Knockdown of miR-26a in zebrafish leads to impairment of the anti-inflammatory function of TnP in the control of neutrophilia

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dc.contributorLETA - Laboratório de Toxinologia Aplicadapt_BR
dc.contributorCentro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS)pt_BR
dc.contributorPrograma de Pós-Graduação em Ciências – Toxinologia (PPGTox)pt_BR
dc.contributor.authorFalcão, Maria Alice Pimentelpt_BR
dc.contributor.authorWalker, Cristiani Isabel Banderópt_BR
dc.contributor.authorDisner, Geonildo Rodrigopt_BR
dc.contributor.authorSilva Filho, João Batista dapt_BR
dc.contributor.authorSoares, Amanda Beatriz Silvapt_BR
dc.contributor.authorLima, Leticia Balanpt_BR
dc.contributor.authorLima, Carlapt_BR
dc.contributor.authorLopes-Ferreira, Monicapt_BR
dc.date.accessioned2021-05-21T14:13:09Z-
dc.date.available2021-05-21T14:13:09Z-
dc.date.issued2021pt_BR
dc.identifier.citationFalcão MAP, Walker CIB, Disner GR, Silva Filho JB, Soares ABS, Lima LB, et al. Knockdown of miR-26a in zebrafish leads to impairment of the anti-inflammatory function of TnP in the control of neutrophilia. Fish Shellfish Immunol. 2021 July;114:301-310. doi:10.1016/j.fsi.2021.04.029.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/3763-
dc.description.abstractOur recent data show the valuable potential of TnP for the development of a new and safe anti-inflammatory drug due to its ability to control the traffic and activation of leukocytes in response to inflammation. Although there is considerable knowledge surrounding the cellular mechanisms of TnP, less is known about the mechanistic molecular role of TnP underlying its immunomodulatory functions. Here, we conducted investigations to identify whether miRNAs could be one of the molecular bases of the therapeutic effect of TnP. Using a zebrafish model of neutrophilic inflammation with a combination of genetic gain- and loss-of-function approaches, we showed that TnP treatment was followed by up-regulation of only four known miRNAs, and mature dre-miR-26a-1, herein referred just as miR-26a was the first most highly expressed. The knockdown of miR-26a ubiquitously resulted in a significant reduction of miR-26a in embryos, accompanied by impaired TnP immunomodulatory function observed by the loss of the control of the removal of neutrophils in response to inflammation, while the overexpression increased the inhibition of neutrophilic inflammation promoted by TnP. The striking importance of miR-26a was confirmed when rescue strategies were used (morpholino and mimic combination). Our results identified miR-26a as an essential molecular regulator of the therapeutic action of TnP, and suggest that miR-26a or its targets could be used as promising therapeutic candidates for enhancing the resolution of inflammation.pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt_BR
dc.format.extent301-310pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofFish & Shellfish Immunologypt_BR
dc.rightsOpen Accesspt_BR
dc.titleKnockdown of miR-26a in zebrafish leads to impairment of the anti-inflammatory function of TnP in the control of neutrophiliapt_BR
dc.typeArticlept_BR
dc.identifier.doi10.1016/j.fsi.2021.04.029pt_BR
dc.identifier.urlhttps://doi.org/10.1016/j.fsi.2021.04.029pt_BR
dc.contributor.externalUniversidade Federal de Sergipe (UFS)pt_BR
dc.identifier.citationvolume114pt_BR
dc.subject.keywordTnP peptidept_BR
dc.subject.keywordZebrafish (Danio rerio)pt_BR
dc.subject.keywordInflammationpt_BR
dc.subject.keywordNeutrophiliapt_BR
dc.subject.keywordmiR-26apt_BR
dc.relation.ispartofabbreviatedFish Shellfish Immunolpt_BR
dc.identifier.citationabntv. 114, p. 301-310, jul. 2021pt_BR
dc.identifier.citationvancouver2021 July;114:301-310pt_BR
dc.contributor.butantanFalcão, Maria Alice Pimentel|:Aluno|:Laboratório Especial de Toxinologia Aplicada (LETA):Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS|:PrimeiroAutorpt_BR
dc.contributor.butantanDisner, Geonildo Rodrigo|:Pesquisador|:Laboratório Especial de Toxinologia Aplicada (LETA):Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS)pt_BR
dc.contributor.butantanSilva Filho, João Batista da|:Aluno|:Laboratório Especial de Toxinologia Aplicada (LETA):Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS):Programa de Pós-Graduação em Ciências – Toxinologia (PPGTox)pt_BR
dc.contributor.butantanSoares, Amanda Beatriz Silva|:Aluno|:Laboratório Especial de Toxinologia Aplicada (LETA):Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS)pt_BR
dc.contributor.butantanLima, Leticia Balan|:Aluno|:Laboratório Especial de Toxinologia Aplicada (LETA):Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS)pt_BR
dc.contributor.butantanLima, Carla|:Pesquisador:Docente permanente PPGTOX|:Laboratório Especial de Toxinologia Aplicada (LETA):Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS)|:Autor de correspondênciapt_BR
dc.contributor.butantanLopes-Ferreira, Monica|:Pesquisador:Laboratório Especial de Toxinologia Aplicada (LETA):Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS)pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2013/07467-1pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦305414/2019-4pt_BR
dc.sponsorship.butantanCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)¦¦001pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
item.grantfulltextembargo_29990101-
item.languageiso639-1English-
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