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- W2765408510 abstract "Vascular resistance is a major determinant of BP and is controlled, in large part, by RhoA-dependent smooth muscle cell (SMC) contraction within small peripheral arterioles and previous studies from our lab indicate that GRAF3 is a critical regulator of RhoA in vascular SMC. The elevated contractile responses we observed in GRAF3 deficient vessels coupled with the hypertensive phenotype provided a mechanistic link for the hypertensive locus recently identified within the GRAF3 gene. On the basis of our previous findings that the RhoA signaling axis also controls SMC contractile gene expression and that GRAF3 expression was itself controlled by this pathway, we postulated that GRAF3 serves as an important counter-regulator of SMC phenotype. Indeed, our new findings presented herein indicate that GRAF3 expression acts as a pressure-sensitive rheostat to control vessel tone by both reducing calcium sensitivity and restraining expression of the SMC-specific contractile proteins that support this function. Collectively, these studies highlight the potential therapeutic value of GRAF3 in the control of human hypertension." @default.
- W2765408510 created "2017-11-10" @default.
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- W2765408510 date "2017-11-03" @default.
- W2765408510 modified "2023-09-26" @default.
- W2765408510 title "GRAF3 serves as a blood volume-sensitive rheostat to control smooth muscle contractility and blood pressure" @default.
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- W2765408510 doi "https://doi.org/10.1080/21541248.2017.1375602" @default.
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