The role of CD44, hyaluronan and NHE1 in cardiac remodeling
Cardiac remodeling, characterized by excessive extracellular matrix (ECM) remodeling, predisposes the heart to failure if left unresolved. Understanding the signaling mechanisms involved in excessive extracellular matrix (ECM) remodeling is necessary to identify the means to regress the development...
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| Veröffentlicht in: | Life sciences (1973) 2018-09, Vol.209, p.197-201 |
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| creator | Suleiman, Muna Abdulrahman, Nabeel Yalcin, Huseyin Mraiche, Fatima |
| description | Cardiac remodeling, characterized by excessive extracellular matrix (ECM) remodeling, predisposes the heart to failure if left unresolved. Understanding the signaling mechanisms involved in excessive extracellular matrix (ECM) remodeling is necessary to identify the means to regress the development of cardiac remodeling and heart failure. Recently, hyaluronan (HA), a ubiquitously expressed glycosaminoglycan in the ECM, was shown to participate in tissue fibrosis and myofibroblast proliferation through interacting with its ubiquitously expressed cell-surface receptor, CD44. CD44 is a multifunctional transmembrane glycoprotein that serves as a cell-surface receptor for a number of ECM proteins. The mechanism by which the interaction between CD44-HA contributes to ECM and cardiac remodeling remains unknown. A previous study performed on a non-cardiac model showed that CD44-HA enhances Na+/H+ exchanger isoform-1 (NHE1) activity, causing ECM remodeling, HA metabolism and tumor invasion. Interestingly, NHE1 has been demonstrated to be involved in cardiac remodeling and myocardial fibrosis. In addition, it has previously been demonstrated that CD44 is upregulated in transgenic mouse hearts expressing active NHE-1. The role of CD44, HA and NHE1 and the cellular interplay of these factors in the ECM and cardiac remodeling is the focus of this review.
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| doi_str_mv | 10.1016/j.lfs.2018.08.009 |
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[Display omitted]</description><subject>Atrial Remodeling</subject><subject>Cardiac fibroblast</subject><subject>Cardiac hypertrophy</subject><subject>Cardiac remodeling</subject><subject>Cardiovascular system</subject><subject>CD44</subject><subject>CD44 antigen</subject><subject>Cell surface</subject><subject>Cells</subject><subject>Extracellular matrix</subject><subject>Extracellular matrix remodeling</subject><subject>Fibrosis</subject><subject>Glycoproteins</subject><subject>Glycosaminoglycans</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart Failure - physiopathology</subject><subject>Humans</subject><subject>Hyaluronan</subject><subject>Hyaluronan Receptors - metabolism</subject><subject>Hyaluronic acid</subject><subject>Hyaluronic Acid - metabolism</subject><subject>Metabolism</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Na+/H+-exchanging ATPase</subject><subject>NHE-1</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Sodium-Hydrogen Exchanger 1 - metabolism</subject><subject>TGF-β</subject><subject>Transgenic mice</subject><subject>Ventricular Remodeling</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rGzEQhkVpaFy3P6CXIOilh6wz-tiVRE7BSZuASS_pWcjSbCKzXiWSt5B_HxmnOfQQGBgGnvdleAj5xmDBgHVnm8XQlwUHphdQB8wHMmNamQY6wT6SGQCXjeDQHpPPpWwAoG2V-ESOBYA2XIgZOb97QJrTgDT1dHkp5Sl9eHbDlNPoRurGQG-vrxiNI_Uuh-g8zbhNAYc43n8hR70bCn593XPy5-fV3fK6Wf3-dbO8WDVegto1be-EUl5jqwKickFKvZbaGNYab0LopA6dCRxBGdWuVb2kgFZL1AZ5p8Sc_Dj0Pub0NGHZ2W0sHofBjZimYjnojneMKVbR7_-hmzTlsX5nOWNaVIqbSrED5XMqJWNvH3PcuvxsGdi9Wbux1azdm7VQB_aZk9fmab3F8Jb4p7IC5wcAq4q_EbMtPuLoMcSMfmdDiu_UvwAa8YTA</recordid><startdate>20180915</startdate><enddate>20180915</enddate><creator>Suleiman, Muna</creator><creator>Abdulrahman, Nabeel</creator><creator>Yalcin, Huseyin</creator><creator>Mraiche, Fatima</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6188-1145</orcidid></search><sort><creationdate>20180915</creationdate><title>The role of CD44, hyaluronan and NHE1 in