CREM-transgene mice: An animal model of atrial fibrillation and thrombogenesis

Abstract Background The molecular pathomechanisms underlying atrial thrombogenesis are multifactorial and still require detailed investigations. Transgenic mice with cardiomyocyte-directed expression of the transcriptional repressor CREM-IbΔC-X (CREM-TG) represent an experimental model of atrial fibrillation (AF) that shows a gradual, age-dependent progression from atrial ectopy to persistent AF. Importantly, this model develops biatrial thrombi. The molecular characteristics related to the thrombogenesis in CREM-TG mice have not been studied, yet. Methods The inflammatory and prothrombotic state was evaluated at the transcriptional (qRT-PCR) and protein level in the left (LA) and right atria (RA) from CREM-TG mice at the age of 20 weeks and compared to wild-type controls. Moreover, histological analyses of atrial thrombi were performed. Results The endocardial dysfunction was mirrored by diminished levels of eNOS-mRNA in both atria (RA: 0.79 ± 0.04, LA: 0.72 ± 0.06; each P P P P P P Conclusions CREM-TG mice represent a valuable model for studying atrial thrombogenesis and assessing therapeutic approaches preventing embolic events in the systemic and pulmonary circulation.