Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation
Autor(a) principal: | |
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Data de Publicação: | 2016 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/172606 |
Resumo: | During brain development, cells proliferate, migrate and differentiate in highly accurate patterns. In this context, published results indicate that bradykinin functions in neural fate determination, favoring neurogenesis and migration. However, mechanisms underlying bradykinin function are yet to be explored. Our findings indicate a previously unidentified role for bradykinin action in inducing neurongenerating division in vitro and in vivo, given that bradykinin lengthened the G1-phase of the neural progenitor cells (NPC) cycle and increased TIS21 (also known as PC3 and BTG2) expression in hippocampus from newborn mice. This role, triggered by activation of the kinin-B2 receptor, was conditioned by ERK1/2 activation. Moreover, immunohistochemistry analysis of hippocampal dentate gyrus showed that the percentage of Ki67+ cells markedly increased in bradykinin-treated mice, and ERK1/2 inhibition affected this neurogenic response. The progress of neurogenesis depended on sustained ERK phosphorylation and resulted in ERK1/2 translocation to the nucleus in NPCs and PC12 cells, changing expression of genes such as Hes1 and Ngn2 (also known as Neurog2). In agreement with the function of ERK in integrating signaling pathways, effects of bradykinin in stimulating neurogenesis were reversed following removal of protein kinase C (PKC)-mediated sustained phosphorylation. |
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Pillat, Micheli MainardiLameu, ClaudianaTrujillo, Cleber A.Glaser, TalitaCappellari, Angélica ReginaNegraes, Priscilla D.Battastini, Ana Maria OliveiraSchwindt, Telma T.Muotri, Alysson RenatoUlrich, Henning2018-02-20T02:25:15Z20160021-9533http://hdl.handle.net/10183/172606001059634During brain development, cells proliferate, migrate and differentiate in highly accurate patterns. In this context, published results indicate that bradykinin functions in neural fate determination, favoring neurogenesis and migration. However, mechanisms underlying bradykinin function are yet to be explored. Our findings indicate a previously unidentified role for bradykinin action in inducing neurongenerating division in vitro and in vivo, given that bradykinin lengthened the G1-phase of the neural progenitor cells (NPC) cycle and increased TIS21 (also known as PC3 and BTG2) expression in hippocampus from newborn mice. This role, triggered by activation of the kinin-B2 receptor, was conditioned by ERK1/2 activation. Moreover, immunohistochemistry analysis of hippocampal dentate gyrus showed that the percentage of Ki67+ cells markedly increased in bradykinin-treated mice, and ERK1/2 inhibition affected this neurogenic response. The progress of neurogenesis depended on sustained ERK phosphorylation and resulted in ERK1/2 translocation to the nucleus in NPCs and PC12 cells, changing expression of genes such as Hes1 and Ngn2 (also known as Neurog2). In agreement with the function of ERK in integrating signaling pathways, effects of bradykinin in stimulating neurogenesis were reversed following removal of protein kinase C (PKC)-mediated sustained phosphorylation.application/pdfengJournal of Cell Science. London. Vol. 129, no. 18 (Sep. 2016), p. 3437-3448BradicininaCiclo celularNeurogêneseSistema de sinalização das MAP quinasesBradykininERKProliferationNeurogenesisNgn2Cell cycleBradykinin promotes neuron-generating division of neural progenitor cells through ERK activationEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSORIGINAL001059634.pdf001059634.pdfTexto completo (inglês)application/pdf4656246http://www.lume.ufrgs.br/bitstream/10183/172606/1/001059634.pdf50019e7b0dd39cc4a4421ef693a1350fMD51TEXT001059634.pdf.txt001059634.pdf.txtExtracted Texttext/plain73317http://www.lume.ufrgs.br/bitstream/10183/172606/2/001059634.pdf.txtf9ddd50d74f5bda7592ba806c7323e82MD52THUMBNAIL001059634.pdf.jpg001059634.pdf.jpgGenerated Thumbnailimage/jpeg2230http://www.lume.ufrgs.br/bitstream/10183/172606/3/001059634.pdf.jpg61064b1f5d1fe9a4a60fbad9725daeb1MD5310183/1726062018-10-29 07:49:41.575oai:www.lume.ufrgs.br:10183/172606Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2018-10-29T10:49:41Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation |
