Downregulation of NLRP2 inhibits HUVEC viability by inhibiting the MAPK signaling pathway.

Abstract

Nucleotide-binding oligomerization domain (NOD)-like receptor proteins (NLRPs) are a subfamily of NOD-like receptors (NLRs) that mainly participate in innate immunity. Among the 14 NLRPs, studies on NLRP2 are few and mostly focus on its functions in reproduction and embryonic development. To the best of the authors' knowledge, there has been no research on the function of NLRP2 in human umbilical vein endothelial cells (HUVECs). The present study knockdown the expression of NLRP2 by transfecting a short interfering (si)RNA (siNLRP2) into HUVECs and investigating its effects on HUVECs. It was identified using a Cell Counting kit-8 assay that knockdown of NLRP2 can inhibit cell proliferation in HUVECs. The results of wound healing and Transwell assays indicated that migration and invasion were also suppressed by siNLRP2 transfection in HUVECs. Flow cytometry demonstrated that siNLRP2 induced cell cycle arrest and apoptosis in HUVECs. Western blot analysis revealed that the expression levels of cell cycle and apoptosis-associated proteins were markedly changed. In addition, knockdown of NLRP2 inhibited the mitogen-activated protein kinase (MAPK) signaling pathway by elevating extracellular signal-regulated kinase phosphorylation levels and reducing proto-oncogene serine/threonine-protein kinase expression. Taken together, it was concluded that NLRP2 served an important role in maintaining cell viability, proliferation and motility in HUVECs, mainly by promoting the MAPK signaling pathway.