BACKGROUND: Stretch marks are a disfiguring skin condition of yet unknown etiology. OBJECTIVE: We wanted to compare the functional disposition of dermal fibroblasts, derived from unaffected skin of patients with stretch marks and fibroblasts from normal age-matched subjects, and develop a test to predict predisposition to stretch mark development. METHODS: Skin biopsies from normal subjects (NS), stretch-marked skin (SM), and normal-looking skin from patients with stretch marks (NL) were analyzed by histochemistry and assays of total protein, DNA, and elastin. Cellular migration, proliferation, and matrix production were also measured in primary cultures of biopsy-derived fibroblasts. RESULTS: We found that NL skin contained less DNA, protein, and elastin than NS skin (-16%, -36%, -44%, respectively) and that such deficiencies were more profound in SM skin (-55%, -64%, -80%, respectively). Both NL- and SM-derived cells had slower than normal outgrowth of their fibroblasts, which also demonstrated low migration and proliferation rates, and produced less elastin, fibrillin 1, collagen 1, and fibronectin than NS-derived cells in primary cultures. All these aberrant features, indicating a dormant phenotype of NL- and SM-derived fibroblasts, were reversed and normalized in the fourth passage of all tested fibroblasts. CONCLUSIONS: A series of in vitro tests led to the discovery of a dormant phenotype in dermal fibroblasts from patients with stretch marks. The described tests may serve as a diagnostic tool for predicting predisposition to stretch marks. The reported reversibility of impaired fibroblast phenotypes opens a new perspective for preventive treatments for people predisposed to stretch mark formation.
BACKGROUND: Stretch marks are a disfiguring skin condition of yet unknown etiology. OBJECTIVE: We wanted to compare the functional disposition of dermal fibroblasts, derived from unaffected skin of patients with stretch marks and fibroblasts from normal age-matched subjects, and develop a test to predict predisposition to stretch mark development. METHODS: Skin biopsies from normal subjects (NS), stretch-marked skin (SM), and normal-looking skin from patients with stretch marks (NL) were analyzed by histochemistry and assays of total protein, DNA, and elastin. Cellular migration, proliferation, and matrix production were also measured in primary cultures of biopsy-derived fibroblasts. RESULTS: We found that NL skin contained less DNA, protein, and elastin than NS skin (-16%, -36%, -44%, respectively) and that such deficiencies were more profound in SM skin (-55%, -64%, -80%, respectively). Both NL- and SM-derived cells had slower than normal outgrowth of their fibroblasts, which also demonstrated low migration and proliferation rates, and produced less elastin, fibrillin 1, collagen 1, and fibronectin than NS-derived cells in primary cultures. All these aberrant features, indicating a dormant phenotype of NL- and SM-derived fibroblasts, were reversed and normalized in the fourth passage of all tested fibroblasts. CONCLUSIONS: A series of in vitro tests led to the discovery of a dormant phenotype in dermal fibroblasts from patients with stretch marks. The described tests may serve as a diagnostic tool for predicting predisposition to stretch marks. The reported reversibility of impaired fibroblast phenotypes opens a new perspective for preventive treatments for people predisposed to stretch mark formation.
Authors: Tamar Matyashov; Ella Pardo; Reut Rotem; Yael Lichtman; Maayan Elnir Katz; Adi Y Weintraub; Amir Horev Journal: PLoS One Date: 2022-03-15 Impact factor: 3.240