Roles of transient receptor potential canonical (TRPC) channels and reverse-mode Na+/Ca2+ exchanger on cell proliferation in human cardiac fibroblasts: Effects of transforming growth factor β1
| Autor: | Yumiko Yamamoto, Fumitaka Nakamura, Issei Komuro, Tomofumi Tanaka, Kenichi Ikeda, Toshiaki Nakajima, Nami Takano, Hironobu Kikuchi, Gaku Oguri, Toshihiro Morita |
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| Rok vydání: | 2013 |
| Předmět: |
Thapsigargin
Physiology Phloroglucinol Biology Sodium-Calcium Exchanger Cell Line TRPC6 Diglycerides Transforming Growth Factor beta1 chemistry.chemical_compound medicine Humans Calcium Signaling RNA Messenger Enzyme Inhibitors RNA Small Interfering Fibroblast Molecular Biology TRPC Cell Proliferation TRPC Cation Channels Terpenes Cell growth Angiotensin II Thiourea Cell Cycle Checkpoints Cell Biology Fibroblasts Cell biology medicine.anatomical_structure chemistry Calcium RNA Interference Intracellular Transforming growth factor |
| Zdroj: | Cell Calcium. 54:213-225 |
| ISSN: | 0143-4160 |
| DOI: | 10.1016/j.ceca.2013.06.005 |
| Popis: | Expression of transient receptor potential canonical channels (TRPC) and the effects of transforming growth factor-β1 (TGF-β1) on Ca2+ signals and fibroblast proliferation were investigated in human cardiac fibroblasts. The conventional and quantitative real-time RT-PCR, western blot, immunocytochemical analysis, and intracellular Ca2+ concentration [Ca2+]i measurement were applied. Cell proliferation and cell cycle progression were assessed using MTT assays and fluorescence activated cell sorting. Human cardiac fibroblasts have the expression of TRPC1,3,4,6 mRNA and proteins. 1-oleoyl-2-acetyl-sn-glycerol (OAG) and thapsigargin induced extracellular Ca(2+)-mediated [Ca2+]i rise. siRNA for knock down of TRPC6 reduced OAG-induced Ca2+ entry. Hyperforin as well as angiotensin II (Ang II) induced Ca2+ entry. KB-R7943, a reverse-mode Na+/Ca2+ exchanger (NCX) inhibitor, and/or replacement of Na+ with NMDG+ inhibited thapsigargin-, OAG- and Ang II-induced Ca2+ entry. Treatment with TGF-β1 increased thapsigargin-, OAG- and Ang II-induced Ca2+ entry with an enhancement of TRPC1,6 protein expression, suppressed by KB-R7943. TGF-β1 and AngII promoted cell cycle progression from G0/G1 to S/G2/M and cell proliferation. A decrease of the extracellular Ca2+ and KB-R7943 suppressed it. Human cardiac fibroblasts contain several TRPC-mediated Ca2+ influx pathways, which activate the reverse-mode NCX. TGF-β1 enhances the Ca2+ influx pathways requiring Ca2+ signals for its effect on fibroblast proliferation. |
| Databáze: | OpenAIRE |
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