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Bidirectional Ca2+ coupling of mitochondria with the endoplasmic reticulum and regulation of multimodal Ca2+ entries in rat brown adipocytes.
Am J Physiol Cell Physiol 2007; 292(2):C896-908AJ

Abstract

How the endoplasmic reticulum (ER) and mitochondria communicate with each other and how they regulate plasmalemmal Ca(2+) entry were studied in cultured rat brown adipocytes. Cytoplasmic Ca(2+) or Mg(2+) and mitochondrial membrane potential were measured by fluorometry. The sustained component of rises in cytoplasmic Ca(2+) concentration ([Ca(2+)](i)) produced by thapsigargin was abolished by removing extracellular Ca(2+), depressed by depleting extracellular Na(+), and enhanced by raising extracellular pH. FCCP, dinitrophenol, and rotenone caused bi- or triphasic rises in [Ca(2+)](i), in which the first phase was accompanied by mitochondrial depolarization. The FCCP-induced first phase was partially inhibited by oligomycin but not by ruthenium red, cyclosporine A, U-73122, a Ca(2+)-free EGTA solution, and an Na(+)-free solution. The FCCP-induced second phase paralleling mitochondrial repolarization was partially blocked by removing extracellular Ca(2+) and fully blocked by oligomycin but not by thapsigargin or an Na(+)-deficient solution, was accompanied by a rise in cytoplasmic Mg(2+) concentration, and was summated with a high pH-induced rise in [Ca(2+)](i), whereas the extracellular Ca(2+)-independent component was blocked by U-73122 and cyclopiazonic acid. The FCCP-induced third phase was blocked by removing Ca(2+) but not by thapsigargin, depressed by decreasing Na(+), and enhanced by raising pH. Cyclopiazonic acid-evoked rises in [Ca(2+)](i) in a Ca(2+)-free solution were depressed after FCCP actions. Thus mitochondrial uncoupling causes Ca(2+) release, activating Ca(2+) release from the ER and store-operated Ca(2+) entry, and directly elicits a novel plasmalemmal Ca(2+) entry, whereas Ca(2+) release from the ER activates Ca(2+) accumulation in, or release from, mitochondria, indicating bidirectional mitochondria-ER couplings in rat brown adipocytes.

Authors+Show Affiliations

Laboratory of Anatomy and Physiology, School of Nutritional Sciences, Nagoya Univ. of Arts and Sciences, 57 Takenoyama, Iwasaki-cho, Nissin, Aichi 470-0196, Japan. kubak@nuas.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16987997

Citation

Kuba, Masako, et al. "Bidirectional Ca2+ Coupling of Mitochondria With the Endoplasmic Reticulum and Regulation of Multimodal Ca2+ Entries in Rat Brown Adipocytes." American Journal of Physiology. Cell Physiology, vol. 292, no. 2, 2007, pp. C896-908.
Kuba M, Higure Y, Susaki H, et al. Bidirectional Ca2+ coupling of mitochondria with the endoplasmic reticulum and regulation of multimodal Ca2+ entries in rat brown adipocytes. Am J Physiol, Cell Physiol. 2007;292(2):C896-908.
Kuba, M., Higure, Y., Susaki, H., Hayato, R., & Kuba, K. (2007). Bidirectional Ca2+ coupling of mitochondria with the endoplasmic reticulum and regulation of multimodal Ca2+ entries in rat brown adipocytes. American Journal of Physiology. Cell Physiology, 292(2), pp. C896-908.
Kuba M, et al. Bidirectional Ca2+ Coupling of Mitochondria With the Endoplasmic Reticulum and Regulation of Multimodal Ca2+ Entries in Rat Brown Adipocytes. Am J Physiol, Cell Physiol. 2007;292(2):C896-908. PubMed PMID: 16987997.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bidirectional Ca2+ coupling of mitochondria with the endoplasmic reticulum and regulation of multimodal Ca2+ entries in rat brown adipocytes. AU - Kuba,Masako, AU - Higure,Yoko, AU - Susaki,Hisashi, AU - Hayato,Ryotaro, AU - Kuba,Kenji, Y1 - 2006/09/20/ PY - 2006/9/22/pubmed PY - 2007/4/6/medline PY - 2006/9/22/entrez SP - C896 EP - 908 JF - American journal of physiology. Cell physiology JO - Am. J. Physiol., Cell Physiol. VL - 292 IS - 2 N2 - How the endoplasmic reticulum (ER) and mitochondria communicate with each other and how they regulate plasmalemmal Ca(2+) entry were studied in cultured rat brown adipocytes. Cytoplasmic Ca(2+) or Mg(2+) and mitochondrial membrane potential were measured by fluorometry. The sustained component of rises in cytoplasmic Ca(2+) concentration ([Ca(2+)](i)) produced by thapsigargin was abolished by removing extracellular Ca(2+), depressed by depleting extracellular Na(+), and enhanced by raising extracellular pH. FCCP, dinitrophenol, and rotenone caused bi- or triphasic rises in [Ca(2+)](i), in which the first phase was accompanied by mitochondrial depolarization. The FCCP-induced first phase was partially inhibited by oligomycin but not by ruthenium red, cyclosporine A, U-73122, a Ca(2+)-free EGTA solution, and an Na(+)-free solution. The FCCP-induced second phase paralleling mitochondrial repolarization was partially blocked by removing extracellular Ca(2+) and fully blocked by oligomycin but not by thapsigargin or an Na(+)-deficient solution, was accompanied by a rise in cytoplasmic Mg(2+) concentration, and was summated with a high pH-induced rise in [Ca(2+)](i), whereas the extracellular Ca(2+)-independent component was blocked by U-73122 and cyclopiazonic acid. The FCCP-induced third phase was blocked by removing Ca(2+) but not by thapsigargin, depressed by decreasing Na(+), and enhanced by raising pH. Cyclopiazonic acid-evoked rises in [Ca(2+)](i) in a Ca(2+)-free solution were depressed after FCCP actions. Thus mitochondrial uncoupling causes Ca(2+) release, activating Ca(2+) release from the ER and store-operated Ca(2+) entry, and directly elicits a novel plasmalemmal Ca(2+) entry, whereas Ca(2+) release from the ER activates Ca(2+) accumulation in, or release from, mitochondria, indicating bidirectional mitochondria-ER couplings in rat brown adipocytes. SN - 0363-6143 UR - https://www.unboundmedicine.com/medline/citation/16987997/Bidirectional_Ca2+_coupling_of_mitochondria_with_the_endoplasmic_reticulum_and_regulation_of_multimodal_Ca2+_entries_in_rat_brown_adipocytes_ L2 - http://www.physiology.org/doi/full/10.1152/ajpcell.00649.2005?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -