The human hypertrophic scar undergoes hyperplasia and regression during progression. This study aimed to investigate whether fibroblasts in scar tissue undergo biological changes during the formation and regression of human hypertrophic scar. Using 32 scar samples, we measured collagen production by Masson's staining and the expression levels of transforming growth factor (TGF)-β1 and vascular endothelial growth factor (VEGF) by immunohistochemistry. In addition, fibroblasts from scar tissue were isolated and cultured, and total RNA was extracted for measurement of TGF-β1, VEGF and collagen transcript levels by reverse transcription-polymerase chain reaction (RT-PCR). Masson's staining showed that the number of fibroblasts and microvessels increased gradually in early and proliferative scars but decreased in regressive scars. Immunohistochemistry revealed that the expression of TGF-β1 and VEGF increased in early scars, peaked in proliferative scars and decreased in regressive scars. Moreover, the expression of TGF-β1, VEGF, collagen I and collagen III mRNAs also increased in early and proliferative scars and decreased significantly in regressive scars. Dynamic changes in fibroblast biology correlated with the formation and progression of hypertrophic scar.

Besides regulating glucose levels, insulin has been reported to participate actively in many other functions such as modulating inflammatory reaction. In this study we investigated how insulin application topically would effort the diabetic wound healing process. We found that the excessive expression of insulin degrading enzyme in diabetic skin led to the insufficient insulin level in diabetic skin during the wound healing, which ultimately reduced the recovery rate of diabetic wounds. We confirmed the topical insulin application could reverse the impaired inflammation reaction in diabetic wound environment and promote diabetic wounds healing. Our study revealed that insulin promoted neutrophils apoptosis and following triggered macrophages phenotype polarization. Both in vivo and in vitro studies verified that insulin reestablished the damaged neutrophils phagocytosis function and promoted the process of phagocytosis induced apoptosis of neutrophils. Furthermore, we found that the insulin treatment also promoted macrophages efferocytosis of the apoptosed neutrophils and thus induced macrophages polarized from M1 to M2. In conclusion, our studies proved that the exogenous application of insulin could improve the diabetic wound healing via the normalization of inflammatory response.

Hypoxia is dynamic in scar tissue and is possibly correlated with scar formation and regression.

To investigate the characteristics of diabetic patients with foot ulcers, their health-related quality of life (HRQoL), and the link between them. The study population included 131 consecutive patients presenting in a diabetic foot clinic with a new foot ulcer between December 1, 2011, and May 1, 2012. The authors collected sociodemographic data, foot and ulcer characteristics using the Wagner Grade, and HRQoL (using the SF-36 Scale) information; 54.2% of the patients were in Wagner 2 or Wagner 3 categories. In all the 8 SF-36 subscales and in the SF-36 summary scales, the patients with diabetic foot ulcer had significantly poorer HRQoL than the general population in China (P < .01). Their Wagner Grade had negative correlation with all the SF-36 subscales and the summary scales (P < .05). In conclusion, new diabetic foot ulcers were already in poor condition when patients first visited the diabetic foot clinic. Concomitantly, patients had worse HRQoL compared with the general population. More effective interventions are needed to improve their self-care level and HRQoL.