Intracellular alkalinization induces cytosolic Ca2+ increases by inhibiting sarco/endoplasmic reticulum Ca2+-ATPase (SERCA)
| Autor: | Hon Cheung Lee, Sen Li, Baixia Hao, Peilin Yu, Yingying Lu, Jianbo Yue |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
ORAI1 Protein
lcsh:Medicine Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism Endoplasmic Reticulum Biochemistry Ion Channels chemistry.chemical_compound Mice Cytosol Molecular Cell Biology Inositol 1 4 5-Trisphosphate Receptors Signaling in Cellular Processes lcsh:Science Oxazoles Multidisciplinary Membrane Glycoproteins Voltage-dependent calcium channel Chemistry Ryanodine receptor ORAI1 Cytosol - metabolism Calcium - metabolism STIM1 Hydrogen-Ion Concentration Cellular Structures Signaling Cascades Cell biology Neoplasm Proteins Cytochemistry Research Article Signal Transduction SERCA Thapsigargin Macrocyclic Compounds Intracellular pH Green Fluorescent Proteins Signaling Pathways Endoplasmic Reticulum - metabolism Sarcoplasmic Reticulum Calcium-Transporting ATPases Animals Humans Stromal Interaction Molecule 1 Biology Endoplasmic reticulum Lentivirus lcsh:R Membrane Proteins Proteins Ryanodine Receptor Calcium Release Channel Calcium Channels - metabolism Cellular Neuroscience NIH 3T3 Cells Calcium lcsh:Q Calcium Channels HeLa Cells Neuroscience |
| Zdroj: | PLoS ONE, Vol 7, Iss 2, p e31905 (2012) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | 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. published_or_final_version |
| Databáze: | OpenAIRE |
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