Angiotensin II Enhances Integrin and α-Actinin Expression in Adult Rat Cardiac Fibroblasts
Key result
Angiotensin II induces integrin and alpha-actinin expression in cardiac fibroblasts, which is associated with adhesion and left ventricular hypertrophy, and is blocked by AT1 receptor inhibition.
Population
Adult rat cardiac fibroblasts in vitro and spontaneously hypertensive rats (SHR) in vivo
Comparison
Angiotensin II with or without AT1 receptor… vs Untreated cardiac fibroblasts; untreated SHR…
Design
Preclinical
Authors
Discussion
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Implication
AT1 blockade may attenuate fibroblast adhesion in Ang II-driven LVH models; leaves open translation to human hypertension therapy.
Structured PICO
P
Population
In vitro study of adult rat cardiac fibroblasts and in vivo study of spontaneously hypertensive rats to investigate the role of Angiotensin II on integrin and alpha-actinin expression.
I
Intervention
Angiotensin II (100 nmol/L) with or without AT1 receptor antagonist (irbesartan 10 micromol/L) or AT2 receptor antagonist (PD 123319 10 micromol/L) in vitro; AT1 receptor blocker (losartan) or hydralazine in vivo
C
Comparator
Untreated cardiac fibroblasts; untreated SHR; Wistar-Kyoto rats
O
Outcome
Expression of integrins (αv, β1, β3, β5), osteopontin, and α-actinin mRNA and protein levels; cell attachment to extracellular matrix; left ventricular masssurrogate
Angiotensin II induces integrin and α-actinin expression in cardiac fibroblasts via the AT1 receptor, contributing to cell adhesion and left ventricular hypertrophy.
Cite This Study
Kawano et al. (2000) studied Cardiac remodeling and left ventricular hypertrophy. Angiotensin II (in vitro) and Losartan (in vivo) vs. Without Ang II (in vitro); Hydralazine or Wistar-Kyoto rats (in vivo) was evaluated on Integrin and alpha-actinin mRNA and protein levels, cell attachment, and left ventricular mass. Angiotensin II induces integrin and alpha-actinin expression in cardiac fibroblasts, which is associated with adhesion and left ventricular hypertrophy, and is blocked by AT1 receptor inhibition.