ETV5 Regulates Sertoli Cell Chemokines Involved in Mouse Stem/Progenitor Spermatogonia Maintenance
Spermatogonial stem cells are the only stem cells in the body that transmit genetic information to offspring. Although growth factors responsible for self‐renewal of these cells are known, the factors and mechanisms that attract and physically maintain these cells within their microenvironment are p...
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| Veröffentlicht in: | Stem cells (Dayton, Ohio) Ohio), 2010-10, Vol.28 (10), p.1882-1892 |
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| creator | Simon, Liz Ekman, Gail C. Garcia, Thomas Carnes, Kay Zhang, Zhen Murphy, Theresa Murphy, Kenneth M. Hess, Rex A. Cooke, Paul S. Hofmann, Marie‐Claude |
| description | Spermatogonial stem cells are the only stem cells in the body that transmit genetic information to offspring. Although growth factors responsible for self‐renewal of these cells are known, the factors and mechanisms that attract and physically maintain these cells within their microenvironment are poorly understood. Mice with targeted disruption of Ets variant gene 5 (Etv5) show total loss of stem/progenitor spermatogonia following the first wave of spermatogenesis, resulting in a Sertoli cell‐only phenotype and aspermia. Microarray analysis of primary Sertoli cells from Etv5 knockout (Etv5−/−) versus wild‐type (WT) mice revealed significant decreases in expression of several chemokines. Chemotaxis assays demonstrated that migration of stem/progenitor spermatogonia toward Etv5−/− Sertoli cells was significantly decreased compared to migration toward WT Sertoli cells. Interestingly, differentiating spermatogonia, spermatocytes, and round spermatids were not chemoattracted by WT Sertoli cells, whereas stem/progenitor spermatogonia showed a high and significant chemotactic index. Rescue assays using recombinant chemokines indicated that C‐C‐motif ligand 9 (CCL9) facilitates Sertoli cell chemoattraction of stem/progenitor spermatogonia, which express C‐C‐receptor type 1 (CCR1). In addition, there is protein‐DNA interaction between ETV5 and Ccl9, suggesting that ETV5 might be a direct regulator of Ccl9 expression. Taken together, our data show for the first time that Sertoli cells are chemoattractive for stem/progenitor spermatogonia, and that production of specific chemokines is regulated by ETV5. Therefore, changes in chemokine production and consequent decreases in chemoattraction by Etv5−/− Sertoli cells helps to explain stem/progenitor spermatogonia loss in Etv5−/− mice. STEM CELLS 2010;28:1882–1892 |
| doi_str_mv | 10.1002/stem.508 |
| format | Article |
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Although growth factors responsible for self‐renewal of these cells are known, the factors and mechanisms that attract and physically maintain these cells within their microenvironment are poorly understood. Mice with targeted disruption of Ets variant gene 5 (Etv5) show total loss of stem/progenitor spermatogonia following the first wave of spermatogenesis, resulting in a Sertoli cell‐only phenotype and aspermia. Microarray analysis of primary Sertoli cells from Etv5 knockout (Etv5−/−) versus wild‐type (WT) mice revealed significant decreases in expression of several chemokines. Chemotaxis assays demonstrated that migration of stem/progenitor spermatogonia toward Etv5−/− Sertoli cells was significantly decreased compared to migration toward WT Sertoli cells. Interestingly, differentiating spermatogonia, spermatocytes, and round spermatids were not chemoattracted by WT Sertoli cells, whereas stem/progenitor spermatogonia showed a high and significant chemotactic index. Rescue assays using recombinant chemokines indicated that C‐C‐motif ligand 9 (CCL9) facilitates Sertoli cell chemoattraction of stem/progenitor spermatogonia, which express C‐C‐receptor type 1 (CCR1). In addition, there is protein‐DNA interaction between ETV5 and Ccl9, suggesting that ETV5 might be a direct regulator of Ccl9 expression. Taken together, our data show for the first time that Sertoli cells are chemoattractive for stem/progenitor spermatogonia, and that production of specific chemokines is regulated by ETV5. Therefore, changes in chemokine production and consequent decreases in chemoattraction by Etv5−/− Sertoli cells helps to explain stem/progenitor spermatogonia loss in Etv5−/− mice. STEM CELLS 2010;28:1882–1892</description><identifier>ISSN: 1066-5099</identifier><identifier>EISSN: 1549-4918</identifier><identifier>DOI: 10.1002/stem.508</identifier><identifier>PMID: 20799334</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Blotting, Western ; Cell Movement - genetics ; Cells, Cultured ; Chemokine CCL7 - genetics ; Chemokine CCL7 - metabolism ; Chemokine CXCL5 - genetics ; Chemokine CXCL5 - metabolism ; chemokines ; Chemokines - genetics ; Chemokines - metabolism ; Chemokines, CC - genetics ; Chemokines, CC - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Electrophoretic Mobility Shift Assay ; Ets‐variant gene 5 ; Immunohistochemistry ; Macrophage Inflammatory Proteins - genetics ; Macrophage Inflammatory Proteins - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Monocyte Chemoattractant Proteins - genetics ; Monocyte Chemoattractant Proteins - metabolism ; Original ; Polymerase Chain Reaction ; Promoter Regions, Genetic - genetics ; Protein Binding ; Receptors, CCR1 - genetics ; Receptors, CCR1 - metabolism ; RNA Interference ; Sertoli cells ; Sertoli Cells - metabolism ; Spermatogonia - cytology ; Spermatogonia - metabolism ; spermatogonial stem cells ; Stem Cells - cytology ; Stem Cells - metabolism ; testis ; Testis - cytology ; Testis - metabolism ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>Stem cells (Dayton, Ohio), 2010-10, Vol.28 (10), p.1882-1892</ispartof><rights>Copyright © 2010 AlphaMed Press</rights><rights>2010 AlphaMed Press. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4758-a2e09c644c1a1450d4a69e630c12b2a287553a8eadd14160508a8fc0700418073</citedby><cites>FETCH-LOGICAL-c4758-a2e09c644c1a1450d4a69e630c12b2a287553a8eadd14160508a8fc0700418073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20799334$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Simon, Liz</creatorcontrib><creatorcontrib>Ekman, Gail C.</creatorcontrib><creatorcontrib>Garcia, Thomas</creatorcontrib><creatorcontrib>Carnes, Kay</creatorcontrib><creatorcontrib>Zhang, Zhen</creatorcontrib><creatorcontrib>Murphy, Theresa</creatorcontrib><creatorcontrib>Murphy, Kenneth M.</creatorcontrib><creatorcontrib>Hess, Rex A.</creatorcontrib><creatorcontrib>Cooke, Paul S.</creatorcontrib><creatorcontrib>Hofmann, Marie‐Claude</creatorcontrib><title>ETV5 Regulates Sertoli Cell Chemokines Involved in Mouse Stem/Progenitor Spermatogonia Maintenance</title><title>Stem cells (Dayton, Ohio)</title><addtitle>Stem Cells</addtitle><description>Spermatogonial stem cells are the only stem cells in the body that transmit genetic information to offspring. Although growth factors responsible for self‐renewal of these cells are known, the factors and mechanisms that attract and physically maintain these cells within their microenvironment are poorly understood. Mice with targeted disruption of Ets variant gene 5 (Etv5) show total loss of stem/progenitor spermatogonia following the first wave of spermatogenesis, resulting in a Sertoli cell‐only phenotype and aspermia. Microarray analysis of primary Sertoli cells from Etv5 knockout (Etv5−/−) versus wild‐type (WT) mice revealed significant decreases in expression of several chemokines. Chemotaxis assays demonstrated that migration of stem/progenitor spermatogonia toward Etv5−/− Sertoli cells was significantly decreased compared to migration toward WT Sertoli cells. Interestingly, differentiating spermatogonia, spermatocytes, and round spermatids were not chemoattracted by WT Sertoli cells, whereas stem/progenitor spermatogonia showed a high and significant chemotactic index. Rescue assays using recombinant chemokines indicated that C‐C‐motif ligand 9 (CCL9) facilitates Sertoli cell chemoattraction of stem/progenitor spermatogonia, which express C‐C‐receptor type 1 (CCR1). In addition, there is protein‐DNA interaction between ETV5 and Ccl9, suggesting that ETV5 might be a direct regulator of Ccl9 expression. Taken together, our data show for the first time that Sertoli cells are chemoattractive for stem/progenitor spermatogonia, and that production of specific chemokines is regulated by ETV5. Therefore, changes in chemokine production and consequent decreases in chemoattraction by Etv5−/− Sertoli cells helps to explain stem/progenitor spermatogonia loss in Etv5−/− mice. STEM CELLS 2010;28:1882–1892</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cell Movement - genetics</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL7 - genetics</subject><subject>Chemokine CCL7 - metabolism</subject><subject>Chemokine CXCL5 - genetics</subject><subject>Chemokine CXCL5 - metabolism</subject><subject>chemokines</subject><subject>Chemokines - genetics</subject><subject>Chemokines - metabolism</subject><subject>Chemokines, CC - genetics</subject><subject>Chemokines, CC - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Electrophoretic Mobility Shift Assay</subject><subject>Ets‐variant gene 5</subject><subject>Immunohistochemistry</subject><subject>Macrophage Inflammatory Proteins - genetics</subject><subject>Macrophage Inflammatory Proteins - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Monocyte Chemoattractant Proteins - genetics</subject><subject>Monocyte Chemoattractant Proteins - metabolism</subject><subject>Original</subject><subject>Polymerase Chain Reaction</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Protein Binding</subject><subject>Receptors, CCR1 - genetics</subject><subject>Receptors, CCR1 - metabolism</subject><subject>RNA Interference</subject><subject>Sertoli cells</subject><subject>Sertoli Cells - metabolism</subject><subject>Spermatogonia - cytology</subject><subject>Spermatogonia - metabolism</subject><subject>spermatogonial stem cells</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - metabolism</subject><subject>testis</subject><subject>Testis - cytology</subject><subject>Testis - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>1066-5099</issn><issn>1549-4918</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp1kUFvEzEQha2qqC0Fqb-g8g0u2453vbv2pVIVBajUCEQCV2vinaSGXTvYm6D-exylVHDoySPPpzdv5jF2IeBKAJTXaaThqgZ1xM5ELXUhtVDHuYamKWrQ-pS9TukHgJC1UifstIRW66qSZ2w5XXyv-Vdab3scKfE5xTH0jk-o7_nkgYbw0_n8f-d3od9Rx53ns7BNxOd55vWXGNbk3Rgin28oDjiGdfAO-QydH8mjt_SGvVphn-jt03vOvn2YLiafivvPH-8mt_eFlW2tCiwJtG2ktAKzT-gkNpqaCqwolyWWqq3rChVh1wkpGsjrolpZaAGkUNBW5-zmoLvZLgfqLPkxYm820Q0YH01AZ_7vePdg1mFnKgFatWUWePckEMOvLaXRDC7ZfAj0lFc2bSNAVkpVmXx_IG0MKUVaPU8RYPaJmH0iJlvM6OW_rp7BvxFkoDgAv11Pjy8KmfliOtsL_gEn85aS</recordid><startdate>201010</startdate><enddate>201010</enddate><creator>Simon, Liz</creator><creator>Ekman, Gail C.</creator><creator>Garcia, Thomas</creator><creator>Carnes, Kay</creator><creator>Zhang, Zhen</creator><creator>Murphy, Theresa</creator><creator>Murphy, Kenneth M.</creator><creator>Hess, Rex A.</creator><creator>Cooke, Paul S.</creator><creator>Hofmann, Marie‐Claude</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>24P</scope><scope>WIN</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>5PM</scope></search><sort><creationdate>201010</creationdate><title>ETV5 Regulates Sertoli Cell Chemokines Involved in Mouse Stem/Progenitor Spermatogonia Maintenance</title><author>Simon, Liz ; 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Although growth factors responsible for self‐renewal of these cells are known, the factors and mechanisms that attract and physically maintain these cells within their microenvironment are poorly understood. Mice with targeted disruption of Ets variant gene 5 (Etv5) show total loss of stem/progenitor spermatogonia following the first wave of spermatogenesis, resulting in a Sertoli cell‐only phenotype and aspermia. Microarray analysis of primary Sertoli cells from Etv5 knockout (Etv5−/−) versus wild‐type (WT) mice revealed significant decreases in expression of several chemokines. Chemotaxis assays demonstrated that migration of stem/progenitor spermatogonia toward Etv5−/− Sertoli cells was significantly decreased compared to migration toward WT Sertoli cells. Interestingly, differentiating spermatogonia, spermatocytes, and round spermatids were not chemoattracted by WT Sertoli cells, whereas stem/progenitor spermatogonia showed a high and significant chemotactic index. Rescue assays using recombinant chemokines indicated that C‐C‐motif ligand 9 (CCL9) facilitates Sertoli cell chemoattraction of stem/progenitor spermatogonia, which express C‐C‐receptor type 1 (CCR1). In addition, there is protein‐DNA interaction between ETV5 and Ccl9, suggesting that ETV5 might be a direct regulator of Ccl9 expression. Taken together, our data show for the first time that Sertoli cells are chemoattractive for stem/progenitor spermatogonia, and that production of specific chemokines is regulated by ETV5. Therefore, changes in chemokine production and consequent decreases in chemoattraction by Etv5−/− Sertoli cells helps to explain stem/progenitor spermatogonia loss in Etv5−/− mice. STEM CELLS 2010;28:1882–1892</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20799334</pmid><doi>10.1002/stem.508</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Blotting, Western Cell Movement - genetics Cells, Cultured Chemokine CCL7 - genetics Chemokine CCL7 - metabolism Chemokine CXCL5 - genetics Chemokine CXCL5 - metabolism chemokines Chemokines - genetics Chemokines - metabolism Chemokines, CC - genetics Chemokines, CC - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Electrophoretic Mobility Shift Assay Ets‐variant gene 5 Immunohistochemistry Macrophage Inflammatory Proteins - genetics Macrophage Inflammatory Proteins - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Monocyte Chemoattractant Proteins - genetics Monocyte Chemoattractant Proteins - metabolism Original Polymerase Chain Reaction Promoter Regions, Genetic - genetics Protein Binding Receptors, CCR1 - genetics Receptors, CCR1 - metabolism RNA Interference Sertoli cells Sertoli Cells - metabolism Spermatogonia - cytology Spermatogonia - metabolism spermatogonial stem cells Stem Cells - cytology Stem Cells - metabolism testis Testis - cytology Testis - metabolism Transcription Factors - genetics Transcription Factors - metabolism |
| title | ETV5 Regulates Sertoli Cell Chemokines Involved in Mouse Stem/Progenitor Spermatogonia Maintenance |
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