CaMKIIδC Drives Early Adaptive Ca²⁺ Change and Late Eccentric Cardiac Hypertrophy.

ABSTRACT:

Rationale

CaMKII (Ca²⁺-Calmodulin dependent protein kinase) δC activation is implicated in pathological progression of heart failure (HF) and CaMKIIδC transgenic mice rapidly develop HF and arrhythmias. However, little is known about early spatio-temporal Ca²⁺ handling and CaMKII activation in hypertrophy and HF.

Objective

To measure time- and location-dependent activation of CaMKIIδC signaling in adult ventricular cardiomyocytes, during transaortic constriction (TAC) and in CaMKIIδC transgenic mice.

Methods and results

We used human tissue from nonfailing and HF hearts, 4 mouse lines: wild-type, KO (CaMKIIδ-knockout), CaMKIIδC transgenic in wild-type (TG), or KO background, and wild-type mice exposed to TAC. Confocal imaging and biochemistry rev

SUBMITTER: Ljubojevic-Holzer S 

PROVIDER: S-EPMC7547876 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature