Key result
Phosphorylation of Serine 727 in TMEM16A by CaMKIIγ inhibits TMEM16A Ca2+-activated chloride channel activity and promotes angiotensin II-induced basilar arterial smooth muscle cell proliferation.
Serine 727 phosphorylation in TMEM16A by CaMKIIγ provides a novel mechanism for regulating TMEM16A CaCC activity and Ang II-induced basilar arterial smooth muscle cell proliferation in hypertensive cerebrovascular remodeling.
Hypothesis-generating for CaMKIIγ-TMEM16A regulation in vascular remodeling; clinical relevance in hypertension remains undetermined.
BACKGROUND: -activated chloride channels (CaCCs) and mediates basilar arterial smooth muscle cell (BASMC) proliferation in hypertensive cerebrovascular remodeling. CaMKII is a negative regulator of CaCC, and four CaMKII isoforms (α, β, γ and δ) are expressed in vasculature; however, it is unknown which and how CaMKII isoforms affect TMEM16A-associated CaCC and BASMC proliferation. METHODS AND RESULTS: in basilar artery proliferative remodeling in Ang II-infused mice. CONCLUSIONS: Serine 727 phosphorylation in TMEM16A by CaMKIIγ provides a new mechanism for regulating TMEM16A CaCC activity and Ang II-induced BASMC proliferation.
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Lin et al. (2017) studied Cerebrovascular remodeling. CaMKIIγ overexpression and TMEM16A mutation vs. Control / Wild-type was evaluated. Phosphorylation of Serine 727 in TMEM16A by CaMKIIγ inhibits TMEM16A Ca2+-activated chloride channel activity and promotes angiotensin II-induced basilar arterial smooth muscle cell proliferation.
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