Glucagon-like peptide 1 reverses myocardial hypertrophy through cAMP/PKA/RhoA/ROCK2 signaling

Autor: Shao-Hua Fan, Qian-Feng Xiong, Li-Hui Zhang, Xin Zhang, Yawei Shi
Rok vydání: 2020
Předmět:
Male
rho GTP-Binding Proteins
0301 basic medicine
endocrine system
medicine.medical_specialty
RHOA
medicine.drug_class
Biophysics
Cardiomegaly
030204 cardiovascular system & hematology
Rats
Inbred WKY
Second Messenger Systems
Biochemistry
Glucagon
Cell Line
03 medical and health sciences
0302 clinical medicine
Atrial natriuretic peptide
Glucagon-Like Peptide 1
Rats
Inbred SHR
Internal medicine
Cyclic AMP
medicine
Natriuretic peptide
Animals
Cardiac muscle cell
rho-Associated Kinases
biology
Chemistry
digestive
oral
and skin physiology
General Medicine
medicine.disease
Cyclic AMP-Dependent Protein Kinases
Glucagon-like peptide-1
Angiotensin II
Rats
030104 developmental biology
medicine.anatomical_structure
Endocrinology
Heart failure
biology.protein
hormones
hormone substitutes
and hormone antagonists
Zdroj: Acta Biochimica et Biophysica Sinica. 52:612-619
ISSN: 1672-9145
Popis: Myocardial hypertrophy is a major pathological and physiological process during heart failure. Glucagon-like peptide 1 (GLP-1) is a glucagon incretin hormone released from the gut endocrine L-cells that has protective effects on various cardiovascular diseases, including hypertension, atherosclerosis, and myocardial hypertrophy. However, the protective mechanisms of GLP-1 in myocardial hypertrophy remain unclear. Here, we showed that the GLP-1 agonist liraglutide and dipeptidyl peptidase 4 inhibitor alogliptin decreased heart weight and cardiac muscle cell volume in spontaneously hypertensive rats (SHR). In H9C2 cell hypertensive models induced by angiotensin II, GLP-1 treatment reduced myocardial cell volume, inhibited the expressions of atrial natriuretic peptide, brain/B-type natriuretic peptide, β-myosin heavy chain, RhoA, and ROCK2, and decreased MLC and MYPT1 phosphorylation. When H9C2 cells were treated with H89, a PKA inhibitor, the inhibitory effect of GLP-1 disappeared, while the inhibitory role was enhanced under the treatment of Y-27632, a ROCK2 inhibitor. These results suggested that GLP-1 might reverse myocardial hypertrophy through the PKA/RhoA/ROCK2 signaling pathway.
Databáze: OpenAIRE
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