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Article: TGF-β3 regulates the blood-testis barrier dynamics via the p38 mitogen activated protein (MAP) kinase pathway: An in vivo study

TitleTGF-β3 regulates the blood-testis barrier dynamics via the p38 mitogen activated protein (MAP) kinase pathway: An in vivo study
Authors
Issue Date2003
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2003, v. 144 n. 4, p. 1139-1142 How to Cite?
AbstractRecent studies using Sertoli cells cultured tn vitro to permit tight junction (TJ) assembly have shown that TJ dynamics are regulated, at least in part, by TGF-β3 via the p38 mitogen activated protein (MAP) kinase pathway. This in turn regulates the production of occludin, a TJ-integral membrane protein, by Sertoli cells. Yet it is not known if this pathway is used by Sertoli cells to regulate the blood-testis barrier (BTB) function in vivo. Using an in vivo model for studying BTB dynamics, we report herein the CdCl 2-induced BTB damage in rats was associated with a significant reduction in testieular oceludin along with a loss of immunoreaetive oeeludin in the seminiferous epithelium at the site of the BTB. Also, this CdCl 2-induced occludin loss from the BTB coincided with a surge in testicular TGF-β3, as well as p-p38 MAP kinase (the phosphorylated/activated form of p38), but not p38 MAP kinase and neither extracellular signal-regulated kinase nor its phosphorylated form (ERK/p-ERK), consistent with results of in vitro studies. More important, intratesticular administration of SB202190, a specific p38 MAP kinase inhibitor, could block the CdCl 2-induced occludin loss from the BTB. These results illustrate that BTB dynamics in vivo are regulated by the TGF-β3/p38 MAP kinase pathway, which in turn determines the level of occludin at the site of Sertoli cell TJs.
Persistent Identifierhttp://hdl.handle.net/10722/178790
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLui, WYen_US
dc.contributor.authorWong, CHen_US
dc.contributor.authorMruk, DDen_US
dc.contributor.authorCheng, CYen_US
dc.date.accessioned2012-12-19T09:49:46Z-
dc.date.available2012-12-19T09:49:46Z-
dc.date.issued2003en_US
dc.identifier.citationEndocrinology, 2003, v. 144 n. 4, p. 1139-1142en_US
dc.identifier.issn0013-7227en_US
dc.identifier.urihttp://hdl.handle.net/10722/178790-
dc.description.abstractRecent studies using Sertoli cells cultured tn vitro to permit tight junction (TJ) assembly have shown that TJ dynamics are regulated, at least in part, by TGF-β3 via the p38 mitogen activated protein (MAP) kinase pathway. This in turn regulates the production of occludin, a TJ-integral membrane protein, by Sertoli cells. Yet it is not known if this pathway is used by Sertoli cells to regulate the blood-testis barrier (BTB) function in vivo. Using an in vivo model for studying BTB dynamics, we report herein the CdCl 2-induced BTB damage in rats was associated with a significant reduction in testieular oceludin along with a loss of immunoreaetive oeeludin in the seminiferous epithelium at the site of the BTB. Also, this CdCl 2-induced occludin loss from the BTB coincided with a surge in testicular TGF-β3, as well as p-p38 MAP kinase (the phosphorylated/activated form of p38), but not p38 MAP kinase and neither extracellular signal-regulated kinase nor its phosphorylated form (ERK/p-ERK), consistent with results of in vitro studies. More important, intratesticular administration of SB202190, a specific p38 MAP kinase inhibitor, could block the CdCl 2-induced occludin loss from the BTB. These results illustrate that BTB dynamics in vivo are regulated by the TGF-β3/p38 MAP kinase pathway, which in turn determines the level of occludin at the site of Sertoli cell TJs.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.rightsEndocrinology . Copyright © The Endocrine Society.-
dc.titleTGF-β3 regulates the blood-testis barrier dynamics via the p38 mitogen activated protein (MAP) kinase pathway: An in vivo studyen_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.2002-0211en_US
dc.identifier.pmid12639893-
dc.identifier.scopuseid_2-s2.0-0037374822en_US
dc.identifier.hkuros100785-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037374822&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume144en_US
dc.identifier.issue4en_US
dc.identifier.spage1139en_US
dc.identifier.epage1142en_US
dc.identifier.isiWOS:000182188900002-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLui, WY=35220192400en_US
dc.identifier.scopusauthoridWong, CH=8849630400en_US
dc.identifier.scopusauthoridMruk, DD=6701823934en_US
dc.identifier.scopusauthoridCheng, CY=7404797787en_US

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