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Article: Blockage of testicular connexins induced apoptosis in rat seminiferous epithelium

TitleBlockage of testicular connexins induced apoptosis in rat seminiferous epithelium
Authors
Issue Date2006
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1360-8185
Citation
Apoptosis, 2006, v. 11 n. 7, p. 1215-1229 How to Cite?
AbstractSpermatogenesis, a tightly regulated developmental process of male germ cells in testis, is associated with temporal and spatial expression of gap junction proteins, such as the connexin family members. Perturbation of their expressions may lead to spermatogenic arrest as manifested by disruption of cell-cell interaction. To explore the role(s) of connexins during spermatogenesis, we utilized the small peptide antagonistic approach to specifically deplete connexin 31, connexin 33, and pan-connexin. Three connexin peptides corresponding to the extracellular binding domain of connexin 31 and connexin 33 and to the extracellular conserved domain of connexins were designed and synthesized commercially. Peptides (at single dosage of 0.5, 1, or 2 mg per animal) were injected into rat testes and testes were collected on day 0, 1, 3, 5, 10, 15, and 30 after microinjection. In situ TUNEL assay demonstrated the induction of apoptosis in the testes after pan-connexin peptide treatment in a dose-dependent manner from day 3 and onward. Unlike the pan-connexin peptide, connexin 31 and connexin 33 peptides appeared to have little effect on inducing apoptosis and germ cell loss. CD45 staining also detected the occasional presence of infiltrating lymphocytes in the seminiferous tubules. Accompanied with the apoptotic events, two apoptotic markers, NF-κB and caspase 3, demonstrated a general up-regulation in their expressions. In adjacent testis sections, eliminations of connexin 31, 32, and 43 were observed. However, an induction of connexin 33 expression was detected. This suggests the versatility and functional diversity of connexins in the testis. The expression of ZO-1, the only known adaptor of connexins in the testis, was reduced and remained in a low level in the seminiferous epithelium. As such, the alterations of connexins in seminiferous epithelium may induce apoptotic signaling in the testis via the caspase 3 and the NF-κB pathway. This demonstrates the significant role of testicular connexins to maintain the survival of germ cells by regulating inter-cellular communications among germ cells and adjacent supporting cells during spermatogenesis. In addition, the inter-relationship between connexins and other junction proteins and associated signaling protein were investigated. After pan-connexin peptide treatment, a dys-localization of N-cadherin, an adherens junction protein, and diminution of occludin, a tight junction protein, level were detected. In addition, inductions of junction regulatory protein, cathepsin L, was observed during the course of peptide-mediated germ cell loss in the testes. In summary, pan-connexin peptide treatment triggered apoptosis and germ cell loss in the testes. This event influenced the localization and expression of different junction proteins and junction-associated protein in the testes. © Springer Science + Business Media, LLC 2006.
Persistent Identifierhttp://hdl.handle.net/10722/173306
ISSN
2015 Impact Factor: 3.592
2015 SCImago Journal Rankings: 1.554
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, NPYen_US
dc.contributor.authorLeung, KWen_US
dc.contributor.authorWo, JYen_US
dc.contributor.authorTam, PCen_US
dc.contributor.authorYeung, WSBen_US
dc.contributor.authorLuk, JMen_US
dc.date.accessioned2012-10-30T06:29:12Z-
dc.date.available2012-10-30T06:29:12Z-
dc.date.issued2006en_US
dc.identifier.citationApoptosis, 2006, v. 11 n. 7, p. 1215-1229en_US
dc.identifier.issn1360-8185en_US
dc.identifier.urihttp://hdl.handle.net/10722/173306-
