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dc.contributor.authorRosselli-Murai, Luciana K.
dc.contributor.authorAlmeida, Luciana O.
dc.contributor.authorZagni, Chiara
dc.contributor.authorGalindo Moreno, Pablo Antonio 
dc.contributor.authorPadial Molina, Miguel 
dc.contributor.authorVolk, Sarah L.
dc.contributor.authorMurai, Marcelo J.
dc.contributor.authorRíos, Héctor F.
dc.contributor.authorSquarize, Cristiane H.
dc.contributor.authorCastilho, Rogerio M.
dc.date.accessioned2014-02-07T10:52:09Z
dc.date.available2014-02-07T10:52:09Z
dc.date.issued2013
dc.identifier.citationRosselli-Murai, L.K.; et al. Periostin Responds to Mechanical Stress and Tension by Activating the MTOR Signaling Pathway . Plos One, 8(12): e83580 (2013). [http://hdl.handle.net/10481/30300]es_ES
dc.identifier.issn1932-6203
dc.identifier.otherdoi: 10.1371/journal.pone.0083580
dc.identifier.urihttp://hdl.handle.net/10481/30300
dc.description.abstractCurrent knowledge about Periostin biology has expanded from its recognized functions in embryogenesis and bone metabolism to its roles in tissue repair and remodeling and its clinical implications in cancer. Emerging evidence suggests that Periostin plays a critical role in the mechanism of wound healing; however, the paracrine effect of Periostin in epithelial cell biology is still poorly understood. We found that epithelial cells are capable of producing endogenous Periostin that, unlike mesenchymal cell, cannot be secreted. Epithelial cells responded to Periostin paracrine stimuli by enhancing cellular migration and proliferation and by activating the mTOR signaling pathway. Interestingly, biomechanical stimulation of epithelial cells, which simulates tension forces that occur during initial steps of tissue healing, induced Periostin production and mTOR activation. The molecular association of Periostin and mTOR signaling was further dissected by administering rapamycin, a selective pharmacological inhibitor of mTOR, and by disruption of Raptor and Rictor scaffold proteins implicated in the regulation of mTORC1 and mTORC2 complex assembly. Both strategies resulted in ablation of Periostin-induced mitogenic and migratory activity. These results indicate that Periostin-induced epithelial migration and proliferation requires mTOR signaling. Collectively, our findings identify Periostin as a mechanical stress responsive molecule that is primarily secreted by fibroblasts during wound healing and expressed endogenously in epithelial cells resulting in the control of cellular physiology through a mechanism mediated by the mTOR signaling cascade.es_ES
dc.description.sponsorshipThis work was funded by the National Institutes of Health (NIH/NCI) P50-CA97248 (University of Michigan Head and Neck SPORE).es_ES
dc.language.isoenges_ES
dc.publisherPublic Library of Science (PLOS)es_ES
dc.subjectCell migrationes_ES
dc.subjectEpithelial cellses_ES
dc.subjectFibroblastses_ES
dc.subjectMechanical stresses_ES
dc.subjectRaptorses_ES
dc.subjectSmall interfering RNAes_ES
dc.subjectTissue repaires_ES
dc.subjectWound headinges_ES
dc.titlePeriostin Responds to Mechanical Stress and Tension by Activating the MTOR Signaling Pathwayes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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