Magnesium inhibits the calcification of the extracellular matrix in tendon-derived stem cells via the ATP-P2R and mitochondrial pathways
Tendon calcification has been widely regarded by researchers to result from the osteogenic differentiation of Tendon-Derived Stem Cells (TDSCs) and ectopic mineralization caused by the calcification of cellular matrix. Recent studies have revealed a correlation between the Mg2+/Ca2+ balance and the...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2016-09, Vol.478 (1), p.314-322 |
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| description | Tendon calcification has been widely regarded by researchers to result from the osteogenic differentiation of Tendon-Derived Stem Cells (TDSCs) and ectopic mineralization caused by the calcification of cellular matrix. Recent studies have revealed a correlation between the Mg2+/Ca2+ balance and the degeneration or calcification of tendon tissues. Furthermore, the ATP–P2X/P2Y receptor pathway has been shown to play a decisive role in the process of calcification, with calcium exportation from mitochondria and calcium oscillations potentially representing the cohesive signal produced by this pathway. Our previous study demonstrated that matrix calcification is inhibited by magnesium. In this study, we examined the effects of extracellular Mg2+ on the deposition of calcium phosphate matrix and cellular pathways in TDSCs. The suppression of the export of calcium from mitochondria has also been detected. We found that a high concentration of extracellular Mg2+ ([Mg2+]e) inhibited the mineralization of the extracellular matrix in TDSCs and that 100 μM ATP reversed this inhibitory effect in vitro. In addition, the spontaneous release of ATP was inhibited by high [Mg2+]e levels. A high [Mg2+]e suppressed the expression of P2X4, P2X5 and P2X7 and activated the expression of P2Y1, P2Y2, P2Y4 and P2Y14. The interaction between Mg2+ and Ca2+ is therefore contradictory, Mg2+ inhibits mitochondrial calcium concentrations, meanwhile it reverses the opening of mPTP that is induced by Ca2+. JC-1 staining verified the protective effect of Mg2+ on mitochondrial membrane potential and the decrease induced by Ca2+. Taken together, these results indicate that high [Mg2+]e interferes with the expression of P2 receptors, resulting in decreased extracellular mineralization. The balance between Mg2+ and Ca2+ influences mitochondrial calcium exportation and provides another explanation for the mechanism underlying matrix calcification in TDSCs. |
| doi_str_mv | 10.1016/j.bbrc.2016.06.108 |
| format | Article |
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Recent studies have revealed a correlation between the Mg2+/Ca2+ balance and the degeneration or calcification of tendon tissues. Furthermore, the ATP–P2X/P2Y receptor pathway has been shown to play a decisive role in the process of calcification, with calcium exportation from mitochondria and calcium oscillations potentially representing the cohesive signal produced by this pathway. Our previous study demonstrated that matrix calcification is inhibited by magnesium. In this study, we examined the effects of extracellular Mg2+ on the deposition of calcium phosphate matrix and cellular pathways in TDSCs. The suppression of the export of calcium from mitochondria has also been detected. We found that a high concentration of extracellular Mg2+ ([Mg2+]e) inhibited the mineralization of the extracellular matrix in TDSCs and that 100 μM ATP reversed this inhibitory effect in vitro. In addition, the spontaneous release of ATP was inhibited by high [Mg2+]e levels. A high [Mg2+]e suppressed the expression of P2X4, P2X5 and P2X7 and activated the expression of P2Y1, P2Y2, P2Y4 and P2Y14. The interaction between Mg2+ and Ca2+ is therefore contradictory, Mg2+ inhibits mitochondrial calcium concentrations, meanwhile it reverses the opening of mPTP that is induced by Ca2+. JC-1 staining verified the protective effect of Mg2+ on mitochondrial membrane potential and the decrease induced by Ca2+. Taken together, these results indicate that high [Mg2+]e interferes with the expression of P2 receptors, resulting in decreased extracellular mineralization. The balance between Mg2+ and Ca2+ influences mitochondrial calcium exportation and provides another explanation for the mechanism underlying matrix calcification in TDSCs.