Calcium-sensing receptor-mediated mitogen-activated protein kinase pathway improves the status of transplanted mouse embryonic stem cells in rats with acute myocardial infarction
Several studies have identified the critical role of calcium-sensing receptors (CaSRs) in cardiac ischaemia/reperfusion injury and cardiac hypertrophy and have demonstrated that CaSRs induce myocardial apoptosis by activating MAPKs. Using acute myocardial infarction rat models, we found that a combi...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2017-07, Vol.431 (1-2), p.151-160 |
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| creator | Sun, Jian Wei, Tao Bai, Shuzhi Zhao, Hongtao Liu, Xiaoqin Yu, Jinfeng Li, Li Song, Gaochen Luan, Hairong Xu, Changqing |
| description | Several studies have identified the critical role of calcium-sensing receptors (CaSRs) in cardiac ischaemia/reperfusion injury and cardiac hypertrophy and have demonstrated that CaSRs induce myocardial apoptosis by activating MAPKs. Using acute myocardial infarction rat models, we found that a combination therapy of CaSR inhibition and embryonic stem cell (ESC) transplantation after acute myocardial infarction (AMI) leads to a dramatic reduction in the infarct size; a significant increase in the maximum rising and falling rate (+dp/dtmax and −dp/dtmax, respectively) of left ventricular pressure; a significant decrease in left ventricular end-diastolic pressure; a significant decrease in the mRNA expression level of CaSR, Bax, Bcl-2, cleaved caspase-3, cleaved caspase-9, p-ERK, p-JNK and p-P38 protein together with apoptosis indexes in the C and E groups; and a significant decrease in cTnT levels as well as LDH and CK activity. These findings indicate that cardiac function could be enhanced significantly by combination therapy with CaSR inhibition and ESC transplantation; the effect was better than ESC transplantation alone, and the mechanism might be associated with a reduction in cell apoptosis via the inhibition of the MAPK pathway. Apoptosis could be reduced through CaSR, which regulates the MAPK pathway and apoptosis-related protein. Our study indicated that CaSR inhibitors have a pivotal role in the treatment of AMI. |
| doi_str_mv | 10.1007/s11010-017-2987-z |
| format | Article |
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Using acute myocardial infarction rat models, we found that a combination therapy of CaSR inhibition and embryonic stem cell (ESC) transplantation after acute myocardial infarction (AMI) leads to a dramatic reduction in the infarct size; a significant increase in the maximum rising and falling rate (+dp/dtmax and −dp/dtmax, respectively) of left ventricular pressure; a significant decrease in left ventricular end-diastolic pressure; a significant decrease in the mRNA expression level of CaSR, Bax, Bcl-2, cleaved caspase-3, cleaved caspase-9, p-ERK, p-JNK and p-P38 protein together with apoptosis indexes in the C and E groups; and a significant decrease in cTnT levels as well as LDH and CK activity. These findings indicate that cardiac function could be enhanced significantly by combination therapy with CaSR inhibition and ESC transplantation; the effect was better than ESC transplantation alone, and the mechanism might be associated with a reduction in cell apoptosis via the inhibition of the MAPK pathway. Apoptosis could be reduced through CaSR, which regulates the MAPK pathway and apoptosis-related protein. Our study indicated that CaSR inhibitors have a pivotal role in the treatment of AMI.