Delayed healing and induction of secretory leukocyte protease inhibitor in polycystic ovary syndrome rat skin wounds

Abstract

Abstract. Secretory leukocyte protease inhibitor (SLPI) and estrogen promote wound healing through a decrease in the excessive inflammatory response, accelerating re-epithelialization and increasing the amount of collagen deposition. The excessive administration of estradiol valerate (EV) using hormonal therapy decreases the concentration of estrogen abruptly and induces the polycystic ovary syndrome (PCOS). In this study, the PCOS rat skin wound area was wider than that of the normal groups and the rate of keratinocyte migration in PCOS was lower than the normal group. The numbers of inflammatory cells and macrophages recruited in the PCOS group were larger than that of the normal group. More collagen was deposited in the healing area of the normal group than in the PCOS group. The level of SLPI expression was higher in the PCOS group than the normal group after wounding, with the exception of the epithelium. On the other hand, mRNA and protein expression levels of transforming growth factor-β1 (TGF-β1) were lower in the PCOS group than in the normal group. Matrix metalloproteinase-2 (MMP-2) and MMP-9 levels in the PCOS group were significantly lower than that of the normal group. Therefore, increased SLPI in PCOS skin wounds may help prevent an excessive inflammatory response and aberrant collagen deposition but not are sufficient to accelerate PCOS skin wound healing, suggesting that SLPI may act as a local rather than a systemic modulating molecule in PCOS rat skin wounds.

Impaired healing of cutaneous wound in a <i>Trpv1</i> deficient mouse

“…TRPV1 in neutrophils from patients of polycystic ovary syndrome (PCOS) might be associated with calcium-entry dependent neutrophilic activation and release of pro-inflammatory cytokines [ 52 ]. Moreover, re-epithelialization of the rat skin in the PCOS model was delayed with increased inflammation and collagen deposition [ 53 ]. Other report implies that TRPV1 involves in migration of neutrophils via leukotriene B4 receptor (LTB4) activation [ 54 ].…”