Disruption of Tubulobulbar Complex by High Intratesticular Estrogens Leading to Failed Spermiation
Spermiation is the final phase of spermatogenesis leading to release of mature spermatids into the lumen of the seminiferous tubules. Morphologically, it involves a series of events, namely removal of excess spermatid cytoplasm, removal of ectoplasmic specialization, formation of tubulobulbar comple...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2009-04, Vol.150 (4), p.1861-1869 |
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| creator | D'Souza, Ryan Pathak, Shilpa Upadhyay, Rahul Gaonkar, Reshma D'Souza, Serena Sonawane, Shobha Gill-Sharma, Manjit Balasinor, Nafisa H |
| description | Spermiation is the final phase of spermatogenesis leading to release of mature spermatids into the lumen of the seminiferous tubules. Morphologically, it involves a series of events, namely removal of excess spermatid cytoplasm, removal of ectoplasmic specialization, formation of tubulobulbar complex, and final disengagement of the spermatid from the Sertoli cell. Previous studies in our laboratory have shown that administration of 17β-estradiol at a dose of 100 μg/kg body weight for 10 d resulted in failure of spermiation. This was accompanied by a suppression of FSH and intratesticular testosterone with a concomitant rise in intratesticular 17β-estradiol. The present study was undertaken to determine the cause of failure and subsequently the molecular events in spermiation. Electron microscopic and confocal studies revealed an absence of tubulobulbar complex in step 19 spermatids after estradiol treatment, highlighting the significance of these structures in spermiation. It was further observed that treatment affected the Sertoli cell cytoskeleton and Arp2/3 complex that is critical for de novo polymerization of actin during tubulobulbar complex formation. In conclusion, the present study reports the role of 17β-estradiol in inhibiting the formation of tubulobulbar complex, which could be one of the mechanism by which environmental estrogens influence male fertility.
High intratesticular estrogen inhibits tubulobulbar complex formation, a testis-specific intercellular junction leading to spermiation failure. |
| doi_str_mv | 10.1210/en.2008-1232 |
| format | Article |
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High intratesticular estrogen inhibits tubulobulbar complex formation, a testis-specific intercellular junction leading to spermiation failure.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2008-1232</identifier><identifier>PMID: 19095743</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Chevy Chase, MD: Endocrine Society</publisher><subject>17β-Estradiol ; Actin ; Actin-Related Protein 3 - metabolism ; Animals ; Biological and medical sciences ; Blotting, Western ; Body weight ; Complex formation ; Cytoplasm ; Cytoskeleton ; Estradiol - pharmacology ; Estrogens ; Fertility ; Fluorescent Antibody Technique ; Follicle-stimulating hormone ; Fundamental and applied biological sciences. Psychology ; Immunohistochemistry ; Integrin alpha6beta1 - metabolism ; Male ; Microscopy ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Polymerase Chain Reaction ; Rats ; Sex hormones ; Spermatids ; Spermatids - drug effects ; Spermatids - metabolism ; Spermatids - ultrastructure ; Spermatogenesis ; Spermatogenesis - drug effects ; Testis - drug effects ; Testis - metabolism ; Testis - ultrastructure ; Testosterone ; Tubules ; Vertebrates: endocrinology ; Vinculin - metabolism</subject><ispartof>Endocrinology (Philadelphia), 2009-04, Vol.150 (4), p.1861-1869</ispartof><rights>Copyright © 2009 by The Endocrine Society 2009</rights><rights>2009 INIST-CNRS</rights><rights>Copyright © 2009 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c527t-6f5efccecc51a0ac71a3e233bbcd62ccab6530ba8517665d6181dd2044b6cc5d3</citedby><cites>FETCH-LOGICAL-c527t-6f5efccecc51a0ac71a3e233bbcd62ccab6530ba8517665d6181dd2044b6cc5d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21289777$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19095743$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>D'Souza, Ryan</creatorcontrib><creatorcontrib>Pathak, Shilpa</creatorcontrib><creatorcontrib>Upadhyay, Rahul</creatorcontrib><creatorcontrib>Gaonkar, Reshma</creatorcontrib><creatorcontrib>D'Souza, Serena</creatorcontrib><creatorcontrib>Sonawane, Shobha</creatorcontrib><creatorcontrib>Gill-Sharma, Manjit</creatorcontrib><creatorcontrib>Balasinor, Nafisa H</creatorcontrib><title>Disruption of Tubulobulbar Complex by High Intratesticular Estrogens Leading to Failed Spermiation</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Spermiation is the final phase of spermatogenesis leading to release of mature spermatids into the lumen of the seminiferous tubules. Morphologically, it involves a series of events, namely removal of excess spermatid cytoplasm, removal of ectoplasmic specialization, formation of tubulobulbar complex, and final disengagement of the spermatid from the Sertoli cell. Previous studies in our laboratory have shown that administration of 17β-estradiol at a dose of 100 μg/kg body weight for 10 d resulted in failure of spermiation. This was accompanied by a suppression of FSH and intratesticular testosterone with a concomitant rise in intratesticular 17β-estradiol. The present study was undertaken to determine the cause of failure and subsequently the molecular events in spermiation. Electron microscopic and confocal studies revealed an absence of tubulobulbar complex in step 19 spermatids after estradiol treatment, highlighting the significance of these structures in spermiation. It was further observed that treatment affected the Sertoli cell cytoskeleton and Arp2/3 complex that is critical for de novo polymerization of actin during tubulobulbar complex formation. In conclusion, the present study reports the role of 17β-estradiol in inhibiting the formation of tubulobulbar complex, which could be one of the mechanism by which environmental estrogens influence male fertility.
