Proliferation Of Scar Fibroblasts Research Articles

Effects of genistein on PCNA expression and cell cycle in human hypertrophic scar fibroblasts in vitro

Objective To observe the effects of genistein on PCNA expression and cell cycle in fibroblasts derived from human hypertrophic scar in order to explore the mechanism of its inhibition on hypertrophic scar （HS） fibroblast proliferation. Methods The human hypertrophic scar fibroblasts were cultured in vitro. Genistein with various concentrations （25, 50, 100 μmol/L） was co-cultured in the medium for 48 hours. The expression of PCNA was detected with immunocytochemical staining method and the cell cycle was measured with flow cytometry. Results Genistein could significantly decrease PCNA expression in HS fibroblasts, especially when its concentration at 50 μmol/L or 100 μmol/L. The cell percentage of G0 - G1 phase decreased with drug＇s concentration, and G2 -M percentage increased conversely, implying the suspension of mitosis. In 100 μmol/L group, most cells blocked at S phase and a hypodiploid apoptosis peak could be observed ahead of G1 phase. Conclusion Genistein can inhibit the proliferation of human hypertrophic scar by blocking cell division as well as decreasing DNA synthesis. Key words: Hypertrophic scar ; Fibroblasts ; Proliferating cell nuclear antigen ; Cell cycle ; Genistein

Pentoxifylline inhibits mature burn scar fibroblasts in culture

Fibroblasts are thought to be (in part) responsible for the persisting contractile forces that result in burn contractures. Using monolayer and fibroblast populated collagen lattice (FPCL) models we subjected burn scar fibroblasts to the anti-fibrinolytic agent Pentoxifylline (PFX) in an attempt to reduce proliferation and contraction of these cells. Fibroblasts were isolated from mature burn scars at reconstructive surgery. Fibroblasts were grown in monolayer or incorporated into FPCL's and exposed to PFX. Fibroblast numbers and FPCL surface areas were calculated using digital photography and image analysis. PFX showed a dose-dependent inhibition of contraction and reduced proliferation of burn scar fibroblasts. In monolayer, cell number proliferation was markedly reduced. FPCL's containing 0, 0.25, 0.5, 1, and 2 mg/ml of PFX had relative surface areas of 31, 40, 43, 59, and 85%, respectively. One and 2 mg/ml FPCL's contracted significantly less than controls ( p < 0.0001). This is the first study to show the dose-dependent effects of Pentoxifylline on the proliferation and contraction of burn scar fibroblasts. This study suggests that Pentoxifylline has a direct effect on inhibiting burn scar fibroblasts. Further study of PFX on burn scars will provide opportunities to reduce burn scar contractures in vivo.

The inhibition of fibroblast proliferation by a novel monokine: an in vitro and in vivo study.

We have identified a product of rabbit macrophages that inhibits fibroblast proliferation. Tested in vitro against several fibroblast populations, this monokine inhibited rabbit conjunctival fibroblast proliferation by 85% (p = 0.005), human conjunctival fibroblast proliferation by 88% (p = 0.005), human hypertrophic scar fibroblast proliferation by 85% (p = 0.005), and human keloid fibroblast proliferation by 79% (p = 0.005). Additionally (in an in vivo model), this monokine was injected into healing rabbit wounds and inhibited fibroblast proliferation by 33% after 7 days (p = 0.0001) and by 27% after 2 weeks (p < 0.0001). Preliminary analysis of the active factor demonstrates that it is not species-specific, has a molecular weight less than 3000 d, is resistant to degradation by trypsin and carboxypeptidase A, is heat-stable, and is produced by macrophages largely in the first 3 days of culture.

Synovial Fluid Stimulates the Proliferation of Rabbit Ligament

This study was designed to test the hypothesis that synovial fluid may be inhibitory to cell proliferation. The effects of bovine synovial fluid (SF) and hyaluronic acid (HA) on the proliferation of normal rabbit medial collateral ligament (MCL), anterior cruciate ligament (ACL), and MCL scar cells were therefore investigated. Cell lines established from rabbit tissues were plated, incubated, and allowed to attach before treatment with varying concentrations of SF, HA, and a balanced salt solution (BSS). The BSS group was added as a control to observe the effects of media dilution alone on cell proliferation. Cell numbers from each group were quantified at 24, 48, 72, and 96 hours. Results showed that for all cell types, cell proliferation during the log phase of growth was significantly stimulated by SF. Maximum stimulation occurred in 20% SF with stimulation decreasing at higher concentrations of SF. HA had virtually no effect on scar and ACL cells, and only a slight stimulatory effect on MCL cells. Media dilution had no effect on scar cells and began to inhibit cell proliferation of ACL and MCL cells only at high dilutions. These findings suggest that low concentrations of bovine SF stimulate proliferation of rabbit ligament and scar fibroblasts in vitro by a mechanism that appears not to involve HA. Even in high concentrations, SF was not inhibitory to proliferation. The implications of these findings to ligament healing and normal ligament physiology require further investigation.