Heart Failure-Induced Diaphragm Myopathy

Author(s):Show less -

Ruiz Lima, Aline Regina ^[1] ; Martinez, Paula Felippe ^[2] ; Damatto, Ricardo Luiz ^[1] ; Mariano Cezar, Marcelo Diarcadia ^[1] ; Guizoni, Daniele Mendes ^[1] ; Bonomo, Camila ^[1] ; Oliveira, Jr., Silvio Assis ^[2] ; Silva, Maeli Dal-Pai ^[3] ; Mamede Zornoff, Leonardo Antonio ^[1] ; Okoshi, Katashi ^[1] ; Okoshi, Marina Politi ^[1]

Affiliation

^[1] UNESP, Botucatu Med Sch, Dept Internal Med, Botocutu, SP - Brazil

^[2] Fed Univ Mato Grosso Do Sul UFMS, Biol Sci & Hlth Ctr, Campo Grande, MS - Brazil

^[3] UNESP, Biosci Inst, Dept Morphol, Botucatu, SP - Brazil

• Document type: Journal article
• Source: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY; v. 34, n. 2, p. 333-345, 2014.
• Web of Science Citations: 20

Abstract

Background: Intracellular signaling pathways involved in skeletal myosin heavy chain (MyHC) isofornn alterations during heart failure (HF) are not completely understood. We tested the hypothesis that diaphragm expression of mitogen-activated protein kinases (MAPK) and myogenic regulatory factors is changed in rats with myocardial infarction (MI) induced HF. Methods: Six months after MI rats were subjected to transthoracic echocardiography. After euthanasia, infarcted rats were subdivided in MI/HF- group (with no HF evidence; n=10), and MI/HF+ (with right ventricular hypertrophy and lung congestion; n=10). Sham operated rats were used as controls (n=10). MyHC isofornns were analyzed by electrophoresis. Statistical analysis: ANOVA and Pearson correlation. Results: MI/HF- had left cardiac chambers dilation with systolic and diastolic left ventricular dysfunction. Cardiac injury was more intense in MI/HF+ than MI/HF-. MyHC I isoform percentage was higher in MI/HF+ than MI/HF-, and IIb isoform lower in MI/HF+ than Sham. Left atrial diameter-to-body weight ratio positively correlated with MyHC I (p=0.005) and negatively correlated with MyHC IIb (p=0.02). TNF-alpha serum concentration positively correlated with MyHC I isoform. Total and phosphorylated ERK was lower in MI/HF- and MI/HF+ than Sham. Phosphorylated JNK was lower in MI/HF- than Sham. JNK and p38 did not differ between groups. Expression of NF-kappa B and the myogenic regulatory factors MyoD, myogenin, and MRF4 was similar between groups. Conclusion: Diaphragm MyHC fast-to-slow shift is related to cardiac dysfunction severity and TNF-alpha serum levels in infarcted rats. Reduced ERK expression seems to participate in MyHC isofornn changes. Myogenic regulatory factors and NF-kappa B do not modulate diaphragm MyHC distribution during chronic HF. Copyright (C) 2014 S. Karger AG, Basel (AU)