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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Photobiomodulation Therapy on Myocardial Infarction in Rats: Transcriptional and Posttranscriptional Implications to Cardiac Remodeling

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Autor(es):
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Feliciano, Regiane dos Santos [1] ; Barboza Atum, Allan Luis [1] ; da Silva Ruiz, Erico Gustavo [1] ; Serra, Andrey Jorge [2] ; Antonio, Ednei Luiz [2] ; Manchini, Martha Trindade [1] ; Augusto Silva, Jairo Montemor [2] ; Ferreira Tucci, Paulo Jose [2] ; Nathanson, Lubov [3] ; Morris, Mariana [3] ; Chavantes, Maria Cristina [1] ; Silva Junior, Jose Antonio [1]
Número total de Autores: 12
Afiliação do(s) autor(es):
[1] Univ Nove Julho, Rua Vergueiro 249, BR-01504001 Sao Paulo, SP - Brazil
[2] Univ Fed Sao Paulo, Rua Pedro Toledo 709, BR-04039001 Sao Paulo, SP - Brazil
[3] Nova Southeastern Univ, 3301 Coll Ave, Ft Lauderdale, FL 33314 - USA
Número total de Afiliações: 3
Tipo de documento: Artigo Científico
Fonte: Lasers in Surgery and Medicine; v. 53, n. 9, p. 1247-1257, NOV 2021.
Citações Web of Science: 0
Resumo

Background and Objectives: Induction of myocardial infarction (MI) in rats by occlusion of the left anterior descending coronary artery is an experimental model used in research to elucidate functional, structural, and molecular modifications associated with ischemic heart disease. Photobiomodulation therapy (PBMT) has become a therapeutic alternative by modulating various biological processes eliciting several effects, including anti-inflammatory and pro-proliferative actions. The main objective of this work was to evaluate the effect of PBMT in the modulation of transcriptional and post-transcriptional changes that occurred in myocardium signal transduction pathways after MI. Study Design/Materials and Methods: Continuous wave (CW) non-thermal laser parameters were: 660 nm wavelength, power 15 mW, with a total energy of 0.9 J, fluence of 1.15 J/cm(2), spot size of 0.785 cm(2), and time of 60 seconds. Using in silico analysis, we selected and then, quantified the expression of messenger RNA (mRNA) of 47 genes of 9 signaling pathways associated with MI (angiogenesis, cell survival, hypertrophy, oxidative stress, apoptosis, extracellular matrix, calcium kinetics, cell metabolism, and inflammation). Messenger RNA expression quantification was performed in myocardial samples by polymerase chain reaction real-time array using TaqMan customized plates. Results: Our results evidenced that MI modified mRNA expression of several well-known biomarkers related to detrimental cardiac activity in almost all signaling pathways analyzed. However, PBMT reverted most of these transcriptional changes. More expressively, PBMT provoked a robust decrease in mRNA expression of molecules that participate in post-MI inflammation and ECM composition, such as IL-6, TNF receptor, TGFb1, and collagen I and III. Global microRNA (miRNA) expression analysis revealed that PBMT decreased miR-221, miR-34c, and miR-93 expressions post-MI, which are related to deleterious effects in cardiac remodeling. Conclusion: Thus, the identification of transcriptional and post-transcriptional changes induced by PBMT may be used to interfere in the molecular dynamics of cardiac remodeling post-MI. (AU)

Processo FAPESP: 09/54225-8 - Fisiopatologia da insuficiência cardíaca congestiva
Beneficiário:Paulo Jose Ferreira Tucci
Modalidade de apoio: Auxílio à Pesquisa - Temático
Processo FAPESP: 12/15808-0 - Caracterização da expressão gênica de vias de transdução do sinal no miocárdio remoto ao infarto induzido por ablação ventricular esquerda e oclusão da artéria coronária em ratos
Beneficiário:Eduardo Tadeu Santana
Modalidade de apoio: Bolsas no Brasil - Doutorado
Processo FAPESP: 15/11028-9 - A modalidade de treinamento físico aeróbio pode determinar a existência de remodelamento cardíaco: identificando peculiaridades estruturais, funcionais e moleculares dos modelos experimentais de natação e corrida
Beneficiário:Andrey Jorge Serra
Modalidade de apoio: Auxílio à Pesquisa - Regular