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-017-2987-z</identifier><identifier>PMID: 28281186</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animal models ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins - biosynthesis ; BAX protein ; Bcl-2 protein ; Biochemistry ; Biomedical and Life Sciences ; Blood pressure ; Calcium ; Calcium-sensing receptors ; Cardiology ; Caspase ; Caspase-3 ; Caspase-9 ; Cell Line ; Detection ; Diastolic pressure ; Embryo cells ; Embryonic stem cells ; Extracellular signal-regulated kinase ; Falling ; Gene expression ; Gene Expression Regulation ; Heart ; Heart attack ; Heart attacks ; Heart diseases ; Heart hypertrophy ; Heterografts ; Hypertrophy ; Inhibitors ; Injuries ; Ischemia ; JNK protein ; Kinases ; Life Sciences ; Male ; MAP kinase ; MAP Kinase Signaling System ; Medical Biochemistry ; Mice ; Mitogens ; Mouse Embryonic Stem Cells - metabolism ; Mouse Embryonic Stem Cells - pathology ; Myocardial infarction ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial Infarction - therapy ; Oncology ; p38 Protein ; Protein kinase ; Protein kinases ; Proteins ; Rats ; Rats, Wistar ; Receptors ; Receptors, Calcium-Sensing - antagonists & inhibitors ; Receptors, Calcium-Sensing - metabolism ; Receptors, G-Protein-Coupled - antagonists & inhibitors ; Receptors, G-Protein-Coupled - metabolism ; Reperfusion ; RNA ; Rodents ; Stem Cell Transplantation ; Stem cells ; Therapy ; Transplantation ; Transplants & implants ; Ventricle</subject><ispartof>Molecular and cellular biochemistry, 2017-07, Vol.431 (1-2), p.151-160</ispartof><rights>Springer Science+Business Media New York 2017</rights><rights>COPYRIGHT 2017 Springer</rights><rights>Molecular and Cellular Biochemistry is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-a6b2e8a362b3e9298c48d71fae831374dfa2587def3638a2fff9d96ba1ce5d143</citedby><cites>FETCH-LOGICAL-c439t-a6b2e8a362b3e9298c48d71fae831374dfa2587def3638a2fff9d96ba1ce5d143</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-017-2987-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-017-2987-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28281186$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Jian</creatorcontrib><creatorcontrib>Wei, Tao</creatorcontrib><creatorcontrib>Bai, Shuzhi</creatorcontrib><creatorcontrib>Zhao, Hongtao</creatorcontrib><creatorcontrib>Liu, Xiaoqin</creatorcontrib><creatorcontrib>Yu, Jinfeng</creatorcontrib><creatorcontrib>Li, Li</creatorcontrib><creatorcontrib>Song, Gaochen</creatorcontrib><creatorcontrib>Luan, Hairong</creatorcontrib><creatorcontrib>Xu, Changqing</creatorcontrib><title>Calcium-sensing receptor-mediated mitogen-activated protein kinase pathway improves the status of transplanted mouse embryonic stem cells in rats with acute myocardial infarction</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Several studies have identified the critical role of calcium-sensing receptors (CaSRs) in cardiac ischaemia/reperfusion injury and cardiac hypertrophy and have demonstrated that CaSRs induce myocardial apoptosis by activating MAPKs. Using acute myocardial infarction rat models, we found that a combination therapy of CaSR inhibition and embryonic stem cell (ESC) transplantation after acute myocardial infarction (AMI) leads to a dramatic reduction in the infarct size; a significant increase in the maximum rising and falling rate (+dp/dtmax and −dp/dtmax, respectively) of left ventricular pressure; a significant decrease in left ventricular end-diastolic pressure; a significant decrease in the mRNA expression level of CaSR, Bax, Bcl-2, cleaved caspase-3, cleaved caspase-9, p-ERK, p-JNK and p-P38 protein together with apoptosis indexes in the C and E groups; and a significant decrease in cTnT levels as well as LDH and CK activity. These findings indicate that cardiac function could be enhanced significantly by combination therapy with CaSR inhibition and ESC transplantation; the effect was better than ESC transplantation alone, and the mechanism might be associated with a reduction in cell apoptosis via the inhibition of the MAPK pathway. Apoptosis could be reduced through CaSR, which regulates the MAPK pathway and apoptosis-related protein. Our study indicated that CaSR inhibitors have a pivotal role in the treatment of AMI.