MURC deficiency in smooth muscle attenuates pulmonary hypertension

Naohiko Nakanishi, Takehiro Ogata, Daisuke Naito, Kotaro Miyagawa, Takuya Taniguchi, Tetsuro Hamaoka, Naoki Maruyama, Takeru Kasahara, Masahiro Nishi, Satoaki Matoba and Tomomi Ueyama ()
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Naohiko Nakanishi: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Takehiro Ogata: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Daisuke Naito: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Kotaro Miyagawa: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Takuya Taniguchi: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Tetsuro Hamaoka: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Naoki Maruyama: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Takeru Kasahara: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Masahiro Nishi: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Satoaki Matoba: Graduate School of Medical Science, Kyoto Prefectural University of Medicine
Tomomi Ueyama: Graduate School of Medical Science, Kyoto Prefectural University of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Emerging evidence suggests that caveolin-1 (Cav1) is associated with pulmonary arterial hypertension. MURC (also called Cavin-4) is a member of the cavin family, which regulates caveolar formation and functions together with caveolins. Here, we show that hypoxia increased Murc mRNA expression in the mouse lung, and that Murc-null mice exhibited attenuation of hypoxia-induced pulmonary hypertension (PH) accompanied by reduced ROCK activity in the lung. Conditional knockout mice lacking Murc in smooth muscle also resist hypoxia-induced PH. MURC regulates the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) through Rho/ROCK signalling. Cav1 suppresses RhoA activity in PASMCs, which is reversed by MURC. MURC binds to Cav1 and inhibits the association of Cav1 with the active form of Gα13, resulting in the facilitated association of the active form of Gα13 with p115RhoGEF. These results reveal that MURC has a function in the development of PH through modulating Rho/ROCK signalling.

Date: 2016
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DOI: 10.1038/ncomms12417

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