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- W2335837243 abstract "β 2 -Spectrin is critical for integrating membrane and cytoskeletal domains in excitable and nonexcitable cells. The role of β 2 -spectrin for vertebrate function is illustrated by dysfunction of β 2 -spectrin-based pathways in disease. Recently, defects in β 2 -spectrin association with protein partner ankyrin-B were identified in congenital forms of human arrhythmia. However, the role of β 2 -spectrin in common forms of acquired heart failure and arrhythmia is unknown. We report that β 2 -spectrin protein levels are significantly altered in human cardiovascular disease as well as in large and small animal cardiovascular disease models. Specifically, β 2 -spectrin levels were decreased in atrial samples of patients with atrial fibrillation compared with tissue from patients in sinus rhythm. Furthermore, compared with left ventricular samples from nonfailing hearts, β 2 -spectrin levels were significantly decreased in left ventricle of ischemic- and nonischemic heart failure patients. Left ventricle samples of canine and murine heart failure models confirm reduced β 2 -spectrin protein levels. Mechanistically, we identify that β 2 -spectrin levels are tightly regulated by posttranslational mechanisms, namely Ca 2+ - and calpain-dependent proteases. Furthermore, consistent with this data, we observed Ca 2+ - and calpain-dependent loss of β 2 -spectrin downstream effector proteins, including ankyrin-B in heart. In summary, our findings illustrate that β 2 -spectrin and downstream molecules are regulated in multiple forms of cardiovascular disease via Ca 2+ - and calpain-dependent proteolysis." @default.
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- W2335837243 date "2016-06-01" @default.
- W2335837243 modified "2023-10-14" @default.
- W2335837243 title "Dysfunction of the β<sub>2</sub>-spectrin-based pathway in human heart failure" @default.
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- W2335837243 doi "https://doi.org/10.1152/ajpheart.00875.2015" @default.
- W2335837243 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4935521" @default.
- W2335837243 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27106045" @default.
- W2335837243 hasPublicationYear "2016" @default.
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