Article ; Online: TRPM7 is involved in angiotensin II induced cardiac fibrosis development by mediating calcium and magnesium influx.
2014 Volume 55, Issue 5, Page(s) 252–260
Abstract: ... both calcium and magnesium changes in cardiac fibroblasts which contribute to fibrosis progress. This study ... TRPM7 expression in CFs, and 2-APB (TRPM7 inhibitor), inhibited Ang II-induced CTGF, α-SMA expression ... Cardiac fibrosis is involved in a lot of cardiovascular pathological processes. Cardiac fibrosis ...
Abstract | Cardiac fibrosis is involved in a lot of cardiovascular pathological processes. Cardiac fibrosis can block conduction, cause hypoxia, strengthen myocardial stiffness, create electrical heterogeneity, and hamper systolic ejection, which is associated with the development of arrhythmia, heart failure and sudden cardiac death. Besides the initial stimulating factors, the cardiac fibroblasts (CFs) are the principal responsible cells in the fibrogenesis cascade of events. TRPM7, a member of the TRPM (Melastatin) subfamily, is a non-selective cation channel, which permeates both Ca(2+) and Mg(2+). Here we demonstrated TRPM7 expression in CFs, and 2-APB (TRPM7 inhibitor), inhibited Ang II-induced CTGF, α-SMA expression and CFs proliferation. Besides, knocking down TRPM7 by shRNA, we proved that TRPM7 mediated both calcium and magnesium changes in cardiac fibroblasts which contribute to fibrosis progress. This study suggested that TRPM7 should play a pivotal role in cardiac fibroblast functions associated to cardiac fibrosis development. |
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MeSH term(s) | Actins/metabolism ; Angiotensin II/pharmacology ; Animals ; Boron Compounds/pharmacology ; Calcium/metabolism ; Cell Proliferation/drug effects ; Cells, Cultured ; Connective Tissue Growth Factor/metabolism ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Down-Regulation/drug effects ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibrosis/chemically induced ; Fibrosis/metabolism ; Fibrosis/pathology ; Magnesium/metabolism ; Male ; NFATC Transcription Factors/metabolism ; Nerve Tissue Proteins/metabolism ; RNA Interference ; RNA, Small Interfering/metabolism ; Rats ; Rats, Sprague-Dawley ; TRPM Cation Channels/antagonists & inhibitors ; TRPM Cation Channels/genetics ; TRPM Cation Channels/metabolism | |||||
Chemical Substances | Actins ; Boron Compounds ; CCN2 protein, rat ; Cdkn1b protein, rat ; NFATC Transcription Factors ; Nerve Tissue Proteins ; Nfatc4 protein, rat ; RNA, Small Interfering ; TRPM Cation Channels ; smooth muscle actin, rat ; Angiotensin II (11128-99-7) ; Connective Tissue Growth Factor (139568-91-5) ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; 2-aminoethoxydiphenyl borate (E4ES684O93) ; Trpm7 protein, rat (EC 2.7.11.1) ; Magnesium (I38ZP9992A) ; Calcium (SY7Q814VUP) | |||||
Language | English | |||||
Publishing date | 2014-03-11 | |||||
Publishing country | Netherlands | |||||
Document type | Journal Article ; Research Support, Non-U.S. Gov't | |||||
ZDB-ID | 757687-0 | |||||
ISSN | 1532-1991 ; 0143-4160 | |||||
ISSN (online) | 1532-1991 | |||||
ISSN | 0143-4160 | |||||
DOI | 10.1016/j.ceca.2014.02.019 | |||||
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Database | MEDical Literature Analysis and Retrieval System OnLINE |
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