Changes in myofibroblast markers and matrix molecule mRNA expression in isolated cardiac fibroblasts after AngII stimulation and PAR2 inhibition.

<p>Cardiac fibroblasts isolated from neonatal rats were treated with anti-PAR2 blocking antibody SAM11 (αPAR2, n = 5 each) and 2μM PAR2 inhibitor AZ3541 (PAR2 I., n = 3 each) or left untreated (0, n = 5 each) or treated with isotype control antibody (iso, n = 3) as a control using unstimulated...

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محفوظ في:

التفاصيل البيبلوغرافية
المؤلف الرئيسي:	Albrecht Meyer zu Schwabedissen (20390671) (author)
مؤلفون آخرون:	Silvia Vergarajauregui (20390674) (author), Marko Bertog (20390677) (author), Kerstin Amann (186160) (author), Felix B. Engel (13861349) (author), Christoph Daniel (282746) (author)
منشور في:	2024
الموضوعات:	Biochemistry Medicine Cell Biology Genetics Molecular Biology Physiology Pharmacology Biotechnology Immunology Developmental Biology Marine Biology Cancer Infectious Diseases Virology relative heart weight left ventricular cross 40 &# 177 rat cardiac fibroblasts untreated control mice deficient mice compared longer significantly different xlink "> hypertension xlink "> activation wt mice resulted par2 deficient mice left ventricular hypertrophy deficient animals compared cardiac interstitial fibrosis wt mice treated similarly treated par2 induced cardiac injury xlink "> deficient animals cardiac injury cardiac expression wt animals untreated controls significantly increased significantly higher angii compared par2 deficiency sectional area one hand mouse model four weeks fibrotic genes expression levels enhancing fibrosis continuous infusion blocking antibody angiotensin ii ambivalent effect additional experiments
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Changes in myofibroblast markers and matrix molecule mRNA expression in isolated cardiac fibroblasts after AngII stimulation and PAR2 inhibition.

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