhesion formation after flexor tendon repair.
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flexor tendon healing in vitro effects of tgf β on tendon cell collagen production
2002Co-Authors: Matthew B Klein, Michael T. Longaker, Hung Pham, Naveen Yalamanchi, James ChangAbstract:Abstract Flexor tendon healing is complicated by adhesions to the surrounding sheath. Transforming growth factor beta (TGF-β) is a cytokine with numerous activities related to wound healing. We examined the effects of TGF-β–1, –2 and –3 on tendon cell proliferation and collagen production. Three separate cell lines—sheath fibroblasts, epitenon and Endotenon tenocytes—were isolated from rabbit flexor tendons and cultured separately. Cell culture media was supplemented with 1 or 5 ng/mL of TGF-β–1, –2, or –3. Cell number and collagen I and III production were measured and compared with unsupplemented control cultures. The addition of TGF-β to cell culture media resulted in a decrease in cell number in all 3 lines that did not reach statistical significance. There was a significant increase (p
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flexor tendon healing in vitro effects of tgf β on tendon cell collagen production
2002Co-Authors: Matthew B Klein, Michael T. Longaker, Hung Pham, Naveen Yalamanchi, James ChangAbstract:Flexor tendon healing is complicated by adhesions to the surrounding sheath. Transforming growth factor beta (TGF-beta) is a cytokine with numerous activities related to wound healing. We examined the effects of TGF-beta-1, -2 and -3 on tendon cell proliferation and collagen production. Three separate cell lines--sheath fibroblasts, epitenon and Endotenon tenocytes--were isolated from rabbit flexor tendons and cultured separately. Cell culture media was supplemented with 1 or 5 ng/mL of TGF-beta-1, -2, or -3. Cell number and collagen I and III production were measured and compared with unsupplemented control cultures. The addition of TGF-beta to cell culture media resulted in a decrease in cell number in all 3 lines that did not reach statistical significance. There was a significant increase (p <.05) in collagen I and III production with the addition of all 3 TGF-beta isoforms. Modulation of TGF-beta production may provide a mechanism to modulate adhesion formation clinically.
Jane M Fedorczyk - One of the best experts on this subject based on the ideXlab platform.
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exposure dependent increases in il 1β substance p ctgf and tendinosis in flexor digitorum tendons with upper extremity repetitive strain injury
2009Co-Authors: Jane M Fedorczyk, Ann E Barr, Shobha Rani, Mamta Amin, Shreya Amin, Judith Litvin, Mary F BarbeAbstract:Upper extremity tendinopathies are associated with performance of forceful repetitive tasks. We used our rat model of repetitive strain injury to study changes induced in forelimb flexor digitorum tendons. Rats were trained to perform a high repetition high force (HRHF) handle-pulling task (12 reaches/min at 60 ± 5 % maximum pulling force (MPF)), or a low repetition negligible force (LRNF) reaching and food retrieval task (3 reaches/min at 5 ± 5% MPF), for 2 hrs/day in 30 min sessions, 3 days/wk for 3–12 weeks. Forelimb grip strength was tested. Flexor digitorum tendons were examined at mid tendon at the level of the carpal tunnel for interleukin (IL)-1β; neutrophil and macrophage influx; Substance P, connective tissue growth factor (CTGF) and periostin like factor (PLF) immunoexpression; and histopathological changes. In HRHF rats, grip strength progressively decreased, while IL-1β levels progressively increased in the flexor digitorum peritendon (para- and epitendon combined) and endotendon with task performance. Macrophage invasion was evident in week 6 and 12 HRHF peritendon but not endotendon. Also in HRHF rats, Substance P immunoexpression increased in week 12 peritendon as did CTGF- and PLF-immunopositive fibroblasts, the increased fibroblasts contributing greatly to peritendon thickening. Endotendon collagen disorganization was evident in week 12 HRHF tendons. LRNF tendons did not differ from controls, even at 12 weeks. Thus, we observed exposure dependent changes in flexor digitorum tendons within the carpal tunnel, including increased inflammation, nociceptor-related neuropeptide immunoexpression, and fibrotic histopathology, changes associated with grip strength declines.
