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Article: Intracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA)
Title | Intracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) |
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Authors | |
Issue Date | 2012 |
Publisher | Public 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? |
Abstract | Intracellular 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 Identifier | http://hdl.handle.net/10722/171793 |
ISSN | 2023 Impact Factor: 2.9 2023 SCImago Journal Rankings: 0.839 |
PubMed Central ID | |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Li, S | en_US |
dc.contributor.author | Hao, B | en_US |
dc.contributor.author | Lu, Y | en_US |
dc.contributor.author | Yu, P | en_US |
dc.contributor.author | Lee, HC | en_US |
dc.contributor.author | Yue, J | en_US |
dc.date.accessioned | 2012-10-30T06:17:09Z | - |
dc.date.available | 2012-10-30T06:17:09Z | - |
dc.date.issued | 2012 | en_US |
dc.identifier.citation | PLoS One, 2012, v. 7 n. 2, article no. e31905 | en_US |
dc.identifier.issn | 1932-6203 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171793 | - |
dc.description.abstract | Intracellular 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.language | eng | en_US |
dc.publisher | Public Library of Science. The Journal's web site is located at http://www.plosone.org/home.action | en_US |
dc.relation.ispartof | PLoS ONE | en_US |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject.mesh | Calcium - metabolism | - |
dc.subject.mesh | Calcium Channels - metabolism | - |
dc.subject.mesh | Cytosol - metabolism | - |
dc.subject.mesh | Endoplasmic Reticulum - metabolism | - |
dc.subject.mesh | Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism | - |
dc.title | Intracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) | en_US |
dc.type | Article | en_US |
dc.identifier.email | Yu, P: ypljj@hku.hk | en_US |
dc.identifier.email | Lee, HC: leehc@hku.hk | - |
dc.identifier.email | Yue, J: jyue@hku.hk | - |
dc.identifier.authority | Yue, J=rp00286 | en_US |
dc.description.nature | published_or_final_version | en_US |
dc.identifier.doi | 10.1371/journal.pone.0031905 | en_US |
dc.identifier.pmid | 22384096 | - |
dc.identifier.pmcid | PMC3288054 | - |
dc.identifier.scopus | eid_2-s2.0-84863269135 | en_US |
dc.identifier.hkuros | 208767 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-84863269135&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 7 | en_US |
dc.identifier.issue | 2, article no. e31905 | en_US |
dc.identifier.isi | WOS:000302918500045 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Yue, J=7101875828 | en_US |
dc.identifier.scopusauthorid | Lee, HC=40761849900 | en_US |
dc.identifier.scopusauthorid | Yu, P=55034912300 | en_US |
dc.identifier.scopusauthorid | Lu, Y=8240340800 | en_US |
dc.identifier.scopusauthorid | Hao, B=55276400800 | en_US |
dc.identifier.scopusauthorid | Li, S=55277258400 | en_US |
dc.identifier.issnl | 1932-6203 | - |