p21(CIP1/WAF1)-dependent inhibition of cardiac hypertrophy in response to Angiotensin II involves Akt/Myc and pRb signaling

• Published in: Peptides (New York, N.Y. : 1980) Vol. 83; pp. 38 - 48
• Main Authors: Hauck, Ludger, Grothe, Daniela, Billia, Filio
• Format: Journal Article
• Language: English
• Published: United States 01.09.2016
• Subjects: Angiotensin II - administration & dosage; Angiotensin II - metabolism; Animals; Cardiomegaly - genetics; Cardiomegaly - physiopathology; Cardiomegaly - therapy; Cyclin-Dependent Kinase Inhibitor p21 - biosynthesis; Cyclin-Dependent Kinase Inhibitor p21 - genetics; Gene Expression Regulation - genetics; Heart - growth & development; Heart - physiopathology; Heart Failure - genetics; Heart Failure - physiopathology; Heart Failure - therapy; Humans; Mice; Mice, Knockout; Oncogene Protein v-akt - genetics; Proto-Oncogene Proteins c-myc - genetics; Retinoblastoma Protein - genetics; Heart failure; Cardiac hypertrophy; Cdk; p21; Cyclin D2; Cardiac fibrosis; p27; Myc; Angiotensin; Cell cycle; Cdkn1a; Retinoblastoma; Cdkn1b

The cyclin-dependent kinase inhibitor p21(CIP1/WAF1) (p21) is highly expressed in the adult heart. However, in response to stress, its expression is downregulated. Therefore, we investigated the role of p21 in the regulation of cardiac hypertrophic growth. At 2 months of age, p21 knockout mice (p21K...