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exposure dependent increases in il 1β substance p ctgf and tendinosis in flexor digitorum tendons with upper extremity repetitive strain injury
2009Co-Authors: Jane M Fedorczyk, Ann E Barr, Shobha Rani, Mamta Amin, Shreya Amin, Judith Litvin, Mary F Barbe, Helen G L GaoAbstract:Upper extremity tendinopathies are associated with performance of forceful repetitive tasks. We used our rat model of repetitive strain injury to study changes induced in forelimb flexor digitorum tendons. Rats were trained to perform a high repetition high force (HRHF) handle-pulling task (12 reaches/min at 60 +/- 5% maximum pulling force [MPF]), or a low repetition negligible force (LRNF) reaching and food retrieval task (three reaches/min at 5 +/- 5% MPF), for 2 h/day in 30 min sessions, 3 days/week for 3-12 weeks. Forelimb grip strength was tested. Flexor digitorum tendons were examined at midtendon at the level of the carpal tunnel for interleukin (IL)-1beta, neutrophil, and macrophage influx, Substance P, connective tissue growth factor (CTGF), and periostin-like factor (PLF) immunoexpression, and histopathological changes. In HRHF rats, grip strength progressively decreased, while IL-1beta levels progressively increased in the flexor digitorum peritendon (para- and epitendon combined) and endotendon with task performance. Macrophage invasion was evident in week 6 and 12 HRHF peritendon but not endotendon. Also in HRHF rats, Substance P immunoexpression increased in week 12 peritendon as did CTGF- and PLF-immunopositive fibroblasts, the increased fibroblasts contributing greatly to peritendon thickening. Endotendon collagen disorganization was evident in week 12 HRHF tendons. LRNF tendons did not differ from controls, even at 12 weeks. Thus, we observed exposure-dependent changes in flexor digitorum tendons within the carpal tunnel, including increased inflammation, nociceptor-related neuropeptide immunoexpression, and fibrotic histopathology, changes associated with grip strength decline.
Ann E Barr - One of the best experts on this subject based on the ideXlab platform.
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exposure dependent increases in il 1β substance p ctgf and tendinosis in flexor digitorum tendons with upper extremity repetitive strain injury
2009Co-Authors: Jane M Fedorczyk, Ann E Barr, Shobha Rani, Mamta Amin, Shreya Amin, Judith Litvin, Mary F BarbeAbstract:Upper extremity tendinopathies are associated with performance of forceful repetitive tasks. We used our rat model of repetitive strain injury to study changes induced in forelimb flexor digitorum tendons. Rats were trained to perform a high repetition high force (HRHF) handle-pulling task (12 reaches/min at 60 ± 5 % maximum pulling force (MPF)), or a low repetition negligible force (LRNF) reaching and food retrieval task (3 reaches/min at 5 ± 5% MPF), for 2 hrs/day in 30 min sessions, 3 days/wk for 3–12 weeks. Forelimb grip strength was tested. Flexor digitorum tendons were examined at mid tendon at the level of the carpal tunnel for interleukin (IL)-1β; neutrophil and macrophage influx; Substance P, connective tissue growth factor (CTGF) and periostin like factor (PLF) immunoexpression; and histopathological changes. In HRHF rats, grip strength progressively decreased, while IL-1β levels progressively increased in the flexor digitorum peritendon (para- and epitendon combined) and endotendon with task performance. Macrophage invasion was evident in week 6 and 12 HRHF peritendon but not endotendon. Also in HRHF rats, Substance P immunoexpression increased in week 12 peritendon as did CTGF- and PLF-immunopositive fibroblasts, the increased fibroblasts contributing greatly to peritendon thickening. Endotendon collagen disorganization was evident in week 12 HRHF tendons. LRNF tendons did not differ from controls, even at 12 weeks. Thus, we observed exposure dependent changes in flexor digitorum tendons within the carpal tunnel, including increased inflammation, nociceptor-related neuropeptide immunoexpression, and fibrotic histopathology, changes associated with grip strength declines.
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exposure dependent increases in il 1β substance p ctgf and tendinosis in flexor digitorum tendons with upper extremity repetitive strain injury
2009Co-Authors: Jane M Fedorczyk, Ann E Barr, Shobha Rani, Mamta Amin, Shreya Amin, Judith Litvin, Mary F Barbe, Helen G L GaoAbstract:Upper extremity tendinopathies are associated with performance of forceful repetitive tasks. We used our rat model of repetitive strain injury to study changes induced in forelimb flexor digitorum tendons. Rats were trained to perform a high repetition high force (HRHF) handle-pulling task (12 reaches/min at 60 +/- 5% maximum pulling force [MPF]), or a low repetition negligible force (LRNF) reaching and food retrieval task (three reaches/min at 5 +/- 5% MPF), for 2 h/day in 30 min sessions, 3 days/week for 3-12 weeks. Forelimb grip strength was tested. Flexor digitorum tendons were examined at midtendon at the level of the carpal tunnel for interleukin (IL)-1beta, neutrophil, and macrophage influx, Substance P, connective tissue growth factor (CTGF), and periostin-like factor (PLF) immunoexpression, and histopathological changes. In HRHF rats, grip strength progressively decreased, while IL-1beta levels progressively increased in the flexor digitorum peritendon (para- and epitendon combined) and endotendon with task performance. Macrophage invasion was evident in week 6 and 12 HRHF peritendon but not endotendon. Also in HRHF rats, Substance P immunoexpression increased in week 12 peritendon as did CTGF- and PLF-immunopositive fibroblasts, the increased fibroblasts contributing greatly to peritendon thickening. Endotendon collagen disorganization was evident in week 12 HRHF tendons. LRNF tendons did not differ from controls, even at 12 weeks. Thus, we observed exposure-dependent changes in flexor digitorum tendons within the carpal tunnel, including increased inflammation, nociceptor-related neuropeptide immunoexpression, and fibrotic histopathology, changes associated with grip strength decline.
