Essential role of Ca2+ release channels in angiotensin II-induced Ca2+ oscillations and mesangial cell contraction
Autor: | Ribao Wei, Bo Fu, Heping Cheng, Xiangmei Chen, Chaoliang Wei, Jianzhong Wang, Xueguang Zhang, Suozhu Shi, Quan Hong, Zhe Feng |
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Rok vydání: | 2006 |
Předmět: |
Male
medicine.medical_specialty Contraction (grammar) Thapsigargin Renal glomerulus Receptors Cytoplasmic and Nuclear chemistry.chemical_compound Internal medicine medicine calcium oscillations Animals Inositol 1 4 5-Trisphosphate Receptors Calcium Signaling Rats Wistar glomerular mesangial contraction Microscopy Confocal Phospholipase C Mesangial cell Chemistry Ryanodine receptor Angiotensin II 1 4 5-trisphosphate receptors Ryanodine Receptor Calcium Release Channel Rats Endocrinology Nephrology Mesangial Cells ryanodine receptors Biophysics Calcium Calcium Channels medicine.symptom Muscle Contraction Muscle contraction |
Zdroj: | Kidney International. 70:130-138 |
ISSN: | 0085-2538 |
DOI: | 10.1038/sj.ki.5000342 |
Popis: | The increased resistance of the glomerulus as a result of contractile dysfunction of mesangial cells (MCs) is associated with reduction of glomerular filtration rate and development of glomerulosclerosis. Evidences show MCs contraction changes with intracellular Ca(2+) concentration ([Ca(2+)](i)). Here, we explore the mechanism of angiotensin II (AngII)-induced Ca(2+) oscillations and MCs contraction. Primary MCs from 3-month-old and 28-month-old rats were used for detection of Ca(2+) oscillations and MC planar area with confocal microscopy. AngII could induce typical Ca(2+) oscillations and contraction of MCs. This process was abolished by thapsigargin, 2-aminoethoxydiphenyl borate, or 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphorylcholine, and partially inhibited by ryanodine, but could not be inhibited in the absence of extracellular Ca(2+). Ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate (InsP(3)) receptors displayed a strong colocalization, which may contribute to the amplification of Ca(2+) response. MLC(20) phosphorylation and MC planar area were associated with AngII-induced Ca(2+) oscillations. The frequency of Ca(2+) oscillations was dependent on the AngII concentration and correlated with the MCs' contractive extent, which could be attenuated by KN-93. The amplitude reduction of oscillations correlated with the decrease in aging-related contraction. In conclusion, [Ca(2+)](i) response of MCs to AngII is characterized by repetitive spikes through the following repetitive cycles: Ca(2+) release by phospholipase C -InsP(3) pathway, Ca(2+) amplification by Ca(2+)-activated RyRs and Ca(2+) reuptake by the endoplasmic reticulum. MCs contraction can be modulated by oscillations not only in an AngII-induced frequency-dependent mode but also in an aging-related, amplitude-dependent mode. |
Databáze: | OpenAIRE |
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