Upregulated expression of @entity19148 , TRPC6, and XXXX contributes to the transition of pulmonary arterial smooth muscle cells from a contractile to proliferative phenotype.

@entity1 @entity712 @entity120 @entity8577 @entity6980 @entity42801 @entity141 @entity204 @entity19148
@entity120 ( @entity120 ) is a progressive disease that, if left untreated, eventually leads to @entity712 and @entity204 . @entity8577 (PAP) in @entity1 with @entity120 is mainly caused by an increase in pulmonary vascular resistance (PVR). Sustained vasoconstriction and excessive @entity6980 are two major causes for elevated PVR in @entity1 with @entity120 . @entity6980 is mediated by increased proliferation of pulmonary arterial smooth muscle cells (PASMC) due to PASMC dedifferentiation from a contractile or quiescent phenotype to a proliferative or synthetic phenotype. Increased cytosolic @entity141 concentration ([ @entity141 ]cyt) in PASMC is a key stimulus for cell proliferation and this phenotypic transition. Voltage-dependent @entity141 entry (VDCE) and store-operated @entity141 entry (SOCE) are important mechanisms for controlling [ @entity141 ]cyt. Stromal interacting molecule proteins (e.g., @entity19148 ) and @entity42801 both contribute to SOCE and we have previously shown that @entity19148 and @entity42801 , specifically, are upregulated in PASMC from @entity1 with idiopathic @entity120 and from animals with @entity120 in comparison to normal controls. In this study, we show that @entity19148 and @entity42801 are upregulated in proliferating PASMC compared with contractile phenotype of PASMC. Additionally, a switch in @entity141 regulation is observed in correlation with a phenotypic transition from contractile PASMC to proliferative PASMC. PASMC in a contractile phenotype or state have increased VDCE, while in the proliferative phenotype or state PASMC have increased SOCE. The data from this study indicate that upregulation of @entity19148 and @entity42801 is involved in the phenotypic transition of PASMC from a contractile state to a proliferative state; the enhanced SOCE due to upregulation of @entity19148 and @entity42801 plays an important role in PASMC proliferation.
