Proinflammatory Role of Angiotensin II in the Aorta of Normotensive Mice

Autor: Silvia Lacchini, Rariane Silva de Lima, Maria Claudia Irigoyen, Marina Gazzano Baladi, Leandro E. Souza, Cintia Taniguti Lima, Maikon Barbosa da Silva, J. C. S. Silva
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Chemokine
medicine.medical_specialty
Article Subject
medicine.medical_treatment
Interleukin-1beta
Nitric Oxide Synthase Type II
Adipose tissue
lcsh:Medicine
Blood Pressure
030204 cardiovascular system & hematology
Muscle
Smooth
Vascular
General Biochemistry
Genetics and Molecular Biology
Proinflammatory cytokine
Mice
03 medical and health sciences
0302 clinical medicine
Transforming Growth Factor beta
medicine.artery
Internal medicine
medicine
Animals
Humans
Saline
Aorta
General Immunology and Microbiology
biology
Cell adhesion molecule
business.industry
Angiotensin II
lcsh:R
General Medicine
Actins
Endocrinology
Gene Expression Regulation
Cardiovascular Diseases
030220 oncology & carcinogenesis
biology.protein
Leukocyte Common Antigens
Immunohistochemistry
Saline Solution
CAMUNDONGOS
business
Research Article
Zdroj: BioMed Research International, Vol 2019 (2019)
Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USP
BioMed Research International
ISSN: 2314-6141
2314-6133
Popis: Angiotensin II plays important functions in cardiovascular system mediating actions leading to inflammatory responses such as activation of VSMC in order to produce ROS, inflammatory cytokines, chemokines, and adhesion molecules. Changes in angiotensin II production could stimulate the recruitment and activation of myeloid cells initiating local inflammatory response without effect on BP. We aimed to verify if angiotensin II induces an inflammatory response in the aorta and if it correlates with variations in BP. C57Bl/6 mice treated with saline solution (0.9%, control group) or angiotensin II (30ng/kg, Ang II group) were used. BP and HR levels were measured. Immunohistochemistry for IL1-β, TGF-β, iNOS, CD45, andα-actin was performed in the aorta. BP and HR do not change. A biphasic response was observed both for IL1-βand TGF-βexpression and also for the presence of CD45 positive cells, with an acute increase (between 30 and 60 minutes) and a second increase, between 24 and 48 hours. Positive staining for iNOS increased in the earlier period (30 minutes) in perivascular adipose tissue and in a longer period (48 hours) in tunica adventitia. Immunoblotting toα-actin showed no alterations, suggesting that the applied dose of angiotensin II does not alter the aortic VSMCs phenotype. The results suggest that angiotensin II, even at doses that do not alter BP, induces the expression of inflammatory markers and migration of inflammatory cells into the aorta of normotensive mice. Thus, angiotensin II may increase the propensity to develop a cardiovascular injury, even in normotensive individuals.
Databáze: OpenAIRE
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