High intratesticular estrogen inhibits tubulobulbar complex formation, a testis-specific intercellular junction leading to spermiation failure.</description><subject>17β-Estradiol</subject><subject>Actin</subject><subject>Actin-Related Protein 3 - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Body weight</subject><subject>Complex formation</subject><subject>Cytoplasm</subject><subject>Cytoskeleton</subject><subject>Estradiol - pharmacology</subject><subject>Estrogens</subject><subject>Fertility</subject><subject>Fluorescent Antibody Technique</subject><subject>Follicle-stimulating hormone</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Immunohistochemistry</subject><subject>Integrin alpha6beta1 - metabolism</subject><subject>Male</subject><subject>Microscopy</subject><subject>Microscopy, Confocal</subject><subject>Microscopy, Electron, Transmission</subject><subject>Polymerase Chain Reaction</subject><subject>Rats</subject><subject>Sex hormones</subject><subject>Spermatids</subject><subject>Spermatids - drug effects</subject><subject>Spermatids - metabolism</subject><subject>Spermatids - ultrastructure</subject><subject>Spermatogenesis</subject><subject>Spermatogenesis - drug effects</subject><subject>Testis - drug effects</subject><subject>Testis - metabolism</subject><subject>Testis - ultrastructure</subject><subject>Testosterone</subject><subject>Tubules</subject><subject>Vertebrates: endocrinology</subject><subject>Vinculin - metabolism</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10M9rFDEUB_Agil2rN88SEPXi1PyYTHaOZW1tYcGD9Rzy482aMpOMyQTsf2-WHSyIHkII-eS9ly9Crym5oIySTxAuGCHbhjLOnqAN7VvRSCrJU7QhhPJGMibP0Iuc7-uxbVv-HJ3RnvRCtnyDzGefU5kXHwOOA74rpoyxLqMT3sVpHuEXNg_4xh9-4NuwJL1AXrwtY72_ykuKBwgZ70E7Hw54ifha-xEc_jZDmrw-1n2Jng16zPBq3c_R9-uru91Ns__65XZ3uW-sYHJpukHAYC1YK6gm2kqqOTDOjbGuY9Zq0wlOjN4KKrtOuI5uqXOMtK3p6hvHz9H7U905xZ-ljqkmny2Mow4QS1adJF39Nqvw7V_wPpYU6myKU05EL_q-r-rjSdkUc04wqDn5SacHRYk6Jq8gqGPy6ph85W_WosVM4B7xGnUF71ags9XjkHSwPv9xjLJtL6Ws7sPJxTL_r2WztuQnCcFFm3yAOUHOj7_556C_AWlZqVg</recordid><startdate>20090401</startdate><enddate>20090401</enddate><creator>D'Souza, Ryan</creator><creator>Pathak, Shilpa</creator><creator>Upadhyay, Rahul</creator><creator>Gaonkar, Reshma</creator><creator>D'Souza, Serena</creator><creator>Sonawane, Shobha</creator><creator>Gill-Sharma, Manjit</creator><creator>Balasinor, Nafisa H</creator><general>Endocrine Society</general><general>Oxford University Press</general><scope>IQODW</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20090401</creationdate><title>Disruption of Tubulobulbar Complex by High Intratesticular Estrogens Leading to Failed Spermiation</title><author>D'Souza, Ryan ; Pathak, Shilpa ; Upadhyay, Rahul ; Gaonkar, Reshma ; D'Souza, Serena ; Sonawane, Shobha ; Gill-Sharma, Manjit ; Balasinor, Nafisa H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c527t-6f5efccecc51a0ac71a3e233bbcd62ccab6530ba8517665d6181dd2044b6cc5d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>17β-Estradiol</topic><topic>Actin</topic><topic>Actin-Related Protein 3 - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Body weight</topic><topic>Complex formation</topic><topic>Cytoplasm</topic><topic>Cytoskeleton</topic><topic>Estradiol - pharmacology</topic><topic>Estrogens</topic><topic>Fertility</topic><topic>Fluorescent Antibody Technique</topic><topic>Follicle-stimulating hormone</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Immunohistochemistry</topic><topic>Integrin alpha6beta1 - metabolism</topic><topic>Male</topic><topic>Microscopy</topic><topic>Microscopy, Confocal</topic><topic>Microscopy, Electron, Transmission</topic><topic>Polymerase Chain Reaction</topic><topic>Rats</topic><topic>Sex hormones</topic><topic>Spermatids</topic><topic>Spermatids - drug effects</topic><topic>Spermatids - metabolism</topic><topic>Spermatids - ultrastructure</topic><topic>Spermatogenesis</topic><topic>Spermatogenesis - drug effects</topic><topic>Testis - drug effects</topic><topic>Testis - metabolism</topic><topic>Testis - ultrastructure</topic><topic>Testosterone</topic><topic>Tubules</topic><topic>Vertebrates: endocrinology</topic><topic>Vinculin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>D'Souza, Ryan</creatorcontrib><creatorcontrib>Pathak, Shilpa</creatorcontrib><creatorcontrib>Upadhyay, Rahul</creatorcontrib><creatorcontrib>Gaonkar, Reshma</creatorcontrib><creatorcontrib>D'Souza, Serena</creatorcontrib><creatorcontrib>Sonawane, Shobha</creatorcontrib><creatorcontrib>Gill-Sharma, Manjit</creatorcontrib><creatorcontrib>Balasinor, Nafisa H</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>D'Souza, Ryan</au><au>Pathak, Shilpa</au><au>Upadhyay, Rahul</au><au>Gaonkar, Reshma</au><au>D'Souza, Serena</au><au>Sonawane, Shobha</au><au>Gill-Sharma, Manjit</au><au>Balasinor, Nafisa H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disruption of Tubulobulbar Complex by High Intratesticular Estrogens Leading to Failed Spermiation</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2009-04-01</date><risdate>2009</risdate><volume>150</volume><issue>4</issue><spage>1861</spage><epage>1869</epage><pages>1861-1869</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>Spermiation is the final phase of spermatogenesis leading to release of mature spermatids into the lumen of the seminiferous tubules. Morphologically, it involves a series of events, namely removal of excess spermatid cytoplasm, removal of ectoplasmic specialization, formation of tubulobulbar complex, and final disengagement of the spermatid from the Sertoli cell. Previous studies in our laboratory have shown that administration of 17β-estradiol at a dose of 100 μg/kg body weight for 10 d resulted in failure of spermiation. This was accompanied by a suppression of FSH and intratesticular testosterone with a concomitant rise in intratesticular 17β-estradiol. The present study was undertaken to determine the cause of failure and subsequently the molecular events in spermiation. Electron microscopic and confocal studies revealed an absence of tubulobulbar complex in step 19 spermatids after estradiol treatment, highlighting the significance of these structures in spermiation. It was further observed that treatment affected the Sertoli cell cytoskeleton and Arp2/3 complex that is critical for de novo polymerization of actin during tubulobulbar complex formation. In conclusion, the present study reports the role of 17β-estradiol in inhibiting the formation of tubulobulbar complex, which could be one of the mechanism by which environmental estrogens influence male fertility.
High intratesticular estrogen inhibits tubulobulbar complex formation, a testis-specific intercellular junction leading to spermiation failure.</abstract><cop>Chevy Chase, MD</cop><pub>Endocrine Society</pub><pmid>19095743</pmid><doi>10.1210/en.2008-1232</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | 17β-Estradiol Actin Actin-Related Protein 3 - metabolism Animals Biological and medical sciences Blotting, Western Body weight Complex formation Cytoplasm Cytoskeleton Estradiol - pharmacology Estrogens Fertility Fluorescent Antibody Technique Follicle-stimulating hormone Fundamental and applied biological sciences. Psychology Immunohistochemistry Integrin alpha6beta1 - metabolism Male Microscopy Microscopy, Confocal Microscopy, Electron, Transmission Polymerase Chain Reaction Rats Sex hormones Spermatids Spermatids - drug effects Spermatids - metabolism Spermatids - ultrastructure Spermatogenesis Spermatogenesis - drug effects Testis - drug effects Testis - metabolism Testis - ultrastructure Testosterone Tubules Vertebrates: endocrinology Vinculin - metabolism |
| title | Disruption of Tubulobulbar Complex by High Intratesticular Estrogens Leading to Failed Spermiation |
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