CADM1 isoforms differentially regulate human mast cell survival and homotypic adhesion
Cell adhesion molecule 1 (CADM1), expressed by human lung mast cells (HLMCs), mediates their adhesion to airway smooth muscle (ASM), and contributes to ASM-dependent HLMC proliferation and survival. CADM1 is expressed in alternatively spliced isoforms, but those present in HLMCs and their function a...
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description | Cell adhesion molecule 1 (CADM1), expressed by human lung mast cells (HLMCs), mediates their adhesion to airway smooth muscle (ASM), and contributes to ASM-dependent HLMC proliferation and survival. CADM1 is expressed in alternatively spliced isoforms, but those present in HLMCs and their function are not known. We cloned three functional and one cryptic non-functional isoform with alternative splicing between exons 7/11 and 1/2, respectively, from HLMCs and human MC lines (HMC-1 and LAD2). Differentiated HLMCs and LAD2 cells expressed the functional isoform SP4 containing exons 7/8/11 (~80% of clones), as well as SP1 (exons 7/8/9/11) and a novel SP6 (exons 7/8/9/10/11). In contrast, immature HMC-1 cells expressed only functional SP4. SP4 overexpression in HMC-1 cells and HLMCs augmented homotypic adhesion to a greater extent than SP1 in various conditions. In contrast, CADM1 downregulation abolished homotypic adhesion, indicating that CADM1 is the sole receptor mediating mast cell aggregation. CADM1-mediated adhesion was enhanced by the presence of cell survival factors. SP1 overexpression in HMC-1 cells compromised survival compared to SP4 overexpression or control. CADM1 downregulation resulted in reduced viability and decreased expression of the pro-survival protein Mcl-1
L
, but not Blc-2 or Bcl-X
L
, and increased caspase-3/7 activity in both HMC-1 cells and HLMCs. This coincided with decreased basal Kit levels in HLMCs. In summary, human MCs express multiple CADM1 isoforms which exhibit differential regulation of survival and homotypic adhesion. The most highly expressed SP4 isoform is likely to contribute to MC aggregation and longevity in mastocytosis, and augment the pathophysiology of allergic diseases. |
doi_str_mv | 10.1007/s00018-012-0948-y |
format | Article |
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L
, but not Blc-2 or Bcl-X
L
, and increased caspase-3/7 activity in both HMC-1 cells and HLMCs. This coincided with decreased basal Kit levels in HLMCs. In summary, human MCs express multiple CADM1 isoforms which exhibit differential regulation of survival and homotypic adhesion. The most highly expressed SP4 isoform is likely to contribute to MC aggregation and longevity in mastocytosis, and augment the pathophysiology of allergic diseases.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-012-0948-y</identifier><identifier>PMID: 22438059</identifier><language>eng</language><publisher>Basel: SP Birkhäuser Verlag Basel</publisher><subject>Adhesion ; Allergies ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Blotting, Western ; Cell Adhesion ; Cell adhesion & migration ; Cell Adhesion Molecule-1 ; Cell Adhesion Molecules - metabolism ; Cell Aggregation ; Cell Biology ; Cell Survival ; Cells, Cultured ; Humans ; Immunoglobulins - metabolism ; Leukemia, Mast-Cell - metabolism ; Leukemia, Mast-Cell - pathology ; Life Sciences ; Lung - cytology ; Lung - metabolism ; Lungs ; Mast Cells - cytology ; Mast Cells - metabolism ; Mast-Cell Sarcoma - metabolism ; Mast-Cell Sarcoma - pathology ; Molecular biology ; Protein Isoforms ; Real-Time Polymerase Chain Reaction ; Research Article ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Signal transduction ; Survival</subject><ispartof>Cellular and molecular life sciences : CMLS, 2012-08, Vol.69 (16), p.2751-2764</ispartof><rights>The Author(s) 2012</rights><rights>Springer Basel AG 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c584t-a61c1154246e03224bbc2ec0459b0900fb86de4c8e8a30d2adbcdb9de859363b3</citedby><cites>FETCH-LOGICAL-c584t-a61c1154246e03224bbc2ec0459b0900fb86de4c8e8a30d2adbcdb9de859363b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3400039/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3400039/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,41493,42562,51324,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22438059$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moiseeva, Elena P.</creatorcontrib><creatorcontrib>Leyland, Mark L.