Cd34-flox Mouse

Cd34 is a cell surface antigen expressed in numerous stem/progenitor cells, such as hematopoietic stem cells (HSCs) and endothelial progenitor cells (EPCs) [1]. These CD34+ cells are involved in angiogenesis, anti-inflammatory, immunomodulatory, and anti-apoptosis/fibrosis roles through paracrine activity, and also contribute to direct incorporation into the expanding vasculature [1].

In heart-related studies, in murine pressure overload models (transverse aortic constriction, TAC), non-bone-marrow-derived CD34+ cells give rise to fibroblasts and endothelial cells, while bone-marrow-derived CD34+ cells turn into immune cells in response to pressure overload. Partial depletion of CD34+ cells in Cd34-CreERT2; Rosa26-eGFP-DTA (Cre/DTA) mice alleviated myocardial fibrosis and improved cardiac function, suggesting a role in heart failure-related fibrosis [2]. Similar findings were observed in ischemia/reperfusion (I/R) injury models, where depletion of Cd34+ cells using a Cd34-CreERT2; R26-DTA mouse model alleviated ventricular fibrosis and improved cardiac function, with Cd34+ cells contributing to mesenchymal cell, endothelial cell, and monocyte/macrophage commitment during heart remodeling [3].

In conclusion, Cd34+ cells play crucial roles in processes like angiogenesis and tissue repair. Studies using gene-knockout (KO) or conditional-knockout (CKO) mouse models have revealed their significance in heart-related diseases, especially in myocardial fibrosis and cardiac remodeling after injury, providing potential therapeutic implications for heart failure treatment.