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Aquaporin 1 (AQP1) Elevates cMyc and Cyclin D1 via β‐Catenin in Pulmonary Arterial Smooth Muscle Cells (PASMCs)

Pulmonary hypertension is a severe pulmonary vascular disease characterized by functional and structural changes in the vessels. During development of hypoxic pulmonary hypertension, primary features of remodeling in distal small pulmonary arteries include PASMC proliferation and migration. Formerly, we showed that hypoxia increased the expression of a water channel, AQP1, which mediates PASMC proliferation and migration by increasing β‐catenin protein levels. β‐catenin is a dual function protein that may interact with AQP1 in certain cell types and activates the transcription of crucial target genes related to cell migration and proliferation. Thus, we determined whether the AQP1 C‐terminal tail was required for AQP1 to increase β‐catenin levels in PASMCs and, if so, whether known β‐catenin target genes, such as c‐myc and cyclin D1, were also elevated. Primary cultured rat distal PASMCs were harvested and infected with adenoviral constructs expressing wild‐type AQP1 (AdWT), AQP1 lacking the C‐terminal tail (AdCT), or green fluorescent protein (AdGFP), as a control for infection. Compared to AdGFP cells, infection with AdWT, but not AdCT, increased β‐catenin protein and the mRNA and protein expression of c‐myc and cyclin D1. Moreover, knockdown of β‐catenin in PASMCs infected with AdWT prevented the AQP1‐induced increase in proliferation and migration.