cardiac remodeling</title><author>Suleiman, Muna ; Abdulrahman, Nabeel ; Yalcin, Huseyin ; Mraiche, Fatima</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c407t-5fa377c8e57dee7ad448b4899159c9dd648d69d2e07975b78d6430584e89e2673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Atrial Remodeling</topic><topic>Cardiac fibroblast</topic><topic>Cardiac hypertrophy</topic><topic>Cardiac remodeling</topic><topic>Cardiovascular system</topic><topic>CD44</topic><topic>CD44 antigen</topic><topic>Cell surface</topic><topic>Cells</topic><topic>Extracellular matrix</topic><topic>Extracellular matrix remodeling</topic><topic>Fibrosis</topic><topic>Glycoproteins</topic><topic>Glycosaminoglycans</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Heart Failure - physiopathology</topic><topic>Humans</topic><topic>Hyaluronan</topic><topic>Hyaluronan Receptors - metabolism</topic><topic>Hyaluronic acid</topic><topic>Hyaluronic Acid - metabolism</topic><topic>Metabolism</topic><topic>Myocytes, Cardiac - cytology</topic><topic>Myocytes, Cardiac - physiology</topic><topic>Na+/H+-exchanging ATPase</topic><topic>NHE-1</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Sodium-Hydrogen Exchanger 1 - metabolism</topic><topic>TGF-β</topic><topic>Transgenic mice</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Suleiman, Muna</creatorcontrib><creatorcontrib>Abdulrahman, Nabeel</creatorcontrib><creatorcontrib>Yalcin, Huseyin</creatorcontrib><creatorcontrib>Mraiche, Fatima</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Suleiman, Muna</au><au>Abdulrahman, Nabeel</au><au>Yalcin, Huseyin</au><au>Mraiche, Fatima</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of CD44, hyaluronan and NHE1 in cardiac remodeling</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2018-09-15</date><risdate>2018</risdate><volume>209</volume><spage>197</spage><epage>201</epage><pages>197-201</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Cardiac remodeling, characterized by excessive extracellular matrix (ECM) remodeling, predisposes the heart to failure if left unresolved. Understanding the signaling mechanisms involved in excessive extracellular matrix (ECM) remodeling is necessary to identify the means to regress the development of cardiac remodeling and heart failure. Recently, hyaluronan (HA), a ubiquitously expressed glycosaminoglycan in the ECM, was shown to participate in tissue fibrosis and myofibroblast proliferation through interacting with its ubiquitously expressed cell-surface receptor, CD44. CD44 is a multifunctional transmembrane glycoprotein that serves as a cell-surface receptor for a number of ECM proteins. The mechanism by which the interaction between CD44-HA contributes to ECM and cardiac remodeling remains unknown. A previous study performed on a non-cardiac model showed that CD44-HA enhances Na+/H+ exchanger isoform-1 (NHE1) activity, causing ECM remodeling, HA metabolism and tumor invasion. Interestingly, NHE1 has been demonstrated to be involved in cardiac remodeling and myocardial fibrosis. In addition, it has previously been demonstrated that CD44 is upregulated in transgenic mouse hearts expressing active NHE-1. The role of CD44, HA and NHE1 and the cellular interplay of these factors in the ECM and cardiac remodeling is the focus of this review.
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| subjects | Atrial Remodeling Cardiac fibroblast Cardiac hypertrophy Cardiac remodeling Cardiovascular system CD44 CD44 antigen Cell surface Cells Extracellular matrix Extracellular matrix remodeling Fibrosis Glycoproteins Glycosaminoglycans Heart Heart diseases Heart failure Heart Failure - physiopathology Humans Hyaluronan Hyaluronan Receptors - metabolism Hyaluronic acid Hyaluronic Acid - metabolism Metabolism Myocytes, Cardiac - cytology Myocytes, Cardiac - physiology Na+/H+-exchanging ATPase NHE-1 Proteins Rodents Signal Transduction Sodium-Hydrogen Exchanger 1 - metabolism TGF-β Transgenic mice Ventricular Remodeling |
| title | The role of CD44, hyaluronan and NHE1 in cardiac remodeling |
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