Hypoxia is a condition found in disease states and during injury and often results in a lack of endothelial cell proliferation. This and perlecan's role as endorepellin prompted one study into the nature of perlecan expression regulation by endothelial cells during hypoxic conditions. Under hypoxic conditions, this study found that perlecan expression by rat cardiac microvascular endothelial cells was decreased sixty-one percent compared to normal controls. The contention of this paper is that perlecan downregulation leads to a loss of FAK activation and thus less ERK signaling, leading to decreased cell proliferation. It does seem counterintuitive that endothelial cells would proliferate less quickly due to loss of perlecan and its endorepellin subunit. It could be that these endothelial cells merely downregulated transcription of many genes in response to hypoxic conditions. In another study, hypoxia led to induction of genes associated with apoptosis and cell death, but repression of genes was not limited to proteins associated with a specific pathway. When T84 intestinal epithelial cells are exposed to hypoxic conditions for 24 hours a significant increase in perlecan mRNA and protein production occurs. They relate this to the fact that many genes elevated in response to hypoxia contain a cAMP response element (CRE) in their promoter, as does pln. This difference between endothelial cells from the study in 2007 and the epithelial cell studied in these experiments is indicative of how varied the regulatory mechanisms of perlecan may be in different cell types.