Pathways of [Ca2+]irise evoked by angiotensin II in MDCK renal tubular cells
| Autor: | Pochuen Shieh, Kuang-Chung Ko, Daih-Huang Kuo, Chung-Pin Liu, Chung-Ren Jan, Chiang-Ting Chou, Ni-Na Chiang, Hong-Tai Chang, Jin-Shiung Cheng, Wei-Zhe Liang, Ru-Fang Wu |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
medicine.medical_specialty
Thapsigargin Phospholipase C Chemistry Endoplasmic reticulum Cell Biology Phospholipase Biochemistry Angiotensin II Cytosol chemistry.chemical_compound Endocrinology Internal medicine cardiovascular system medicine Extracellular Molecular Biology hormones hormone substitutes and hormone antagonists |
| Zdroj: | Journal of Receptors and Signal Transduction. 33:380-386 |
| ISSN: | 1532-4281 1079-9893 |
| Popis: | The effect of angiotensin II (Ang II) on cytosolic Ca2+ concentrations ([Ca2+]i) in MDCK renal tubular cells was explored. The Ca2+-sensitive fluorescent dye fura-2 was applied to measure [Ca2+]i. Ang II at concentrations of 5–40 µM induced a [Ca2+]i rise in a concentration-dependent manner. The response was reduced partly by removing Ca2+. Ang II evoked store-operated Ca2+ entry that was inhibited by La3+ and Gd3+. In the absence of extracellular Ca2+, incubation with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) or thapsigargin abolished Ang II-induced Ca2+ release. Inhibition of phospholipase C with U73122 abolished Ang II-induced [Ca2+]i rise. Three Ang II analogues [(ASN1,VAL5)-Ang II acetate, (SAR1,THR8)-Ang II acetate, (VAL5)-Ang II acetate] failed to induce a [Ca2+]i rise. Together, in MDCK cells, Ang II induced a [Ca2+]i rise via Ca2+ entry through store-operated Ca2+ channels and phospholipase C-dependent Ca2+ release from the endoplasmic reticulum. Mo... |
| Databáze: | OpenAIRE |
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