</description><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - biosynthesis</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Blood pressure</subject><subject>Calcium</subject><subject>Calcium-sensing receptors</subject><subject>Cardiology</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>Cell Line</subject><subject>Detection</subject><subject>Diastolic pressure</subject><subject>Embryo cells</subject><subject>Embryonic stem cells</subject><subject>Extracellular signal-regulated kinase</subject><subject>Falling</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Heart</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Heart hypertrophy</subject><subject>Heterografts</subject><subject>Hypertrophy</subject><subject>Inhibitors</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Male</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System</subject><subject>Medical Biochemistry</subject><subject>Mice</subject><subject>Mitogens</subject><subject>Mouse Embryonic Stem Cells - metabolism</subject><subject>Mouse Embryonic Stem Cells - pathology</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - therapy</subject><subject>Oncology</subject><subject>p38 Protein</subject><subject>Protein kinase</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors</subject><subject>Receptors, Calcium-Sensing - antagonists & inhibitors</subject><subject>Receptors, Calcium-Sensing - metabolism</subject><subject>Receptors, G-Protein-Coupled - antagonists & inhibitors</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Reperfusion</subject><subject>RNA</subject><subject>Rodents</subject><subject>Stem Cell Transplantation</subject><subject>Stem cells</subject><subject>Therapy</subject><subject>Transplantation</subject><subject>Transplants & implants</subject><subject>Ventricle</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1ks1u1DAUhSMEokPhAdggS2zYpNhJJraX1QgKUiU2sLbuONczLok92E6r6WPxhL3TKb8CZRHJ9ztH59qnql4KfiY4l2-zEFzwmgtZN1rJ-vZRtRBL2dadFvpxteAt57USUp5Uz3K-4gRzIZ5WJ41qlBCqX1TfVzBaP091xpB92LCEFnclpnrCwUPBgU2-xA2GGmzx1_cnuxQL-sC--gAZ2Q7K9gb2zE80uMbMyhZZLlDmzKJjJUHIuxHCvVmcSYHTOu1j8JYwnJjFccyMDBOUzG582TKwc0E27aOFRDlGmjpIlCCG59UTB2PGFw__0-rL-3efVx_qy08XH1fnl7XtWl1q6NcNKmj7Zt2ipvuxnRqkcICqFa3sBgfNUskBXdu3ChrnnB50vwZhcTmIrj2t3hx9aatvM-ZiJp8PUSEgbWGEkn2neS85oa__Qq_inAKlM0JzKYXu2uYXtYERDS0U6WrswdScd3rJNV_2iqizf1D0DTh5GwM6T-d_CMRRYFPMOaEzu-QnSHsjuDn0xBx7Yqgn5tATc0uaVw-B5zU99E_Fj2IQ0ByBTKOwwfTbRv91vQPJe8ze</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Sun, Jian</creator><creator>Wei, Tao</creator><creator>Bai, Shuzhi</creator><creator>Zhao, Hongtao</creator><creator>Liu, Xiaoqin</creator><creator>Yu, Jinfeng</creator><creator>Li, Li</creator><creator>Song, Gaochen</creator><creator>Luan, Hairong</creator><creator>Xu, Changqing</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20170701</creationdate><title>Calcium-sensing receptor-mediated mitogen-activated protein kinase pathway improves the status of transplanted mouse embryonic stem cells in rats with acute myocardial infarction</title><author>Sun, Jian ; Wei, Tao ; Bai, Shuzhi ; Zhao, Hongtao ; Liu, Xiaoqin ; Yu, Jinfeng ; Li, Li ; Song, Gaochen ; Luan, Hairong ; Xu, Changqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-a6b2e8a362b3e9298c48d71fae831374dfa2587def3638a2fff9d96ba1ce5d143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - biosynthesis</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Blood pressure</topic><topic>Calcium</topic><topic>Calcium-sensing receptors</topic><topic>Cardiology</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Caspase-9</topic><topic>Cell Line</topic><topic>Detection</topic><topic>Diastolic pressure</topic><topic>Embryo cells</topic><topic>Embryonic stem cells</topic><topic>Extracellular signal-regulated kinase</topic><topic>Falling</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Heart</topic><topic>Heart attack</topic><topic>Heart attacks</topic><topic>Heart diseases</topic><topic>Heart hypertrophy</topic><topic>Heterografts</topic><topic>Hypertrophy</topic><topic>Inhibitors</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Male</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System</topic><topic>Medical