17β2-Estradiol modifies diabetic wound healing by decreasing matrix metalloproteinase activity

David J. Pincus, Noor Kassira, Michael Gombosh, Mariana Berho, Marilyn Glassberg, Michael Karl, Sharon J. Elliot, Seth Thaller

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

Postmenopausal women are more susceptible to poor wound healing. This phenomenon can be reversed by estrogen replacement therapy in non-diabetic individuals. Postmenopausal women with type 2 diabetes are more susceptible to wound healing complications, potentially secondary to an estrogen deficiency. Few studies have examined the mechanism of action and effects of estrogens on diabetic wound healing in females. It appears that multiple factors influence delayed wound healing among individuals with diabetes including: an imbalance in cytokines, growth factors, extracellular matrix (ECM) turnover, and oxidant stress (OS). Estrogens have been shown to regulate the expression of genes important for extracellular matrix turnover, including collagen and matrix metalloproteinases (MMP). Methods. For this reason, the effects of 17β2-estradiol (E2) on MMP-2, MMP-13, and MMP-14 and estrogen receptor alpha and beta (ER-α and -β) expression in the wound tissue of estrogen-deficient female mice with established type 2 diabetes mellitus (C57BL/6J-m Leprdb/2+) were studied. Results. Topical E2 upregulates ER in wound tissue thereby improving and accelerating diabetic wound healing in estrogen deficient mice. Conclusion. The mechanism appears to decrease MMP-2, MMP-13, and MMP-14 mediated tissue matrix destruction and increasing collagen content.

Original languageEnglish (US)
Pages (from-to)171-178
Number of pages8
JournalWounds
Volume22
Issue number7
StatePublished - Jul 1 2010

ASJC Scopus subject areas

  • Surgery
  • Medical–Surgical

Fingerprint Dive into the research topics of '17β2-Estradiol modifies diabetic wound healing by decreasing matrix metalloproteinase activity'. Together they form a unique fingerprint.

  • Cite this