Involvement of capacitive calcium entry and calcium store refilling in osteoclastic survival and bone resorption process
Bone resorption is closely dependent on osteoclastic survival and osteoclast apoptotic cell death could represent a key step at the end of this process. In order to precise the possible role of calcium movement in osteoclastic cell death, we investigated whether intracellular calcium store replenish...
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| Veröffentlicht in: | Cell calcium (Edinburgh) 2003-08, Vol.34 (2), p.169-175 |
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| creator | Mentaverri, R Kamel, S Brazier, M |
| description | Bone resorption is closely dependent on osteoclastic survival and osteoclast apoptotic cell death could represent a key step at the end of this process. In order to precise the possible role of calcium movement in osteoclastic cell death, we investigated whether intracellular calcium store replenishment and capacitive calcium entry (CCE) are involved in osteoclastic survival and bone resorption. We demonstrate that (i). thapsigargin, a sarco-endoplasmic reticulum calcium ATPase pump (SERCA) blocker, decreases both osteoclastic survival and bone resorption process, (ii). 2-aminoethoxydiphenyl borate (2-APB) and SKF-96365, two store-operated channel (SOC) blockers, dramatically decrease osteoclastic survival and bone resorption and (iii). culture in calcium-free medium and thapsigargin exposure synergically inhibit osteoclastic survival which falls dramatically to a value close to 0% (P |
| doi_str_mv | 10.1016/s0143-4160(03)00080-0 |
| format | Article |
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In order to precise the possible role of calcium movement in osteoclastic cell death, we investigated whether intracellular calcium store replenishment and capacitive calcium entry (CCE) are involved in osteoclastic survival and bone resorption. We demonstrate that (i). thapsigargin, a sarco-endoplasmic reticulum calcium ATPase pump (SERCA) blocker, decreases both osteoclastic survival and bone resorption process, (ii). 2-aminoethoxydiphenyl borate (2-APB) and SKF-96365, two store-operated channel (SOC) blockers, dramatically decrease osteoclastic survival and bone resorption and (iii). culture in calcium-free medium and thapsigargin exposure synergically inhibit osteoclastic survival which falls dramatically to a value close to 0% (P<0.001). Inversely, osteoclastic survival increases significantly when thapsigargin-treated cells are cultured in the presence of 20mM calcium, suggesting that increasing extracellular calcium concentration stimulates osteoclasts survival when the filling of intracellular stores is prevented. Taken together, our data strongly suggest that in osteoclasts, calcium movements between cellular compartments involved in the regulation of calcium signalling, such as calcium stores refilling and CCE, are closely associated to the regulation of osteoclast survival and bone resorption.</description><identifier>ISSN: 0143-4160</identifier><identifier>DOI: 10.1016/s0143-4160(03)00080-0</identifier><identifier>PMID: 12810059</identifier><language>eng</language><publisher>Netherlands</publisher><subject>Animals ; Bone Resorption - metabolism ; Calcium - metabolism ; Calcium Signaling ; Caspase 1 - metabolism ; Cell Survival - drug effects ; Cells, Cultured ; DNA Fragmentation - drug effects ; Osteoclasts - metabolism ; Rabbits ; Thapsigargin - pharmacology</subject><ispartof>Cell calcium (Edinburgh), 2003-08, Vol.34 (2), p.169-175</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-90104a0a56a5f624ead61fb68eb438403c3a68b8dcf57921ff658e22e16f4edf3</citedby><cites>FETCH-LOGICAL-c402t-90104a0a56a5f624ead61fb68eb438403c3a68b8dcf57921ff658e22e16f4edf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12810059$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mentaverri, R</creatorcontrib><creatorcontrib>Kamel, S</creatorcontrib><creatorcontrib>Brazier, M</creatorcontrib><title>Involvement of capacitive calcium entry and calcium store refilling in osteoclastic survival and bone resorption process</title><title>Cell calcium (Edinburgh)</title><addtitle>Cell Calcium</addtitle><description>Bone resorption is closely dependent on osteoclastic survival and osteoclast apoptotic cell death could represent a key step at the end of this process. In order to precise the possible role of calcium movement in osteoclastic cell death, we investigated whether intracellular calcium store replenishment and capacitive calcium entry (CCE) are involved in osteoclastic survival and bone resorption. We demonstrate that (i). thapsigargin, a sarco-endoplasmic reticulum calcium ATPase pump (SERCA) blocker, decreases both osteoclastic survival and bone resorption process, (ii). 