Contribution of TRPC Channels to Intracellular Ca2 + Dyshomeostasis in Smooth Muscle From mdx Mice

Frontiers in Physiology
José R LopezJosé A Adams

Abstract

Duchenne muscular dystrophy (DMD) is an irreversible muscle disease characterized by a progressive loss of muscle function, decreased ambulation, and ultimately death as a result of cardiac or respiratory failure. DMD is caused by the lack of dystrophin, a protein that is important for membrane stability and signaling in excitable cells. Although vascular smooth muscle cells (VSMCs) dysfunction occurs in many pathological conditions, little is known about vascular smooth muscle function in DMD. We have previously shown that striated muscle cells, as well as neurons isolated from dystrophic (mdx) mice have higher intracellular Ca2+ ([Ca2+]i) and Na+ ([Na+]i) concentrations and decreased cell viability in comparison with wild type (Wt). Experiments were carried out in isolated VSMCs from mdx (a murine model of DMD) and congenic C57BL/10SnJ Wt mice. We found elevated [Ca2+]i and [Na+]i in VSMCs from mdx mice compared to Wt. Exposure to 1-oleoyl-2-acetyl-sn-glycerol (OAG), a TRPC3 and TRPC6 channel activator, induced a greater elevation of [Ca2+]i and [Na+]i in mdx than Wt VSMCs. The OAG induced increases in [Ca2+]i could be abolished by either removal of extracellular Ca2+ or by SAR7334, a blocker of TRPC3 and TRPC 6 channels in b...Continue Reading

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Citations

Dec 15, 2020·The Journal of General Physiology·Aldo Meizoso-Huesca, Bradley S Launikonis
Apr 27, 2021·Frontiers in Physiology·Satvik MareeduGopal J Babu
May 14, 2021·International Journal of Immunopathology and Pharmacology·Guangyi BaWeitian Zhang
May 22, 2021·Frontiers in Physiology·Arkady UryashJose R Lopez

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