title |
Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation |
spellingShingle |
Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation Pillat, Micheli Mainardi Bradicinina Ciclo celular Neurogênese Sistema de sinalização das MAP quinases Bradykinin ERK Proliferation Neurogenesis Ngn2 Cell cycle |
title_short |
Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation |
title_full |
Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation |
title_fullStr |
Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation |
title_full_unstemmed |
Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation |
title_sort |
Bradykinin promotes neuron-generating division of neural progenitor cells through ERK activation |
author |
Pillat, Micheli Mainardi |
author_facet |
Pillat, Micheli Mainardi Lameu, Claudiana Trujillo, Cleber A. Glaser, Talita Cappellari, Angélica Regina Negraes, Priscilla D. Battastini, Ana Maria Oliveira Schwindt, Telma T. Muotri, Alysson Renato Ulrich, Henning |
author_role |
author |
author2 |
Lameu, Claudiana Trujillo, Cleber A. Glaser, Talita Cappellari, Angélica Regina Negraes, Priscilla D. Battastini, Ana Maria Oliveira Schwindt, Telma T. Muotri, Alysson Renato Ulrich, Henning |
author2_role |
author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Pillat, Micheli Mainardi Lameu, Claudiana Trujillo, Cleber A. Glaser, Talita Cappellari, Angélica Regina Negraes, Priscilla D. Battastini, Ana Maria Oliveira Schwindt, Telma T. Muotri, Alysson Renato Ulrich, Henning |
dc.subject.por.fl_str_mv |
Bradicinina Ciclo celular Neurogênese Sistema de sinalização das MAP quinases |
topic |
Bradicinina Ciclo celular Neurogênese Sistema de sinalização das MAP quinases Bradykinin ERK Proliferation Neurogenesis Ngn2 Cell cycle |
dc.subject.eng.fl_str_mv |
Bradykinin ERK Proliferation Neurogenesis Ngn2 Cell cycle |
description |
During brain development, cells proliferate, migrate and differentiate in highly accurate patterns. In this context, published results indicate that bradykinin functions in neural fate determination, favoring neurogenesis and migration. However, mechanisms underlying bradykinin function are yet to be explored. Our findings indicate a previously unidentified role for bradykinin action in inducing neurongenerating division in vitro and in vivo, given that bradykinin lengthened the G1-phase of the neural progenitor cells (NPC) cycle and increased TIS21 (also known as PC3 and BTG2) expression in hippocampus from newborn mice. This role, triggered by activation of the kinin-B2 receptor, was conditioned by ERK1/2 activation. Moreover, immunohistochemistry analysis of hippocampal dentate gyrus showed that the percentage of Ki67+ cells markedly increased in bradykinin-treated mice, and ERK1/2 inhibition affected this neurogenic response. The progress of neurogenesis depended on sustained ERK phosphorylation and resulted in ERK1/2 translocation to the nucleus in NPCs and PC12 cells, changing expression of genes such as Hes1 and Ngn2 (also known as Neurog2). In agreement with the function of ERK in integrating signaling pathways, effects of bradykinin in stimulating neurogenesis were reversed following removal of protein kinase C (PKC)-mediated sustained phosphorylation. |
publishDate |
2016 |
dc.date.issued.fl_str_mv |
2016 |
dc.date.accessioned.fl_str_mv |
2018-02-20T02:25:15Z |
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Estrangeiro info:eu-repo/semantics/article |
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http://hdl.handle.net/10183/172606 |
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0021-9533 |
dc.identifier.nrb.pt_BR.fl_str_mv |
001059634 |
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url |
http://hdl.handle.net/10183/172606 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
Journal of Cell Science. London. Vol. 129, no. 18 (Sep. 2016), p. 3437-3448 |
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info:eu-repo/semantics/openAccess |
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openAccess |
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