Delayed healing and induction of secretory leukocyte protease inhibitor             in polycystic ovary syndrome rat skin wounds.
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.
Department of Oral Histology and Developmental Biology, School of Dentistry, Chosun University, Gwangju 501-759, Republic of Korea.
Soon-Jeong
SJ
Jeong
Sung-Shin
SS
Kim
Chun-Sik
CS
Bae
Jin-Ju
JJ
Park
Baik-Dong
BD
Choi
Guanlin
G
Wang
Myung-Ju
MJ
Jung
Hyun-Sun
HS
Jang
Byung-Ock
BO
Kim
Do-Seon
DS
Lim
Young-Sik
YS
Cho
Moon-Jin
MJ
Jeong
D000818:Animals; D002465:Cell Movement; D003094:Collagen / Q000378:metabolism; D004967:Estrogens / Q000097:blood; D005260:Female; D015603:Keratinocytes / Q000378:metabolism; D008264:Macrophages / Q000276:immunology; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000235:genetics / Q000378:metabolism*; D012867:Skin / Q000293:injuries* / Q000378:metabolism* / Q000473:pathology; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism; D014945:Wound Healing / Q000235:genetics
D004967:Estrogens; D053481:Secretory Leukocyte Peptidase Inhibitor; D053773:Transforming Growth Factor beta1; D003094:Collagen; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9