Effects of diabetes on myocardial capillary density and serum angiogenesis biomarkers in male rats

Khazaei, Majid; Fallahzadeh, Ali Reza; Sharifi, Mohammad Reza; Afshar-Moghaddam, Noushin; Javanmard, Shaghayegh Haghjooy; Salehi, Ensieh

doi:10.1590/s1807-59322011000800019

Cited by 33 publications

(23 citation statements)

References 38 publications

(53 reference statements)

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“…[4344] High levels of VEGF-A also lead to vascular permeability in the glomeruli,[45] Physiological levels of NO (nitric oxide) creates low vascular permeability but NO levels too high or too low can lead to hyper-permeability that in turn lead to glomerular injury and diabetic nephropathy. [39]…”

Section: Introductionmentioning

confidence: 99%

Imbalance of angiogenesis in diabetic complications: The mechanisms

2012

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Type 2 diabetes mellitus is a complex disease and a chronic health-care problem. Nowadays, because of alteration of lifestyle such as lack of exercise, intake of high fat diet subsequently obesity and aging population, the prevalence of diabetes mellitus is increasing quickly in around the world. The international diabetes federation estimated in 2008, that 246 million adults in worldwide suffered from diabetes mellitus and the prevalence of disease is expected to reach to 380 million by 2025. Although, mainly in management of diabetes focused on hyperglycemia, however, it is documented that abnormalities of angiogenesis may contribute in the pathogenesis of diabetes complications. Angiogenesis is the generation of new blood vessels from pre-existing ones. Normal angiogenesis depends on the intricate balance between angiogenic factors (such as VEGF, FGF2, TGF-β, angiopoietins) and angiostatic factors (angiostatin, endostatin, thrombospondins). Vascular abnormalities in different tissues including retina and kidney can play a role in pathogenesis of micro-vascular complications of diabetes; also vascular impairment contributes in macrovascular complications e.g., diabetic neuropathy and impaired formation of coronary collaterals. Therefore, identifying of different mechanisms of the diabetic complications can give us an opportunity to prevent and/or treat the following complications and improves quality of life for patients and society. In this review, we studied the mechanisms of angiogenesis in micro-vascular and macro-vascular complications of diabetes mellitus.

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Section: Introductionmentioning

confidence: 99%

Imbalance of angiogenesis in diabetic complications: The mechanisms

2012

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“…[9] Furthermore, it is suggested that VEGF to sVEGFR-1 ratio is a better marker for evaluation of angiogenesis status. [2122] Thus, in the present study, we measured VEGF: sVEGFR1 ratio and we found that this ratio was decreased after BIIE0742 treatment in normal and obese animals. On the other hand, serum NO concentration was also decreased in treatment groups.…”

Section: Discussionmentioning

confidence: 51%

Myocardial capillary density after neuropeptide Y antagonist administration in normal and high-fat diet C57BL6 mice

Alasvand¹,

Javanmard

Rashidi

et al. 2016

Adv Biomed Res

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Background:Neuropeptide Y (NPY), a 36 amino acid peptide, has several effects on cardiovascular system. It is demonstrated that the angiogenic activity of NPY is similar to fibroblast growth factor and vascular endothelial growth factor (VEGF). The aim of this study was to evaluate the effect of systemic administration of antagonist of NPY receptor (BIIE0742) on coronary angiogenesis in normal and diet-induced obese animals.Materials and Methods:Twenty-four male mice were received high-fat diet (HFD) or normal diet (ND) for 14 weeks. Then, each group was randomized to the treatment of antagonist of NPY receptor (BIIE0246) or saline as following: ND+ BIIE0246 (100 μl/kg; i.p.), ND+ saline, HFD+ BIIE0246, HFD+ saline. After 14 days, blood samples were taken, and myocardial tissue (left ventricle) from all experimental groups was evaluated by immunohistochemistry.Results:Serum VEGF concentration and VEGF: Soluble VEGF receptor (sVEGFR)-1 ratio in obese animals was higher than normal group. Administration of BIIE0246 significantly reduced serum VEGF and VEGF: sVEGFR-1 ratio and increased serum sVEGFR-1 concentrations in obese animals (P < 0.05). In normal animals, BIIE0246 increased serum sVEGFR-1 level and decreased VEGF: sVEGFR-1 ratio. Serum nitrite did not alter after administration of BIIE0246 in both groups (P > 0.05). Myocardial capillary density expressed as the number of CD31 positive cells/mm2 was reduced after NPY antagonist treatment in obese and normal animals (P > 0.05).Conclusion:Administration of NPY antagonist impairs myocardial capillary density, reduces angiogenic factors and elevates anti-angiogenic factors, and there are no differences between obese and normal animals.

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“…As, angiogenesis and capillary density decreases in heart of diabetic rats. 18 Similarly, clinical studies have shown an abnormality in endothelium dependent vasodilation in patients with diabetes. 19 Diabetes has been shown to cause structural and functional disturbances in the myocardium through myocardial fibrosis, collagen formation, myocyte hypertrophy, mitochondrial dysfunction, and ROS accumulation.…”

Section: Discussionmentioning

confidence: 98%

Testosterone and Voluntary Exercise, Alone or Together Increase Cardiac Activation of AKT and ERK1/2 in Diabetic Rats

Chodari¹,

Mohammadi²,

Mohaddes³

et al. 2016

Arquivos Brasileiros De Cardiologia

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BackgroundImpaired angiogenesis in cardiac tissue is a major complication of diabetes. Protein kinase B (AKT) and extracellular signal regulated kinase (ERK) signaling pathways play important role during capillary-like network formation in angiogenesis process.ObjectivesTo determine the effects of testosterone and voluntary exercise on levels of vascularity, phosphorylated Akt (P- AKT) and phosphorylated ERK (P-ERK) in heart tissue of diabetic and castrated diabetic rats.MethodsType I diabetes was induced by i.p injection of 50 mg/kg of streptozotocin in animals. After 42 days of treatment with testosterone (2mg/kg/day) or voluntary exercise alone or in combination, heart tissue samples were collected and used for histological evaluation and determination of P-AKT and P-ERK levels by ELISA method.ResultsOur results showed that either testosterone or exercise increased capillarity, P-AKT, and P-ERK levels in the heart of diabetic rats. Treatment of diabetic rats with testosterone and exercise had a synergistic effect on capillarity, P-AKT, and P-ERK levels in heart. Furthermore, in the castrated diabetes group, capillarity, P-AKT, and P-ERK levels significantly decreased in the heart, whereas either testosterone treatment or exercise training reversed these effects. Also, simultaneous treatment of castrated diabetic rats with testosterone and exercise had an additive effect on P-AKT and P-ERK levels.ConclusionOur findings suggest that testosterone and exercise alone or together can increase angiogenesis in the heart of diabetic and castrated diabetic rats. The proangiogenesis effects of testosterone and exercise are associated with the enhanced activation of AKT and ERK1/2 in heart tissue.

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Effects of diabetes on myocardial capillary density and serum angiogenesis biomarkers in male rats

Cited by 33 publications

References 38 publications

Imbalance of angiogenesis in diabetic complications: The mechanisms

Imbalance of angiogenesis in diabetic complications: The mechanisms

Myocardial capillary density after neuropeptide Y antagonist administration in normal and high-fat diet C57BL6 mice

Testosterone and Voluntary Exercise, Alone or Together Increase Cardiac Activation of AKT and ERK1/2 in Diabetic Rats

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