Biochemistry</topic><topic>Mice</topic><topic>Mitogens</topic><topic>Mouse Embryonic Stem Cells - 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Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Jian</au><au>Wei, Tao</au><au>Bai, Shuzhi</au><au>Zhao, Hongtao</au><au>Liu, Xiaoqin</au><au>Yu, Jinfeng</au><au>Li, Li</au><au>Song, Gaochen</au><au>Luan, Hairong</au><au>Xu, Changqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcium-sensing receptor-mediated mitogen-activated protein kinase pathway improves the status of transplanted mouse embryonic stem cells in rats with acute myocardial infarction</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>431</volume><issue>1-2</issue><spage>151</spage><epage>160</epage><pages>151-160</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Several studies have identified the critical role of calcium-sensing receptors (CaSRs) in cardiac ischaemia/reperfusion injury and cardiac hypertrophy and have demonstrated that CaSRs induce myocardial apoptosis by activating MAPKs. Using acute myocardial infarction rat models, we found that a combination therapy of CaSR inhibition and embryonic stem cell (ESC) transplantation after acute myocardial infarction (AMI) leads to a dramatic reduction in the infarct size; a significant increase in the maximum rising and falling rate (+dp/dtmax and −dp/dtmax, respectively) of left ventricular pressure; a significant decrease in left ventricular end-diastolic pressure; a significant decrease in the mRNA expression level of CaSR, Bax, Bcl-2, cleaved caspase-3, cleaved caspase-9, p-ERK, p-JNK and p-P38 protein together with apoptosis indexes in the C and E groups; and a significant decrease in cTnT levels as well as LDH and CK activity. These findings indicate that cardiac function could be enhanced significantly by combination therapy with CaSR inhibition and ESC transplantation; the effect was better than ESC transplantation alone, and the mechanism might be associated with a reduction in cell apoptosis via the inhibition of the MAPK pathway. Apoptosis could be reduced through CaSR, which regulates the MAPK pathway and apoptosis-related protein. Our study indicated that CaSR inhibitors have a pivotal role in the treatment of AMI.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28281186</pmid><doi>10.1007/s11010-017-2987-z</doi><tpages>10</tpages></addata></record> |
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| subjects | Animal models Animals Apoptosis Apoptosis Regulatory Proteins - biosynthesis BAX protein Bcl-2 protein Biochemistry Biomedical and Life Sciences Blood pressure Calcium Calcium-sensing receptors Cardiology Caspase Caspase-3 Caspase-9 Cell Line Detection Diastolic pressure Embryo cells Embryonic stem cells Extracellular signal-regulated kinase Falling Gene expression Gene Expression Regulation Heart Heart attack Heart attacks Heart diseases Heart hypertrophy Heterografts Hypertrophy Inhibitors Injuries Ischemia JNK protein Kinases Life Sciences Male MAP kinase MAP Kinase Signaling System Medical Biochemistry Mice Mitogens Mouse Embryonic Stem Cells - metabolism Mouse Embryonic Stem Cells - pathology Myocardial infarction Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial Infarction - therapy Oncology p38 Protein Protein kinase Protein kinases Proteins Rats Rats, Wistar Receptors Receptors, Calcium-Sensing - antagonists & inhibitors Receptors, Calcium-Sensing - metabolism Receptors, G-Protein-Coupled - antagonists & inhibitors Receptors, G-Protein-Coupled - metabolism Reperfusion RNA Rodents Stem Cell Transplantation Stem cells Therapy Transplantation Transplants & implants Ventricle |
| title | Calcium-sensing receptor-mediated mitogen-activated protein kinase pathway improves the status of transplanted mouse embryonic stem cells in rats with acute myocardial infarction |
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