pone.0244768.g006.tif (3.43 MB)
Fig 6 -
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posted on 2021-09-08, 17:25 authored by Thaoan Bruno Mariano, Anthony César de Souza Castilho, Ana Karenina Dias de Almeida Sabela, André Casanova de Oliveira, Sarah Santiloni Cury, Andreo Fernando Aguiar, Raisa de Jesus Dutra Dias, Antonio Carlos Cicogna, Katashi Okoshi, Luis Antonio Justulin Junior, Robson Francisco Carvalho, Francis Lopes PacagnelliThe mRNA abundance of A. Myh6 gene expression. B. Myh7 gene expression. C. Myh7b gene expression. D. Col1a1 gene expression. E. Col1a2 gene expression. F. Col3a1 gene expression. G. Mmp2 gene expression in RV of experimental groups. S (n = 8): Sedentary Control; T (n = 8): Control with Training; SPAH (8): Sedentary Pulmonary Arterial Hypertension; TPAH (n = 8): Pulmonary Arterial Hypertension with Training. p <0.05 compared to S. Kruskal-Wallis and Dunn’s post hoc.
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right hypertrophied ventriclesreduced cardiac hypertrophypulmonary arterial hypertensionextracellular matrix remodelingextracellular matrix genesweek adaptation periodencoding proteins associateddiv >< passessed exercise capacity8 ); sedentary8 ); controlweek training periodtpah groups receivedtpah group rats8 );sedentary controlgroups receivedtpah groupspreventive exercisefunctional capacityencoding myosin8 ).13th week11th weekfour groupstranscript abundancetraining protocolspah groupsectional areasreverse transcriptionrats underwentquantitative pcrqpcr ).preventive trainingpah ),myocyte cellsmyh7 kg ).induce alterationsgain insightfulton ’fractal dimensionfindings demonstratefd ).echocardiography analysiscollagen expressioncollagen contentcol1a1 60 mg
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