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Updated: Jan 31, 2026

Epigenetic Conversion as a Safe and Simple Method to Obtain Insulin-secreting Cells from Adult Skin Fibroblasts
Published on: March 18, 2016
Oligomeric Procyanidins (OPCs) Inhibit Procollagen Type I Secretion of Fibroblasts
Byung Jun Kim1, Jung-Keun Park2, Byeong Kyu Kim1
11Department of Plastic and Reconstructive Surgery, College of Medicine, Seoul National University, 103 Daehak-ro, Jongno-gu, Seoul, 03080 Korea.
Abstract:
Wound healing is composed of a complex process that requires harmonies of various cell populations where fibroblasts play the main role. Oligomeric procyanidins (OPC) are main components of grape (Vitis vinifera) seed extracts, and recent studies showed OPC's effects on inflammation, cell migration, and proliferation. We investigated the effect of OPC on fibroblasts to regulate wound healing process. Human dermal fibroblast known as Hs27 cells were treated with various concentrations of OPC (0, 2.5, 5, 10, and 20 μg/μl). Cell cytotoxicity was evaluated by the Cell Counting Kit assay, and the expression levels of secreted procollagen were analyzed. Procollagen levels in OPC treated cells exposed to transforming growth factor beta 1 (TGF-β1) or ascorbic acid were evaluated using Western blot and immunocytochemistry. Relative mRNA expressions of procollagen, molecular chaperone such as HSP47, P4H were determined by real-time PCR in OPC treated cells. OPC showed no cytotoxicity on Hs27 cells at every concentration but inhibited procollagen secretion in a dose-dependent manner. The inhibitory effect also appeared under TGF-β1 induced collagen overproduction. Immunocytochemistry showed that higher levels of intracytoplasmic procollagen were accumulated in TGF-β1 treatment group, whereas ascorbic acid induced a release of accumulated procollagen under OPC treatment. The mRNA expressions of procollagen, molecular chaperone were not affected by OPC, but procollagen level was increased when exposed to TGF-β1. OPC inhibits procollagen secretion from fibroblasts with no effects on cell proliferations even under the environment of TGF-β1-induced collagen overproduction. OPC could regulate the diseases and symptoms of abnormal overabundant collagen production.
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