Biphasic Regulation of HMG-CoA Reductase Expression and Activity During Wound Healing and Its Functional Role in the Control of Keratinocyte Angiogenic and Proliferative Responses

    April 2008 in “ Journal of Biological Chemistry ”
    Dana Schiefelbein, Itamar Goren, Beate Fißlthaler, Helmut Schmidt, Gerd Geißlinger, Josef Pfeilschifter, Stefan L. Frank
    TLDR HMG-CoA reductase is crucial for skin wound healing by regulating keratinocyte growth and blood vessel formation.
    This study examined the role of HMG-CoA reductase (HMGR) in skin wound healing in mice, revealing a biphasic increase in HMGR expression and activity with peaks at days 3 and 13 post-injury. Keratinocytes at wound margins were identified as a source of HMGR expression. In vitro, epidermal growth factor (EGF), transforming growth factor (TGF)-α, and insulin co-induced HMGR activity and VEGF expression in keratinocytes. Simvastatin inhibited insulin-induced VEGF expression and keratinocyte proliferation, effects reversible by mevalonate. In vivo, simvastatin reduced VEGF expression and disrupted keratinocyte proliferation, highlighting HMGR's role in keratinocyte angiogenic and proliferative responses during wound healing.
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