Shobha Rani - One of the best experts on this subject based on the ideXlab platform.
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exposure dependent increases in il 1β substance p ctgf and tendinosis in flexor digitorum tendons with upper extremity repetitive strain injury
2009Co-Authors: Jane M Fedorczyk, Ann E Barr, Shobha Rani, Mamta Amin, Shreya Amin, Judith Litvin, Mary F BarbeAbstract:Upper extremity tendinopathies are associated with performance of forceful repetitive tasks. We used our rat model of repetitive strain injury to study changes induced in forelimb flexor digitorum tendons. Rats were trained to perform a high repetition high force (HRHF) handle-pulling task (12 reaches/min at 60 ± 5 % maximum pulling force (MPF)), or a low repetition negligible force (LRNF) reaching and food retrieval task (3 reaches/min at 5 ± 5% MPF), for 2 hrs/day in 30 min sessions, 3 days/wk for 3–12 weeks. Forelimb grip strength was tested. Flexor digitorum tendons were examined at mid tendon at the level of the carpal tunnel for interleukin (IL)-1β; neutrophil and macrophage influx; Substance P, connective tissue growth factor (CTGF) and periostin like factor (PLF) immunoexpression; and histopathological changes. In HRHF rats, grip strength progressively decreased, while IL-1β levels progressively increased in the flexor digitorum peritendon (para- and epitendon combined) and endotendon with task performance. Macrophage invasion was evident in week 6 and 12 HRHF peritendon but not endotendon. Also in HRHF rats, Substance P immunoexpression increased in week 12 peritendon as did CTGF- and PLF-immunopositive fibroblasts, the increased fibroblasts contributing greatly to peritendon thickening. Endotendon collagen disorganization was evident in week 12 HRHF tendons. LRNF tendons did not differ from controls, even at 12 weeks. Thus, we observed exposure dependent changes in flexor digitorum tendons within the carpal tunnel, including increased inflammation, nociceptor-related neuropeptide immunoexpression, and fibrotic histopathology, changes associated with grip strength declines.
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exposure dependent increases in il 1β substance p ctgf and tendinosis in flexor digitorum tendons with upper extremity repetitive strain injury
2009Co-Authors: Jane M Fedorczyk, Ann E Barr, Shobha Rani, Mamta Amin, Shreya Amin, Judith Litvin, Mary F Barbe, Helen G L GaoAbstract:Upper extremity tendinopathies are associated with performance of forceful repetitive tasks. We used our rat model of repetitive strain injury to study changes induced in forelimb flexor digitorum tendons. Rats were trained to perform a high repetition high force (HRHF) handle-pulling task (12 reaches/min at 60 +/- 5% maximum pulling force [MPF]), or a low repetition negligible force (LRNF) reaching and food retrieval task (three reaches/min at 5 +/- 5% MPF), for 2 h/day in 30 min sessions, 3 days/week for 3-12 weeks. Forelimb grip strength was tested. Flexor digitorum tendons were examined at midtendon at the level of the carpal tunnel for interleukin (IL)-1beta, neutrophil, and macrophage influx, Substance P, connective tissue growth factor (CTGF), and periostin-like factor (PLF) immunoexpression, and histopathological changes. In HRHF rats, grip strength progressively decreased, while IL-1beta levels progressively increased in the flexor digitorum peritendon (para- and epitendon combined) and endotendon with task performance. Macrophage invasion was evident in week 6 and 12 HRHF peritendon but not endotendon. Also in HRHF rats, Substance P immunoexpression increased in week 12 peritendon as did CTGF- and PLF-immunopositive fibroblasts, the increased fibroblasts contributing greatly to peritendon thickening. Endotendon collagen disorganization was evident in week 12 HRHF tendons. LRNF tendons did not differ from controls, even at 12 weeks. Thus, we observed exposure-dependent changes in flexor digitorum tendons within the carpal tunnel, including increased inflammation, nociceptor-related neuropeptide immunoexpression, and fibrotic histopathology, changes associated with grip strength decline.