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2016.06.108</identifier><identifier>PMID: 27402270</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>adenosine triphosphate ; Adenosine Triphosphate - metabolism ; Animals ; bone formation ; calcification ; Calcification, Physiologic - drug effects ; Calcification, Physiologic - physiology ; calcium ; calcium phosphates ; Cells, Cultured ; Dose-Response Relationship, Drug ; extracellular matrix ; Extracellular Matrix - drug effects ; Extracellular Matrix - metabolism ; Magnesium ; Magnesium - administration & dosage ; Male ; membrane potential ; mineralization ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; mitochondrial membrane ; P2 receptors ; protective effect ; Rats ; Rats, Sprague-Dawley ; receptors ; Signal Transduction - drug effects ; staining ; stem cells ; Stem Cells - cytology ; Stem Cells - drug effects ; Stem Cells - metabolism ; Tendon calcification ; Tendon-derived stem cells ; Tendons - cytology ; Tendons - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2016-09, Vol.478 (1), p.314-322</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-3af5ca627ae552cd49046cfd4e1a003b4e5edf478896765a207cdeb7baf531993</citedby><cites>FETCH-LOGICAL-c413t-3af5ca627ae552cd49046cfd4e1a003b4e5edf478896765a207cdeb7baf531993</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2016.06.108$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27402270$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yue, Jiaji</creatorcontrib><creatorcontrib>Jin, Shanzi</creatorcontrib><creatorcontrib>Li, Yaqiang</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Jiang, Wenwei</creatorcontrib><creatorcontrib>Yang, Chunxi</creatorcontrib><creatorcontrib>Du, Jiang</creatorcontrib><title>Magnesium inhibits the calcification of the extracellular matrix in tendon-derived stem cells via the ATP-P2R and mitochondrial pathways</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Tendon calcification has been widely regarded by researchers to result from the osteogenic differentiation of Tendon-Derived Stem Cells (TDSCs) and ectopic mineralization caused by the calcification of cellular matrix. Recent studies have revealed a correlation between the Mg2+/Ca2+ balance and the degeneration or calcification of tendon tissues. Furthermore, the ATP–P2X/P2Y receptor pathway has been shown to play a decisive role in the process of calcification, with calcium exportation from mitochondria and calcium oscillations potentially representing the cohesive signal produced by this pathway. Our previous study demonstrated that matrix calcification is inhibited by magnesium. In this study, we examined the effects of extracellular Mg2+ on the deposition of calcium phosphate matrix and cellular pathways in TDSCs. The suppression of the export of calcium from mitochondria has also been detected. We found that a high concentration of extracellular Mg2+ ([Mg2+]e) inhibited the mineralization of the extracellular matrix in TDSCs and that 100 μM ATP reversed this inhibitory effect in vitro. In addition, the spontaneous release of ATP was inhibited by high [Mg2+]e levels. A high [Mg2+]e suppressed the expression of P2X4, P2X5 and P2X7 and activated the expression of P2Y1, P2Y2, P2Y4 and P2Y14. The interaction between Mg2+ and Ca2+ is therefore contradictory, Mg2+ inhibits mitochondrial calcium concentrations, meanwhile it reverses the opening of mPTP that is induced by Ca2+. JC-1 staining verified the protective effect of Mg2+ on mitochondrial membrane potential and the decrease induced by Ca2+. Taken together, these results indicate that high [Mg2+]e interferes with the expression of P2 receptors, resulting in decreased extracellular mineralization. The balance between Mg2+ and Ca2+ influences mitochondrial calcium exportation and provides another explanation for the mechanism underlying matrix calcification in TDSCs.