Targeted proteolysis sustains calcineurin activation

Calcineurin (CnA) is important in the regulation of myocardial hypertrophy. We demonstrated that targeted proteolysis of the CnA autoinhibitory domain under pathological myocardial workload leads to increased CnA activity in human myocardium. Here, we investigated the proteolytic mechanism leading t...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Circulation (New York, N.Y.) N.Y.), 2005-03, Vol.111 (8), p.1045-1053
Hauptverfasser:	BURKARD, Natalie, BECHER, Jan, HEINDL, Cornelia, NEYSES, Ludwig, SCHUH, Kai, RITTER, Oliver
Format:	Artikel
Sprache:	eng
Schlagworte:	Active Transport, Cell Nucleus - physiology Amino Acid Sequence Animals Animals, Newborn Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Calcineurin - chemistry Calcineurin - genetics Calcineurin - metabolism Calpain - metabolism Cardiology. Vascular system Cardiomegaly - pathology Cardiovascular system Cell Extracts - chemistry Cell Nucleus - chemistry Cells, Cultured Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Enzyme Activation - physiology Frozen Sections Humans Hydrolysis Medical sciences Miscellaneous Molecular Sequence Data Myocardium - chemistry Myocardium - enzymology Myocardium - metabolism Myocardium - pathology Myocytes, Cardiac - chemistry Myocytes, Cardiac - cytology Myocytes, Cardiac - enzymology Myocytes, Cardiac - metabolism Pharmacology. Drug treatments Phosphoric Monoester Hydrolases - metabolism Proteins - metabolism Rats Rats, Wistar Transcription, Genetic - genetics
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Beschreibung
Zusammenfassung:	Calcineurin (CnA) is important in the regulation of myocardial hypertrophy. We demonstrated that targeted proteolysis of the CnA autoinhibitory domain under pathological myocardial workload leads to increased CnA activity in human myocardium. Here, we investigated the proteolytic mechanism leading to activation of CnA. In patients with diseased myocardium, we found strong nuclear translocation of CnA. In contrast, in normal human myocardium, there was a cytosolic distribution of CnA. Stimulation of rat cardiomyocytes with angiotensin (Ang) II increased calpain activity significantly (433+/-11%; P
ISSN:	0009-7322 1524-4539
DOI:	10.1161/01.cir.0000156458.80515.f7