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Article: Intracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA)

TitleIntracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA)
Authors
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2012, v. 7 n. 2, article no. e31905 How to Cite?
AbstractIntracellular pH (pHi) and Ca(2+) regulate essentially all aspects of cellular activities. Their inter-relationship has not been mechanistically explored. In this study, we used bases and acetic acid to manipulate the pHi. We found that transient pHi rise induced by both organic and inorganic bases, but not acidification induced by acid, produced elevation of cytosolic Ca(2+). The sources of the Ca(2+) increase are from the endoplasmic reticulum (ER) Ca(2+) pools as well as from Ca(2+) influx. The store-mobilization component of the Ca(2+) increase induced by the pHi rise was not sensitive to antagonists for either IP(3)-receptors or ryanodine receptors, but was due to inhibition of the sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), leading to depletion of the ER Ca(2+) store. We further showed that the physiological consequence of depletion of the ER Ca(2+) store by pHi rise is the activation of store-operated channels (SOCs) of Orai1 and Stim1, leading to increased Ca(2+) influx. Taken together, our results indicate that intracellular alkalinization inhibits SERCA activity, similar to thapsigargin, thereby resulting in Ca(2+) leak from ER pools followed by Ca(2+) influx via SOCs.
Persistent Identifierhttp://hdl.handle.net/10722/171793
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Sen_US
dc.contributor.authorHao, Ben_US
dc.contributor.authorLu, Yen_US
dc.contributor.authorYu, Pen_US
dc.contributor.authorLee, HCen_US
dc.contributor.authorYue, Jen_US
dc.date.accessioned2012-10-30T06:17:09Z-
dc.date.available2012-10-30T06:17:09Z-
dc.date.issued2012en_US
dc.identifier.citationPLoS One, 2012, v. 7 n. 2, article no. e31905en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://hdl.handle.net/10722/171793-
dc.description.abstractIntracellular pH (pHi) and Ca(2+) regulate essentially all aspects of cellular activities. Their inter-relationship has not been mechanistically explored. In this study, we used bases and acetic acid to manipulate the pHi. We found that transient pHi rise induced by both organic and inorganic bases, but not acidification induced by acid, produced elevation of cytosolic Ca(2+). The sources of the Ca(2+) increase are from the endoplasmic reticulum (ER) Ca(2+) pools as well as from Ca(2+) influx. The store-mobilization component of the Ca(2+) increase induced by the pHi rise was not sensitive to antagonists for either IP(3)-receptors or ryanodine receptors, but was due to inhibition of the sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), leading to depletion of the ER Ca(2+) store. We further showed that the physiological consequence of depletion of the ER Ca(2+) store by pHi rise is the activation of store-operated channels (SOCs) of Orai1 and Stim1, leading to increased Ca(2+) influx. Taken together, our results indicate that intracellular alkalinization inhibits SERCA activity, similar to thapsigargin, thereby resulting in Ca(2+) leak from ER pools followed by Ca(2+) influx via SOCs.en_US
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_US
dc.relation.ispartofPLoS Oneen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCalcium - metabolism-
dc.subject.meshCalcium Channels - metabolism-
dc.subject.meshCytosol - metabolism-
dc.subject.meshEndoplasmic Reticulum - metabolism-
dc.subject.meshSarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism-
dc.titleIntracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA)en_US
dc.typeArticleen_US
dc.identifier.emailYu, P: ypljj@hku.hken_US
dc.identifier.emailLee, HC: leehc@hku.hk-
dc.identifier.emailYue, J: jyue@hku.hk-
dc.identifier.authorityYue, J=rp00286en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1371/journal.pone.0031905en_US
dc.identifier.pmid22384096-
dc.identifier.pmcidPMC3288054-
dc.identifier.scopuseid_2-s2.0-84863269135en_US
dc.identifier.hkuros208767-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84863269135&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume7en_US
dc.identifier.issue2, article no. e31905en_US
dc.identifier.isiWOS:000302918500045-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYue, J=7101875828en_US
dc.identifier.scopusauthoridLee, HC=40761849900en_US
dc.identifier.scopusauthoridYu, P=55034912300en_US
dc.identifier.scopusauthoridLu, Y=8240340800en_US
dc.identifier.scopusauthoridHao, B=55276400800en_US
dc.identifier.scopusauthoridLi, S=55277258400en_US

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