Mast cell-deficiency protects mice from streptozotocin-induced diabetic cardiomyopathy.

Mast cell-deficiency protects mice from streptozotocin-induced diabetic cardiomyopathy. Transl Res. 2019 Jan 19;: Authors: He A, Fang W, Zhao K, Wang Y, Li J, Yang C, Benadjaoud F, Shi GP Abstract Mast cells (MCs) have been implicated in the pathogenesis of cardiometabolic diseases by releasing pro-inflammatory mediators. Patients and animals with diabetic cardiomyopathy (DCM) also show inflammatory cell accumulation in the heart. Here, we detected MCs in mouse heart after streptozotocin (STZ)-induced DCM. DCM production caused significant systole and diastole interventricular septum and left ventricular (LV) posterior wall thinning, and systolic LV internal dilation in wild-type (WT) mice. DCM production also led to significant reductions of fractional shortening percentage, heart rate, body weight, heart weight, and significant increases of kidney, pancreas, and lung weight to body weight ratios, and blood hemoglobin HbA1c and glucose levels in WT mice. All these changes were improved or disappeared in MC-deficient KitW-sh/W-sh mice. In the myocardium from WT DCM mice, we detected significant decrease of cardiac cell proliferation and increases of cardiac cell death, chemokine expression, macrophage infiltration, inflammatory cytokine expression, and collagen deposition. These changes were also improved or disappeared in KitW-sh/W-sh DCM mice. Adoptive transfer of bone marrow-derived MCs (BMMCs) from WT mice fully or partially reve...
Source: Translational Research : the journal of laboratory and clinical medicine - Category: Laboratory Medicine Authors: Tags: Transl Res Source Type: research