The anoxic fibroblast response is an early-stage wound healing program

When fibroblasts experience anoxia, a cellular program is initiated which results in stepwise activation of an endogenous SVL30 retroelement, metabolic adaptation to reliance on glycolysis, protease secretion, and endonuclease induction. This response is reversible and occurs with no reduction in cellular viability. Examination of experimental wounds reveals that this same response is physiologically activated during the early phase of wound healing when near-anoxic conditions prevail and wound debridement predominates. Procathepsin D has been identified as one of three major anoxia-inducible secretory proteins; its secretion is the result of altered routing within the cell, with no apparent change in the amount of the protein synthesized. A delayed cellular contractile response occurs approximately 1 week after fibroblasts experience as little as 16 hr of anoxia; this response appears to contribute to wound contraction.