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Article: Post-transcriptional regulation of CLMP mRNA is controlled by tristetraprolin in response to TNFα via c-Jun N-terminal kinase signalling

TitlePost-transcriptional regulation of CLMP mRNA is controlled by tristetraprolin in response to TNFα via c-Jun N-terminal kinase signalling
Authors
Issue Date2008
PublisherPortland Press Ltd. The Journal's web site is located at http://www.biochemj.org
Citation
Biochemical Journal, 2008, v. 410 n. 3, p. 575-583 How to Cite?
AbstractDuring spermatogenesis, extensive restructuring of blood-testis barrier takes place to facilitate the migration of preleptotene/leptotene spermatocytes from the basal to the adluminal compartment in the seminiferous epithelium. However, the biochemical mechanisms involved in this event remain elusive. Recent studies have shown that pro-inflammatory cytokine TNFα (tumour necrosis factor α) plays a crucial role in this event by inhibiting the expression of tight junction proteins in Sertoli cells. In the present study, we sought to examine the detailed mechanism on how TNFα affects the expression of CLMP (coxsackie- and adenovirus-receptor-like membrane protein), a newly identified tight junction transmembrane protein, in the testis. Addition of TNFα (10 ng/ml) to Sertoli cell culture (TM4 cells) significantly reduced the steady-state CLMP mRNA and protein levels. In an mRNA stability assay, it was shown that the rate of CLMP mRNA degradation was significantly increased when cells treated with TNFα were compared with vehicle. Blockage of the JNK (c-Jun N-terminal kinase) signalling pathway by SP600125 significantly abolished the TNFα-mediated destabilization of CLMP mRNA. Activation of the JNK signalling pathway by TNFα up-regulated the expression of an RNA-binding protein, TTP (tristetraprolin). TTP was present in the RNA-protein complex in the RNA EMSA (electrophoretic mobility shift assay) and decreased the CLMP 3′-UTR (untranslated region)-dependent luciferase activity. Taken together, these results suggest that the TNFα-mediated mRNA degradation of the CLMP gene is controlled by TTP through the JNK signalling cascade. © The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/179047
ISSN
2015 Impact Factor: 3.562
2015 SCImago Journal Rankings: 2.582
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSze, KLen_US
dc.contributor.authorLui, WYen_US
dc.contributor.authorLee, WMen_US
dc.date.accessioned2012-12-19T09:51:38Z-
dc.date.available2012-12-19T09:51:38Z-
dc.date.issued2008en_US
dc.identifier.citationBiochemical Journal, 2008, v. 410 n. 3, p. 575-583en_US
dc.identifier.issn0264-6021en_US
dc.identifier.urihttp://hdl.handle.net/10722/179047-
dc.description.abstractDuring spermatogenesis, extensive restructuring of blood-testis barrier takes place to facilitate the migration of preleptotene/leptotene spermatocytes from the basal to the adluminal compartment in the seminiferous epithelium. However, the biochemical mechanisms involved in this event remain elusive. Recent studies have shown that pro-inflammatory cytokine TNFα (tumour necrosis factor α) plays a crucial role in this event by inhibiting the expression of tight junction proteins in Sertoli cells. In the present study, we sought to examine the detailed mechanism on how TNFα affects the expression of CLMP (coxsackie- and adenovirus-receptor-like membrane protein), a newly identified tight junction transmembrane protein, in the testis. Addition of TNFα (10 ng/ml) to Sertoli cell culture (TM4 cells) significantly reduced the steady-state CLMP mRNA and protein levels. In an mRNA stability assay, it was shown that the rate of CLMP mRNA degradation was significantly increased when cells treated with TNFα were compared with vehicle. Blockage of the JNK (c-Jun N-terminal kinase) signalling pathway by SP600125 significantly abolished the TNFα-mediated destabilization of CLMP mRNA. Activation of the JNK signalling pathway by TNFα up-regulated the expression of an RNA-binding protein, TTP (tristetraprolin). TTP was present in the RNA-protein complex in the RNA EMSA (electrophoretic mobility shift assay) and decreased the CLMP 3′-UTR (untranslated region)-dependent luciferase activity. Taken together, these results suggest that the TNFα-mediated mRNA degradation of the CLMP gene is controlled by TTP through the JNK signalling cascade. © The Authors.en_US
dc.languageengen_US
dc.publisherPortland Press Ltd. The Journal's web site is located at http://www.biochemj.orgen_US
dc.relation.ispartofBiochemical Journalen_US
dc.subject.mesh3' Untranslated Regionsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshDna Primersen_US
dc.subject.meshElectrophoretic Mobility Shift Assayen_US
dc.subject.meshMembrane Proteins - Genetics - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshRna Processing, Post-Transcriptionalen_US
dc.subject.meshRna, Messenger - Geneticsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshTristetraprolin - Pharmacologyen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Pharmacologyen_US
dc.titlePost-transcriptional regulation of CLMP mRNA is controlled by tristetraprolin in response to TNFα via c-Jun N-terminal kinase signallingen_US
dc.typeArticleen_US
dc.identifier.emailLui, WY: wylui@hku.hken_US
dc.identifier.emailLee, WM: hrszlwm@hku.hken_US
dc.identifier.authorityLui, WY=rp00756en_US
dc.identifier.authorityLee, WM=rp00728en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1042/BJ20070901en_US
dc.identifier.pmid18047469-
dc.identifier.scopuseid_2-s2.0-41149120601en_US
dc.identifier.hkuros141271-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-41149120601&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume410en_US
dc.identifier.issue3en_US
dc.identifier.spage575en_US
dc.identifier.epage583en_US
dc.identifier.eissn1470-8728-
dc.identifier.isiWOS:000254218300014-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridSze, KL=12779346400en_US
dc.identifier.scopusauthoridLui, WY=35220192400en_US
dc.identifier.scopusauthoridLee, WM=24799156600en_US

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