2-aminoethoxydiphenyl borate (2-APB) and SKF-96365, two store-operated channel (SOC) blockers, dramatically decrease osteoclastic survival and bone resorption and (iii). culture in calcium-free medium and thapsigargin exposure synergically inhibit osteoclastic survival which falls dramatically to a value close to 0% (P<0.001). Inversely, osteoclastic survival increases significantly when thapsigargin-treated cells are cultured in the presence of 20mM calcium, suggesting that increasing extracellular calcium concentration stimulates osteoclasts survival when the filling of intracellular stores is prevented. Taken together, our data strongly suggest that in osteoclasts, calcium movements between cellular compartments involved in the regulation of calcium signalling, such as calcium stores refilling and CCE, are closely associated to the regulation of osteoclast survival and bone resorption.</description><subject>Animals</subject><subject>Bone Resorption - metabolism</subject><subject>Calcium - metabolism</subject><subject>Calcium Signaling</subject><subject>Caspase 1 - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>DNA Fragmentation - drug effects</subject><subject>Osteoclasts - metabolism</subject><subject>Rabbits</subject><subject>Thapsigargin - pharmacology</subject><issn>0143-4160</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUbtOxDAQdAHicfAJIFcIisA6dnxOiRAvCYkCqC3HWSMjJz7sJIK_JwcnKKl2NTuzI80QcsTgnAGTFxmY4IVgEk6BnwGAggK2yN4vvEv2c36bDzVfsh2yy0rFAKp6j3zc91MME3bYDzQ6as3KWD_4Cec1WD92dL6kT2r69hfJQ0xIEzofgu9fqe9pzANGG0wevKV5TJOfTPgWNbFfc3NMq8HHnq5StJjzAdl2JmQ83MwFebm5fr66Kx4eb--vLh8KK6AcihoYCAOmkqZyshRoWslcIxU2gisB3HIjVaNa66plXTLnZKWwLJFJJ7B1fEFOfv7Ovu8j5kF3PlsMwfQYx6yXnFc1U-W_RKaWtZK1mInVD9GmmPOcgl4l35n0qRnodR_6aR28XgevgevvPuZlQY43BmPTYfun2pTBvwDF2osB</recordid><startdate>200308</startdate><enddate>200308</enddate><creator>Mentaverri, R</creator><creator>Kamel, S</creator><creator>Brazier, M</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7X8</scope></search><sort><creationdate>200308</creationdate><title>Involvement of capacitive calcium entry and calcium store refilling in osteoclastic survival and bone resorption process</title><author>Mentaverri, R ; Kamel, S ; Brazier, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-90104a0a56a5f624ead61fb68eb438403c3a68b8dcf57921ff658e22e16f4edf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Bone Resorption - metabolism</topic><topic>Calcium - metabolism</topic><topic>Calcium Signaling</topic><topic>Caspase 1 - metabolism</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>DNA Fragmentation - drug effects</topic><topic>Osteoclasts - metabolism</topic><topic>Rabbits</topic><topic>Thapsigargin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mentaverri, R</creatorcontrib><creatorcontrib>Kamel, S</creatorcontrib><creatorcontrib>Brazier, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell calcium (Edinburgh)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mentaverri, R</au><au>Kamel, S</au><au>Brazier, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of capacitive calcium entry and calcium store refilling in osteoclastic survival and bone resorption process</atitle><jtitle>Cell calcium (Edinburgh)</jtitle><addtitle>Cell Calcium</addtitle><date>2003-08</date><risdate>2003</risdate><volume>34</volume><issue>2</issue><spage>169</spage><epage>175</epage><pages>169-175</pages><issn>0143-4160</issn><abstract>Bone resorption is closely dependent on osteoclastic survival and osteoclast apoptotic cell death could represent a key step at the end of this process. In order to precise the possible role of calcium movement in osteoclastic cell death, we investigated whether intracellular calcium store replenishment and capacitive calcium entry (CCE) are involved in osteoclastic survival and bone resorption. We demonstrate that (i). thapsigargin, a sarco-endoplasmic reticulum calcium ATPase pump (SERCA) blocker, decreases both osteoclastic survival and bone resorption process, (ii). 2-aminoethoxydiphenyl borate (2-APB) and SKF-96365, two store-operated channel (SOC) blockers, dramatically decrease osteoclastic survival and bone resorption and (iii). culture in calcium-free medium and thapsigargin exposure synergically inhibit osteoclastic survival which falls dramatically to a value close to 0% (P<0.001). Inversely, osteoclastic survival increases significantly when thapsigargin-treated cells are cultured in the presence of 20mM calcium, suggesting that increasing extracellular calcium concentration stimulates osteoclasts survival when the filling of intracellular stores is prevented. Taken together, our data strongly suggest that in osteoclasts, calcium movements between cellular compartments involved in the regulation of calcium signalling, such as calcium stores refilling and CCE, are closely associated to the regulation of osteoclast survival and bone resorption.</abstract><cop>Netherlands</cop><pmid>12810059</pmid><doi>10.1016/s0143-4160(03)00080-0</doi><tpages>7</tpages></addata></record> |
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| ispartof | Cell calcium (Edinburgh), 2003-08, Vol.34 (2), p.169-175 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Animals Bone Resorption - metabolism Calcium - metabolism Calcium Signaling Caspase 1 - metabolism Cell Survival - drug effects Cells, Cultured DNA Fragmentation - drug effects Osteoclasts - metabolism Rabbits Thapsigargin - pharmacology |
| title | Involvement of capacitive calcium entry and calcium store refilling in osteoclastic survival and bone resorption process |
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