</creatorcontrib><creatorcontrib>Bradding, Peter</creatorcontrib><title>CADM1 isoforms differentially regulate human mast cell survival and homotypic adhesion</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell. Mol. Life Sci</addtitle><addtitle>Cell Mol Life Sci</addtitle><description>Cell adhesion molecule 1 (CADM1), expressed by human lung mast cells (HLMCs), mediates their adhesion to airway smooth muscle (ASM), and contributes to ASM-dependent HLMC proliferation and survival. CADM1 is expressed in alternatively spliced isoforms, but those present in HLMCs and their function are not known. We cloned three functional and one cryptic non-functional isoform with alternative splicing between exons 7/11 and 1/2, respectively, from HLMCs and human MC lines (HMC-1 and LAD2). Differentiated HLMCs and LAD2 cells expressed the functional isoform SP4 containing exons 7/8/11 (~80% of clones), as well as SP1 (exons 7/8/9/11) and a novel SP6 (exons 7/8/9/10/11). In contrast, immature HMC-1 cells expressed only functional SP4. SP4 overexpression in HMC-1 cells and HLMCs augmented homotypic adhesion to a greater extent than SP1 in various conditions. In contrast, CADM1 downregulation abolished homotypic adhesion, indicating that CADM1 is the sole receptor mediating mast cell aggregation. CADM1-mediated adhesion was enhanced by the presence of cell survival factors. SP1 overexpression in HMC-1 cells compromised survival compared to SP4 overexpression or control. CADM1 downregulation resulted in reduced viability and decreased expression of the pro-survival protein Mcl-1
L
, but not Blc-2 or Bcl-X
L
, and increased caspase-3/7 activity in both HMC-1 cells and HLMCs. This coincided with decreased basal Kit levels in HLMCs. In summary, human MCs express multiple CADM1 isoforms which exhibit differential regulation of survival and homotypic adhesion. The most highly expressed SP4 isoform is likely to contribute to MC aggregation and longevity in mastocytosis, and augment the pathophysiology of allergic diseases.</description><subject>Adhesion</subject><subject>Allergies</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blotting, Western</subject><subject>Cell Adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion Molecule-1</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cell Aggregation</subject><subject>Cell Biology</subject><subject>Cell Survival</subject><subject>Cells, Cultured</subject><subject>Humans</subject><subject>Immunoglobulins - metabolism</subject><subject>Leukemia, Mast-Cell - metabolism</subject><subject>Leukemia, Mast-Cell - pathology</subject><subject>Life Sciences</subject><subject>Lung - cytology</subject><subject>Lung - metabolism</subject><subject>Lungs</subject><subject>Mast Cells - cytology</subject><subject>Mast Cells - metabolism</subject><subject>Mast-Cell Sarcoma - metabolism</subject><subject>Mast-Cell Sarcoma - pathology</subject><subject>Molecular biology</subject><subject>Protein Isoforms</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Research Article</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Signal transduction</subject><subject>Survival</subject><issn>1420-682X</issn><issn>1420-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kUtv1DAUhS0EoqXwA9ggS2zYBK4fSZwNUjW8KrXqBhA7y7FvZlwl8WAnI-Xf42iGqlRiZUv3u8fn-BDymsF7BlB_SADAVAGMF9BIVSxPyDmTHIoGavb0dK8U_3VGXqR0l-FS8eo5OeNcCgVlc05-bi4_3TDqU-hCHBJ1vusw4jh50_cLjbidezMh3c2DGelg0kQt9j1Nczz4g-mpGR3dhSFMy95batwOkw_jS_KsM33CV6fzgvz48vn75ltxffv1anN5XdhSyakwFbOMlZLLCkFkV21rOVqQZdNCA9C1qnIorUJlBDhuXGtd2zhUZSMq0YoL8vGou5_bAZ3NxqPp9T76wcRFB-P1v5PR7_Q2HLSQ-e9EkwXenQRi-D1jmvTg05rQjBjmpBnwWtRQQp3Rt4_QuzDHMcdbqUqVDNRKsSNlY0gpYndvhoFeW9PH1nRuTa-t6SXvvHmY4n7jb00Z4Ecg5dG4xfjw6f-p_gFTtqRa</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>Moiseeva, Elena P.</creator><creator>Leyland, Mark L.</creator><creator>Bradding, Peter</creator><general>SP Birkhäuser Verlag Basel</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</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>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120801</creationdate><title>CADM1 isoforms differentially regulate human mast cell survival and homotypic adhesion</title><author>Moiseeva, Elena P. ; Leyland, Mark L. ; Bradding, Peter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c584t-a61c1154246e03224bbc2ec0459b0900fb86de4c8e8a30d2adbcdb9de859363b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adhesion</topic><topic>Allergies</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blotting, Western</topic><topic>Cell Adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Adhesion Molecule-1</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cell Aggregation</topic><topic>Cell Biology</topic><topic>Cell Survival</topic><topic>Cells, Cultured</topic><topic>Humans</topic><topic>Immunoglobulins - metabolism</topic><topic>Leukemia, Mast-Cell - metabolism</topic><topic>Leukemia, Mast-Cell - pathology</topic><topic>Life Sciences</topic><topic>Lung - cytology</topic><topic>Lung - metabolism</topic><topic>Lungs</topic><topic>Mast Cells - cytology</topic><topic>Mast Cells - metabolism</topic><topic>Mast-Cell Sarcoma - metabolism</topic><topic>Mast-Cell Sarcoma - pathology</topic><topic>Molecular biology</topic><topic>Protein Isoforms</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Research Article</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Signal transduction</topic><topic>Survival</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moiseeva, Elena P.</creatorcontrib><creatorcontrib>Leyland, Mark L.</creatorcontrib><creatorcontrib>Bradding, Peter</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cellular and molecular life sciences : CMLS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moiseeva, Elena P.</au><au>Leyland, Mark L.</au><au>Bradding, Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CADM1 isoforms differentially regulate human mast cell survival and homotypic adhesion</atitle><jtitle>Cellular and molecular life sciences : CMLS</jtitle><stitle>Cell. Mol. Life Sci</stitle><addtitle>Cell Mol Life Sci</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>69</volume><issue>16</issue><spage>2751</spage><epage>2764</epage><pages>2751-2764</pages><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>Cell adhesion molecule 1 (CADM1), expressed by human lung mast cells (HLMCs), mediates their adhesion to airway smooth muscle (ASM), and contributes to ASM-dependent HLMC proliferation and survival. CADM1 is expressed in alternatively spliced isoforms, but those present in HLMCs and their function are not known. We cloned three functional and one cryptic non-functional isoform with alternative splicing between exons 7/11 and 1/2, respectively, from HLMCs and human MC lines (HMC-1 and LAD2). Differentiated HLMCs and LAD2 cells expressed the functional isoform SP4 containing exons 7/8/11 (~80% of clones), as well as SP1 (exons 7/8/9/11) and a novel SP6 (exons 7/8/9/10/11). In contrast, immature HMC-1 cells expressed only functional SP4. SP4 overexpression in HMC-1 cells and HLMCs augmented homotypic adhesion to a greater extent than SP1 in various conditions. In contrast, CADM1 downregulation abolished homotypic adhesion, indicating that CADM1 is the sole receptor mediating mast cell aggregation. CADM1-mediated adhesion was enhanced by the presence of cell survival factors. SP1 overexpression in HMC-1 cells compromised survival compared to SP4 overexpression or control. CADM1 downregulation resulted in reduced viability and decreased expression of the pro-survival protein Mcl-1
L
, but not Blc-2 or Bcl-X
L
, and increased caspase-3/7 activity in both HMC-1 cells and HLMCs. This coincided with decreased basal Kit levels in HLMCs. In summary, human MCs express multiple CADM1 isoforms which exhibit differential regulation of survival and homotypic adhesion. The most highly expressed SP4 isoform is likely to contribute to MC aggregation and longevity in mastocytosis, and augment the pathophysiology of allergic diseases.</abstract><cop>Basel</cop><pub>SP Birkhäuser Verlag Basel</pub><pmid>22438059</pmid><doi>10.1007/s00018-012-0948-y</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adhesion Allergies Apoptosis Biochemistry Biomedical and Life Sciences Biomedicine Blotting, Western Cell Adhesion Cell adhesion & migration Cell Adhesion Molecule-1 Cell Adhesion Molecules - metabolism Cell Aggregation Cell Biology Cell Survival Cells, Cultured Humans Immunoglobulins - metabolism Leukemia, Mast-Cell - metabolism Leukemia, Mast-Cell - pathology Life Sciences Lung - cytology Lung - metabolism Lungs Mast Cells - cytology Mast Cells - metabolism Mast-Cell Sarcoma - metabolism Mast-Cell Sarcoma - pathology Molecular biology Protein Isoforms Real-Time Polymerase Chain Reaction Research Article Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Signal transduction Survival |
title | CADM1 isoforms differentially regulate human mast cell survival and homotypic adhesion |
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