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Role of PTEN in Hypoxic Pulmonary Vasoconstriction

Hypoxic pulmonary vasoconstricition (HPV) optimizes ventilation/perfusion matching in the lung, and critically depends on transient receptor potential canonical (TRPC) 6 activation and trafficking to caveolae. In endothelial cells, phosphatase and tensin homolog (PTEN) has been shown to serve as a scaffold for TRPC6, enabling cell surface expression of the channel and subsequent Ca2+ entry. Moreover, Rho kinase (ROCK) is known to phosphorylate PTEN and play a role in its localization in chemotaxing neutrophils. Hence, we hypothesized that the interaction between PTEN and TRPC6 in PASMC may be required for TRPC6 translocation to caveolae and an intact HPV response in a ROCK‐dependent manner.