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Article: Opposite effects of interleukin-1α and transforming growth factor-β2 induce stage-specific regulation of junctional adhesion molecule-B gene in sertoli cells

TitleOpposite effects of interleukin-1α and transforming growth factor-β2 induce stage-specific regulation of junctional adhesion molecule-B gene in sertoli cells
Authors
Issue Date2009
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2009, v. 150 n. 5, p. 2404-2412 How to Cite?
AbstractIn the mammalian testis, junctional adhesion molecule-B (JAM-B) is found at the blood-testis barrier between Sertoli cells and the apical ectoplasmic specializations between Sertoli and germ cells. The expression of JAM-B is tightly regulated to allow the transit of developing germ cells across the blood-testis barrier and the timely release of mature spermatids at stage VIII. In this study, the basal transcription of JAM-B in the mouse Sertoli cell line, MSC-1 cells, was examined. We found that the constitutive expression of JAM-B is carried out by the binding of specificity proteins (Sps), ETS domain transcription factor Elk-1 (Elk1), neuron-restrictive silencer factor (NRSF), and E2F transcription factor 3 (E2F3) to various cis-acting elements including TG interacting factor (TGIF), Elk-1, NRSF, and proximal Sp1 (pSp1) + E2F binding motifs. We also investigated the effects of two cytokines IL-1α and TGF-β2 on JAM-B expression. IL-1α promotes JAM-B expression by facilitating the binding of Elk-1 to TGIF and pSp1 + E2F motifs in a p38-dependent manner, which leads to an additive effect on Sp1- and NRSF-mediated JAM-B transactivation. TGF-/32 inhibits JAM-B transcription via the activation of mothers against decapentaplegic (Smad) proteins and activated Smads compete with specificity proteins (Sp1 and Sp3) for the TGIF motif, resulting in JAM-B repression. IL-1a and Smad3 expression have been reported to be stage specific. IL-1α is absent in theseminferous epithelium at stages VII-VIII, whereas a high level of nuclear Smad3 level is found at the same stages. This study shows for the first time that IL-1 a and TGF-/32 regulate JAM-B expression in an opposite manner, and in vitro data obtained herein provide some clues on how junctions are regulated in the testis. Copyright © 2009 by The Endocrine Society.
Persistent Identifierhttp://hdl.handle.net/10722/179133
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_US
dc.contributor.authorLui, WYen_US
dc.date.accessioned2012-12-19T09:52:15Z-
dc.date.available2012-12-19T09:52:15Z-
dc.date.issued2009en_US
dc.identifier.citationEndocrinology, 2009, v. 150 n. 5, p. 2404-2412en_US
dc.identifier.issn0013-7227en_US
dc.identifier.urihttp://hdl.handle.net/10722/179133-
dc.description.abstractIn the mammalian testis, junctional adhesion molecule-B (JAM-B) is found at the blood-testis barrier between Sertoli cells and the apical ectoplasmic specializations between Sertoli and germ cells. The expression of JAM-B is tightly regulated to allow the transit of developing germ cells across the blood-testis barrier and the timely release of mature spermatids at stage VIII. In this study, the basal transcription of JAM-B in the mouse Sertoli cell line, MSC-1 cells, was examined. We found that the constitutive expression of JAM-B is carried out by the binding of specificity proteins (Sps), ETS domain transcription factor Elk-1 (Elk1), neuron-restrictive silencer factor (NRSF), and E2F transcription factor 3 (E2F3) to various cis-acting elements including TG interacting factor (TGIF), Elk-1, NRSF, and proximal Sp1 (pSp1) + E2F binding motifs. We also investigated the effects of two cytokines IL-1α and TGF-β2 on JAM-B expression. IL-1α promotes JAM-B expression by facilitating the binding of Elk-1 to TGIF and pSp1 + E2F motifs in a p38-dependent manner, which leads to an additive effect on Sp1- and NRSF-mediated JAM-B transactivation. TGF-/32 inhibits JAM-B transcription via the activation of mothers against decapentaplegic (Smad) proteins and activated Smads compete with specificity proteins (Sp1 and Sp3) for the TGIF motif, resulting in JAM-B repression. IL-1a and Smad3 expression have been reported to be stage specific. IL-1α is absent in theseminferous epithelium at stages VII-VIII, whereas a high level of nuclear Smad3 level is found at the same stages. This study shows for the first time that IL-1 a and TGF-/32 regulate JAM-B expression in an opposite manner, and in vitro data obtained herein provide some clues on how junctions are regulated in the testis. Copyright © 2009 by The Endocrine Society.en_US
dc.languageengen_US
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_US
dc.relation.ispartofEndocrinologyen_US
dc.rights.uriEndocrinology. Copyright © The Endocrine Society.-
dc.titleOpposite effects of interleukin-1α and transforming growth factor-β2 induce stage-specific regulation of junctional adhesion molecule-B gene in sertoli cellsen_US
dc.typeArticleen_US
dc.identifier.emailLui, WY: wylui@hku.hken_US
dc.identifier.authorityLui, WY=rp00756en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1210/en.2008-1239en_US
dc.identifier.pmid19164472-
dc.identifier.scopuseid_2-s2.0-66449100451en_US
dc.identifier.hkuros156256-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-66449100451&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume150en_US
dc.identifier.issue5en_US
dc.identifier.spage2404en_US
dc.identifier.epage2412en_US
dc.identifier.eissn1945-7170-
dc.identifier.isiWOS:000265407500048-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, Y=7601513691en_US
dc.identifier.scopusauthoridLui, WY=35220192400en_US

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