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Phenotypic differences between dermal fibroblasts from different body sites determine their responses to tension and TGFβ1

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Publisher
BioMed Central
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PMC
Keywords
  • Research Article

Abstract

1471-5945-2-13.fm ral ss BioMed CentBMC Dermatology Open AcceBMC Dermatology 2002, 2 xResearch article Phenotypic differences between dermal fibroblasts from different body sites determine their responses to tension and TGFβ1 Constantin C Chipev and Marcia Simon* Address: Living Skin Bank, University Hospital, Dept. Oral Biology and Pathology, Dept. of Dermatology, HSC, SUNY at Stony Brook, NY 11794- 9702, USA E-mail: Constantin C Chipev - [email protected]; Marcia Simon* - [email protected] *Corresponding author Abstract Background: Wounds in the nonglabrous skin of keloid-prone individuals tend to cause large disordered accumulations of collagen which extend beyond the original margins of the wound. In addition to abnormalities in keloid fibroblasts, comparison of dermal fibroblasts derived from nonwounded glabrous or nonglabrous skin revealed differences that may account for the observed location of keloids. Methods: Fibroblast apoptosis and the cellular content of α-smooth-muscle actin, TGFβ1 receptorII and ED-A fibronectin were estimated by FACS analysis. The effects of TGFβ1 and serum were examined. Results: In monolayer cultures non-glabrous fibroblasts were slower growing, had higher granularity and accumulated more α-smooth-muscle actin than fibroblasts from glabrous tissues. Keloid fibroblasts had the highest level of α-smooth-muscle actin in parallel with their expression level of ED-A fibronectin. TGFβ1 positively regulated α-smooth-muscle actin expression in all fibroblast cultures, although its effects on apoptosis in fibroblasts from glabrous and non-glabrous tissues were found to differ. The presence of collagen I in the ECM resulted in reduction of α- smooth-muscle actin. A considerable percentage of the apoptotic fibroblasts in attached gels were α-smooth-muscle actin positive. The extent of apoptosis correlated positively with increased cell and matrix relaxation. TGFβ1 was unable to overcome this apoptotic effect of matrix relaxatio

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