Obesity suppresses circulating level and function of endothelial progenitor cells and heart function

Abstract

Background and aimThis study tested the hypothesis that obesity suppresses circulating number as well as the function of endothelial progenitor cells (EPCs) and left ventricular ejection fraction (LVEF).MethodsHigh fat diet (45 Kcal% fat) was given to 8-week-old C57BL/6 J mice (n = 8) for 20 weeks to induce obesity (group 1). Another age-matched group (n = 8) were fed with control diet for 20 weeks as controls (group 2). The animals were sacrificed at the end of 20 weeks after obesity induction.ResultsBy the end of study period, the heart weight, body weight, abdominal fat weight, serum levels of total cholesterol and fasting blood sugar were remarkably higher in group 1 than in group 2 (all p<0.01). The circulating level of EPCs (C-kit/CD31, Sca-1/KDR, CXCR4/CD34) was significantly lower in group 1 than in group 2 (p<0.03) at 18 h after critical limb ischemia induction. The angiogenesis and migratory ability of bone marrow-derived EPCs was remarkably impaired in group 1 compared to that in group 2 (all p<0.01). The repair ability of aortic endothelium damage by lipopolysaccharide was notably attenuated in group 1 compared with that in group 2 (p<0.01). Collagen deposition (Sirius red staining) and fibrotic area (Masson's Trichrome staining) in LV myocardium were notably increased in group 1 compared with group 2 (p<0.001). LVEF was notably lower, whereas LV end-diastolic and end-systolic dimensions were remarkably higher in group 1 than in group 2 (all p<0.001).ConclusionsObesity diminished circulating EPC level, impaired the recovery of damaged endothelium, suppressed EPC angiogenesis ability and LVEF, and increased LV remodeling.

Daily melatonin protects the endothelial lineage and functional integrity against the aging process, oxidative stress, and toxic environment and restores blood flow in critical limb ischemia area in mice

“…The protocol and procedure of EPC culture and the assessment of angiogenesis were based on our recent report . In brief, mononuclear cells (MNCs) from young mice (3 months old), old mice (8 months old), and old mice (8 months old) being treated daily with Mel were isolated by density‐gradient centrifugation of Ficoll 400 (Sigma‐Aldrich, St. Louis, Mo, USA).…”

Functional Neural–Bone Marrow Pathways

“…29–31, 36, 37, 52–59 In fact, a correlation exists between elevated inflammatory responses and disease progression, 31, 57, 60, 61 and immunosupression can delay or even arrest the progression of CVD. 62–67 Second , following an acute injury, the BM cells with angiogenic and reparative properties such as endothelial progenitor cells (EPCs) 17, 68–73 are immediately recruited to the site of injury, aiding in repair of the tissue damage. 74–78 Unfortunately, some patients with advancing CVD and other related diseases have significantly decreased pools of EPCs, 79, 80 and this decreased vascular potential further exacerbates the dysfunctional vasculature already seen in CVD.…”

Preactivated and Disaggregated Shape-Changed Platelets Protected Against Acute Respiratory Distress Syndrome Complicated by Sepsis Through Inflammation Suppression

“…Additionally, to mimic the clinical setting of ARDS complicated by sepsis, LPS (1.5 mg/kg i.p for each rat) was administered to groups 3 and 4 at 24 h later after ARDS induction. The administration of LPS to animals for sepsis induction was based on our previous report with minimal modification (31).…”