TY - JOUR
T1 - Molecular evidence of tissue remodeling in an animal model of heart failure
AU - Nascimento, Lais Silva
AU - Tedesco, Larissa Martins
AU - Araujo, Natiele Silva
AU - Priviero, Fernanda Bruschi Marinho
AU - Claudino, Mario Angelo
AU - Priolli, Denise Gonçalves
AU - Rocha, Thalita
N1 - Funding Information:
Acknowledgements. This study was financed in part with the supported of Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brazil (CAPES) - Finance Code 1263493 and by Conselho Nacional de Desenvolvimento Científico e Tecnológico – Brazil (CNPq) - Finance Code 139087/2015-0.
Publisher Copyright:
© 2019, Histology and Histopathology. All rights reserved.
PY - 2019
Y1 - 2019
N2 - Summary. Heart failure (HF) is the final common pathway of many cardiovascular diseases. Metalloproteinases and their inhibitors, such as MMP9 and TIMP-1, assist in maintaining the extracellular matrix, leading to tissue remodeling observed after HF. Previous studies have shown that L-Arginine (LA) appears to have beneficial effects for the treatment of HF, contributing to vasodilation, the reestablishment of the endothelial function and an increase in muscle contractile force. This study analyzed heart tissue remodeling in an animal model of HF induced by aortocaval fistula (ACF) and submitted to LA treatment. After 4 weeks of ACF, animals were treated with LA for 4 weeks (SHAM-LA, HF-LA) or for 8-12 weeks with saline (SHAM, HF8, HF12). Rats were euthanized and the hearts removed for histological processing. The samples were stained with Hematoxylin-Eosin (HE), Masson’s Thichome (MT), or submitted to immunohistochemistry (IHC) for MMP9 and TIMP-1. Light microscopy analysis showed cardiac striated muscle without fibrosis in all experimental groups. Immunostaining of MMP9 and TIMP-1 were positive for all experimental groups. LA administration significatively reduced MMP9 content after HF. These data indicate molecular changes in metalloproteinases expression prior to tissue remodeling and point out LA as an adjuvant therapy to pharmacological treatment of patients with HF.
AB - Summary. Heart failure (HF) is the final common pathway of many cardiovascular diseases. Metalloproteinases and their inhibitors, such as MMP9 and TIMP-1, assist in maintaining the extracellular matrix, leading to tissue remodeling observed after HF. Previous studies have shown that L-Arginine (LA) appears to have beneficial effects for the treatment of HF, contributing to vasodilation, the reestablishment of the endothelial function and an increase in muscle contractile force. This study analyzed heart tissue remodeling in an animal model of HF induced by aortocaval fistula (ACF) and submitted to LA treatment. After 4 weeks of ACF, animals were treated with LA for 4 weeks (SHAM-LA, HF-LA) or for 8-12 weeks with saline (SHAM, HF8, HF12). Rats were euthanized and the hearts removed for histological processing. The samples were stained with Hematoxylin-Eosin (HE), Masson’s Thichome (MT), or submitted to immunohistochemistry (IHC) for MMP9 and TIMP-1. Light microscopy analysis showed cardiac striated muscle without fibrosis in all experimental groups. Immunostaining of MMP9 and TIMP-1 were positive for all experimental groups. LA administration significatively reduced MMP9 content after HF. These data indicate molecular changes in metalloproteinases expression prior to tissue remodeling and point out LA as an adjuvant therapy to pharmacological treatment of patients with HF.
KW - Aortocaval fistula
KW - Histochemistry
KW - Metalloproteinases
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U2 - 10.14670/HH-18-128
DO - 10.14670/HH-18-128
M3 - Article
C2 - 31099017
AN - SCOPUS:85075623407
SN - 0213-3911
VL - 34
SP - 1345
EP - 1354
JO - Histology and Histopathology
JF - Histology and Histopathology
IS - 12
ER -