Adiponectin prevents islet ischemia–reperfusion injury through the COX2–TNFα–NF-κB-dependent signal transduction pathway in mice

Du, Xinying; He, Sirong; Jiang, Yao‐Wen; Wei, Lingling; Hu, Weiming

doi:10.1530/joe-12-0568

Cited by 29 publications

(29 citation statements)

References 28 publications

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“…In addition, adiponectin can inhibit damaged vascular intimal hyperplasia, smooth muscle cell proliferation, and migration to reduce plaque size (Uemura et al, 2013). Animal experiments further confirmed the anti-inflammatory and anti-atherosclerotic effects of adiponectin (Du et al, 2013). Because adiponectin has a variety of biological effects through adiponectin receptors, the adiponectin receptor gene (ADIPOR) may be a susceptibility gene for ischemic stroke.…”

Section: Introductionmentioning

confidence: 95%

Association between adiponectin receptor 2 gene polymorphisms and cerebral infarction

Yuan¹,

Teng²

2014

Genet. Mol. Res.

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ABSTRACT. We examined the association between the adiponectin receptor 2 gene and the risk of ischemic stroke. Polymerase chain reaction-restriction fragment length polymorphism was used to detect rs12342 genotypes of the adiponectin receptor 2 gene in 300 ischemic stroke patients and 320 age-and gender-matched healthy controls. In the patient group, the AA, GA, and GG genotype frequencies were 39.3, 42.7, and 18.0%, respectively. The A and G allele frequencies were 0.607 and 0.393, respectively. In the control group, the AA, GA, and GG genotype frequencies were 29.0, 51.7, and 19.3%, respectively. The A and G allele frequencies were 0.548 and 0.452, respectively. The AA genotype and A allele frequencies in the patient group were significantly higher than those in the control group (both P < 0.01). The risk of ischemic stroke in AA genotype carriers was 1.786-fold greater than that in GG genotype carriers (odds ratio = 1.786, 95% confidence interval: 1.432-2.775; P = 0.013). After adjusting for various confounding factors, the difference remained significant (odds ratio = 1.874, 95% confidence interval: 1.221-2.765; P = 0.012). The AA genotype and A allele of rs12342 in the adiponectin receptor 2 7809 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (3): 7808-7814 (2014) Adiponectin and cerebral infarction gene may increase the risk of ischemic stroke, particularly the risk of atherosclerosis cerebral infarction.

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Section: Introductionmentioning

confidence: 95%

Association between adiponectin receptor 2 gene polymorphisms and cerebral infarction

Yuan¹,

Teng²

2014

Genet. Mol. Res.

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“…Simvastatin is a cholesterol-lowering agent that reduces local and systemic inflammatory responses through unknown mechanisms 6 Previous data has suggested that simvastatin blocks the activities of many important proinflammatory cytokines, 7,8 such as TNF-alpha and NF-κB. These cytokines are found to be actively involved in apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Simvastatin Reduces Burn Injury-induced Splenic Apoptosis via Downregulation of the TNF-α/NF-κB Pathway

Zhao

Kaneki

et al. 2015

Annals of Surgery

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Objective Recent studies have suggested that epidermal burn injuries are associated with inflammation and immune dysfunction. Simvastatin has been shown to possess potent anti-inflammatory properties. Thus we hypothesized that simvastatin protects against burn-induced apoptosis in spleen via its anti-inflammatory activity. Methods Wild-type, tumor necrosis factor alpha knockout (TNF-αKO) and NF-κB KO mice were subjected to full-thickness burn injury or sham treatment. The mice then were treated with or without simvastatin and the spleen were harvested to measure the extent of apoptosis. Expression levels of TNF-αand NF-κB were also determined in spleen tissue and serum. Results Burn injury induced significant splenic apoptosis and systemic cytokine production. Simvastatin protected the spleen from apoptosis, reduced cytokine production in the serum and increased the survival rate. Simvastatin decreased burn-induced TNF-αand NF-κB expression in spleen and serum. TNF-αand NF-κB KO mice demonstrated lower levels of apoptosis in spleen in response to burn. Simvastatin did not further decrease burn-caused apoptosis and mortality in either strain of KO mice. Conclusions Simvastatin reduces burn-induced splenic apoptosis via down-regulation of the TNF-α/ NF-κB pathway.

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“…There is evidence that adipoVEGF−/− mice have reduced adiponectin and increased TNFα expression (26). This raises the possibility that the protective effect of adiponectin on inflammatory-mediated apoptosis on pancreatic β-cells (7, 20, 21) may be lost or reduced in adipoVEGF−/− mice, and therefore may explain, at least in part, the reductions in circulating insulin we have observed in our study. It should be noted that this seems to be an adipocyte-specific effect, since circulating basal insulin and glucose have been reported to be unchanged in muscle-specific VEGF deficient mice compared to littermate controls (2).…”

Section: Discussionmentioning

confidence: 77%

Loss of Adipocyte VEGF Impairs Endurance Exercise Capacity in Mice

Zachwieja

O’Connell

Stricker

et al. 2015

Medicine &Amp; Science in Sports &Amp; Exercise

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Purpose Reducing vascular endothelial growth factor (VEGF) in adipose tissue alters adipose vascularity and metabolic homeostasis. We hypothesized that this would also affect metabolic responses during exercise-induced stress, and that adipocyte-specific VEGF deficient (adipoVEGF−/−) mice would have impaired endurance capacity. Methods Endurance exercise capacity in adipoVEGF−/− (n=10) and littermate control (n=11) mice was evaluated every 4 weeks between 6 & 24 weeks of age using a submaximal endurance run to exhaustion at 20 m/min, 10-degree incline. Maximal running speed, using incremental increases in speed at 30-second intervals, was tested at 25 weeks of age. Results White and brown adipose tissue capillarity were reduced by 40% in adipoVEGF−/−, and no difference in skeletal muscle capillarity was observed. Endurance run time to exhaustion was 30% lower in adipoVEGF−/− compared to controls at all time points (p<0.001), but no difference in maximal running speed was observed between the groups. Following exercise (1 hour at 50% maximum running speed), adipoVEGF−/− mice displayed lower circulating insulin, (p<0.001), lower glycerol (p<0.05), and a tendency for lower blood glucose (p=0.06) compared to controls. There was no evidence of altered oxidative damage or changes in carnitine palmitoyltransferase-1β expression in skeletal muscle of adipoVEGF−/− mice. Conclusions These data suggest that VEGF-mediated deficits in adipose tissue blunts the availability of lipid substrates during endurance exercise, both of which likely reduce endurance performance. Surprisingly, we also find an unchanged basal blood glucose, despite lower circulating insulin in adipoVEGF−/− mice, suggesting loss of adipocyte VEGF can blunt insulin release and/or increase basal insulin sensitivity.

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Adiponectin prevents islet ischemia–reperfusion injury through the COX2–TNFα–NF-κB-dependent signal transduction pathway in mice

Cited by 29 publications

References 28 publications

Association between adiponectin receptor 2 gene polymorphisms and cerebral infarction

Association between adiponectin receptor 2 gene polymorphisms and cerebral infarction

Simvastatin Reduces Burn Injury-induced Splenic Apoptosis via Downregulation of the TNF-α/NF-κB Pathway

Loss of Adipocyte VEGF Impairs Endurance Exercise Capacity in Mice

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