dc.description.abstractSpermatogenesis, a tightly regulated developmental process of male germ cells in testis, is associated with temporal and spatial expression of gap junction proteins, such as the connexin family members. Perturbation of their expressions may lead to spermatogenic arrest as manifested by disruption of cell-cell interaction. To explore the role(s) of connexins during spermatogenesis, we utilized the small peptide antagonistic approach to specifically deplete connexin 31, connexin 33, and pan-connexin. Three connexin peptides corresponding to the extracellular binding domain of connexin 31 and connexin 33 and to the extracellular conserved domain of connexins were designed and synthesized commercially. Peptides (at single dosage of 0.5, 1, or 2 mg per animal) were injected into rat testes and testes were collected on day 0, 1, 3, 5, 10, 15, and 30 after microinjection. In situ TUNEL assay demonstrated the induction of apoptosis in the testes after pan-connexin peptide treatment in a dose-dependent manner from day 3 and onward. Unlike the pan-connexin peptide, connexin 31 and connexin 33 peptides appeared to have little effect on inducing apoptosis and germ cell loss. CD45 staining also detected the occasional presence of infiltrating lymphocytes in the seminiferous tubules. Accompanied with the apoptotic events, two apoptotic markers, NF-κB and caspase 3, demonstrated a general up-regulation in their expressions. In adjacent testis sections, eliminations of connexin 31, 32, and 43 were observed. However, an induction of connexin 33 expression was detected. This suggests the versatility and functional diversity of connexins in the testis. The expression of ZO-1, the only known adaptor of connexins in the testis, was reduced and remained in a low level in the seminiferous epithelium. As such, the alterations of connexins in seminiferous epithelium may induce apoptotic signaling in the testis via the caspase 3 and the NF-κB pathway. This demonstrates the significant role of testicular connexins to maintain the survival of germ cells by regulating inter-cellular communications among germ cells and adjacent supporting cells during spermatogenesis. In addition, the inter-relationship between connexins and other junction proteins and associated signaling protein were investigated. After pan-connexin peptide treatment, a dys-localization of N-cadherin, an adherens junction protein, and diminution of occludin, a tight junction protein, level were detected. In addition, inductions of junction regulatory protein, cathepsin L, was observed during the course of peptide-mediated germ cell loss in the testes. In summary, pan-connexin peptide treatment triggered apoptosis and germ cell loss in the testes. This event influenced the localization and expression of different junction proteins and junction-associated protein in the testes. © Springer Science + Business Media, LLC 2006.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1360-8185en_US
dc.relation.ispartofApoptosisen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCadherins - Metabolismen_US
dc.subject.meshCaspase 3en_US
dc.subject.meshCaspases - Metabolismen_US
dc.subject.meshCathepsin Len_US
dc.subject.meshCathepsins - Metabolismen_US
dc.subject.meshConnexin 43 - Metabolismen_US
dc.subject.meshConnexins - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshCysteine Endopeptidases - Metabolismen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIn Situ Nick-End Labelingen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Proteins - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Balb Cen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshPhosphoproteins - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSeminiferous Epithelium - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshTestis - Cytology - Drug Effects - Metabolismen_US
dc.titleBlockage of testicular connexins induced apoptosis in rat seminiferous epitheliumen_US
dc.typeArticleen_US
dc.identifier.emailLee, NPY:nikkilee@hku.hken_US
dc.identifier.emailYeung, WSB:wsbyeung@hkucc.hku.hken_US
dc.identifier.emailLuk, JM:jmluk@hkucc.hku.hken_US
dc.identifier.authorityLee, NPY=rp00263en_US
dc.identifier.authorityYeung, WSB=rp00331en_US
dc.identifier.authorityLuk, JM=rp00349en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s10495-006-6981-2en_US
dc.identifier.pmid16699959-
dc.identifier.scopuseid_2-s2.0-33745841944en_US
dc.identifier.hkuros136467-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745841944&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume11en_US
dc.identifier.issue7en_US
dc.identifier.spage1215en_US
dc.identifier.epage1229en_US
dc.identifier.isiWOS:000238766900014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLee, NPY=7402722690en_US
dc.identifier.scopusauthoridLeung, KW=23097859100en_US
dc.identifier.scopusauthoridWo, JY=7003466728en_US
dc.identifier.scopusauthoridTam, PC=7202539419en_US
dc.identifier.scopusauthoridYeung, WSB=7102370745en_US
dc.identifier.scopusauthoridLuk, JM=7006777791en_US

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