</description><subject>adenosine triphosphate</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>bone formation</subject><subject>calcification</subject><subject>Calcification, Physiologic - drug effects</subject><subject>Calcification, Physiologic - physiology</subject><subject>calcium</subject><subject>calcium phosphates</subject><subject>Cells, Cultured</subject><subject>Dose-Response Relationship, Drug</subject><subject>extracellular matrix</subject><subject>Extracellular Matrix - drug effects</subject><subject>Extracellular Matrix - metabolism</subject><subject>Magnesium</subject><subject>Magnesium - administration & dosage</subject><subject>Male</subject><subject>membrane potential</subject><subject>mineralization</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>mitochondrial membrane</subject><subject>P2 receptors</subject><subject>protective effect</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>receptors</subject><subject>Signal Transduction - drug effects</subject><subject>staining</subject><subject>stem cells</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - metabolism</subject><subject>Tendon calcification</subject><subject>Tendon-derived stem cells</subject><subject>Tendons - cytology</subject><subject>Tendons - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU9v1DAQxS0EotvCF-AAPnLJYjuJnUhcqqr8kYqooJW4WRN70vUqiRfbWdpv0I-N0y0cEacZPf3e02geIa84W3PG5bvtuuuCWYu8r5nMWvOErDhrWSE4q56SFWNMFqLlP47IcYxbxjivZPucHAlVMSEUW5H7L3AzYXTzSN20cZ1LkaYNUgODcb0zkJyfqO8fRLxNAQwOwzxAoCOk4G6zjSacrJ8Ki8Ht0dKYcKQLFunewYPz9OqyuBTfKEyWji55s_GTDQ4GuoO0-QV38QV51sMQ8eXjPCHXH86vzj4VF18_fj47vShMxctUlNDXBqRQgHUtjK1aVknT2wo5MFZ2FdZo-0o1TSuVrEEwZSx2qsu-krdteULeHnJ3wf-cMSY9urgcCxP6OWrecN40SjX8f9D84LoUMqPigJrgYwzY611wI4Q7zZleytJbvZSll7I0k1lrsun1Y_7cjWj_Wv60k4E3B6AHr-EmuKivvy8Jucm25lJk4v2BwPyyvcOgo3E4GbQuoEnaevevC34DkwuwYw</recordid><startdate>20160909</startdate><enddate>20160909</enddate><creator>Yue, Jiaji</creator><creator>Jin, Shanzi</creator><creator>Li, Yaqiang</creator><creator>Zhang, Li</creator><creator>Jiang, Wenwei</creator><creator>Yang, Chunxi</creator><creator>Du, Jiang</creator><general>Elsevier Inc</general><scope>FBQ</scope><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>7X8</scope><scope>7QP</scope></search><sort><creationdate>20160909</creationdate><title>Magnesium inhibits the calcification of the extracellular matrix in tendon-derived stem cells via the ATP-P2R and mitochondrial pathways</title><author>Yue, Jiaji ; Jin, Shanzi ; Li, Yaqiang ; Zhang, Li ; Jiang, Wenwei ; Yang, Chunxi ; Du, Jiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-3af5ca627ae552cd49046cfd4e1a003b4e5edf478896765a207cdeb7baf531993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>adenosine triphosphate</topic><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>bone formation</topic><topic>calcification</topic><topic>Calcification, Physiologic - drug effects</topic><topic>Calcification, Physiologic - physiology</topic><topic>calcium</topic><topic>calcium phosphates</topic><topic>Cells, Cultured</topic><topic>Dose-Response Relationship, Drug</topic><topic>extracellular matrix</topic><topic>Extracellular Matrix - drug effects</topic><topic>Extracellular Matrix - metabolism</topic><topic>Magnesium</topic><topic>Magnesium - administration & dosage</topic><topic>Male</topic><topic>membrane potential</topic><topic>mineralization</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>mitochondrial membrane</topic><topic>P2 receptors</topic><topic>protective effect</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>receptors</topic><topic>Signal Transduction - drug effects</topic><topic>staining</topic><topic>stem cells</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - metabolism</topic><topic>Tendon calcification</topic><topic>Tendon-derived stem cells</topic><topic>Tendons - cytology</topic><topic>Tendons - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yue, Jiaji</creatorcontrib><creatorcontrib>Jin, Shanzi</creatorcontrib><creatorcontrib>Li, Yaqiang</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Jiang, Wenwei</creatorcontrib><creatorcontrib>Yang, Chunxi</creatorcontrib><creatorcontrib>Du, Jiang</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Calcium & Calcified Tissue Abstracts</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yue, Jiaji</au><au>Jin, Shanzi</au><au>Li, Yaqiang</au><au>Zhang, Li</au><au>Jiang, Wenwei</au><au>Yang, Chunxi</au><au>Du, Jiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Magnesium inhibits the calcification of the extracellular matrix in tendon-derived stem cells via the ATP-P2R and mitochondrial pathways</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2016-09-09</date><risdate>2016</risdate><volume>478</volume><issue>1</issue><spage>314</spage><epage>322</epage><pages>314-322</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Tendon calcification has been widely regarded by researchers to result from the osteogenic differentiation of Tendon-Derived Stem Cells (TDSCs) and ectopic mineralization caused by the calcification of cellular matrix. Recent studies have revealed a correlation between the Mg2+/Ca2+ balance and the degeneration or calcification of tendon tissues. Furthermore, the ATP–P2X/P2Y receptor pathway has been shown to play a decisive role in the process of calcification, with calcium exportation from mitochondria and calcium oscillations potentially representing the cohesive signal produced by this pathway. Our previous study demonstrated that matrix calcification is inhibited by magnesium. In this study, we examined the effects of extracellular Mg2+ on the deposition of calcium phosphate matrix and cellular pathways in TDSCs. The suppression of the export of calcium from mitochondria has also been detected. We found that a high concentration of extracellular Mg2+ ([Mg2+]e) inhibited the mineralization of the extracellular matrix in TDSCs and that 100 μM ATP reversed this inhibitory effect in vitro. In addition, the spontaneous release of ATP was inhibited by high [Mg2+]e levels. A high [Mg2+]e suppressed the expression of P2X4, P2X5 and P2X7 and activated the expression of P2Y1, P2Y2, P2Y4 and P2Y14. The interaction between Mg2+ and Ca2+ is therefore contradictory, Mg2+ inhibits mitochondrial calcium concentrations, meanwhile it reverses the opening of mPTP that is induced by Ca2+. JC-1 staining verified the protective effect of Mg2+ on mitochondrial membrane potential and the decrease induced by Ca2+. Taken together, these results indicate that high [Mg2+]e interferes with the expression of P2 receptors, resulting in decreased extracellular mineralization. The balance between Mg2+ and Ca2+ influences mitochondrial calcium exportation and provides another explanation for the mechanism underlying matrix calcification in TDSCs.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27402270</pmid><doi>10.1016/j.bbrc.2016.06.108</doi><tpages>9</tpages></addata></record> |
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| subjects | adenosine triphosphate Adenosine Triphosphate - metabolism Animals bone formation calcification Calcification, Physiologic - drug effects Calcification, Physiologic - physiology calcium calcium phosphates Cells, Cultured Dose-Response Relationship, Drug extracellular matrix Extracellular Matrix - drug effects Extracellular Matrix - metabolism Magnesium Magnesium - administration & dosage Male membrane potential mineralization Mitochondria Mitochondria - drug effects Mitochondria - metabolism mitochondrial membrane P2 receptors protective effect Rats Rats, Sprague-Dawley receptors Signal Transduction - drug effects staining stem cells Stem Cells - cytology Stem Cells - drug effects Stem Cells - metabolism Tendon calcification Tendon-derived stem cells Tendons - cytology Tendons - metabolism |
| title | Magnesium inhibits the calcification of the extracellular matrix in tendon-derived stem cells via the ATP-P2R and mitochondrial pathways |
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