Deletion of P110 δ promotes the development of myocarditis in ApoE‑deficient mice by increasing mononuclear cell peritoneal infiltration.

Deletion of P110δ promotes the development of myocarditis in ApoE‑deficient mice by increasing mononuclear cell peritoneal infiltration. Mol Med Rep. 2020 Nov;22(5):3629-3634 Authors: Zhang QZ, Xue AY, Wei W, Pang AM, Cao LN, Liu F Abstract Phosphoinositide 3-kinase catalytic subunit δ isoform (P110δ) is mainly expressed in white blood cells. It is involved in T and B lymphocyte differentiation, maturation and the neutrophil chemotaxis process. Apolipoprotein E (ApoE) is an arginine‑rich alkaline protein, which is present in plasma chylomicron, low‑density lipoprotein and very low‑density lipoprotein. The present study aimed to determine the effects of P110δ deletion on myocarditis in ApoE‑/‑ mice. A mouse model of ApoE and P110δ double deletion was initially constructed; hematoxylin and eosin (H&E) staining was performed to detect the histological alterations in the mouse myocardium. Systolic and diastolic alterations, and alterations in the left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) were examined by electrocardiogram. Blood cell of ApoE and P110δ double mice was used to detect changes in white blood cells and monocytes. Western blotting was used to detect the expression levels of apoptosis‑associated proteins, whereas flow cytometry was used to detect the percentage of apoptosis. Morphological alterations in myocardial cells were observed under a microscope. T...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research