Anti-apoptotic and angiogenic effects of intelectin-1 in rat cerebral ischemia

Gu, Naibing; Dong, Yaru; Tian, Ye; Zhang, Di; Liu, Zhiqin; Chang, Mingze; Jia, Xiao-Tao; Qian, Yi‐Hua; Zhang, Weiping

doi:10.1016/j.brainresbull.2016.12.006

Cited by 25 publications

(17 citation statements)

References 37 publications

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“…Preclinical studies using mouse models of atherosclerosis or ischaemia/reperfusion injury demonstrated that systemic administration or overexpression of omentin delayed the development of aortic atherosclerotic lesions and reduced myocardial infarct size [15][16][17]. Additionally, lentiviral overexpression of omentin reduced the brain infarction volume in a mouse model of ischaemic stroke [31]. In vitro studies investigating the impact of omentin on endothelial cells, smooth muscle cells and macrophages suggested atheroprotective properties reflected by reduced monocyte adhesion, improved cell differentiation and survival rate, enhanced vasodilation and attenuation of inflammatory processes [32,33], although omentin treatment appeared to have proinflammatory effects on adipocytes [34].…”

Section: Association Between Omentin and Cardiovascular Outcomesmentioning

confidence: 99%

Higher circulating omentin is associated with increased risk of primary cardiovascular events in individuals with diabetes

et al. 2019

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Aims/hypothesis Higher concentrations of the adipokine omentin are associated with lower levels of cardiometabolic risk factors in experimental and cross-sectional studies, but with higher risk of type 2 diabetes and cardiovascular diseases in population-based cohort studies. However, it is unknown whether high omentin concentrations are associated with increased risk of cardiovascular events in people with established diabetes. Therefore, the present study investigated the association between serum omentin concentrations and the risk of cardiovascular events in individuals with diabetes. Methods This prospective study was based on participants of the German ESTHER cohort with diabetes and without previous cardiovascular event. The ESTHER cohort consists of individuals aged 50-75 years at baseline who were recruited by their general practitioners. After exclusion of individuals with serum C-reactive protein ≥10 mg/l (≥95.24 nmol/l), the final analysis population consisted of 933 individuals. At baseline, serum omentin concentrations were measured by ELISA. Cox regression models were fitted to estimate HRs and their corresponding 95% CIs for associations of omentin tertiles with a composite endpoint of cardiovascular events and separately with incident myocardial infarction, stroke and cardiovascular death. Results During 14 years of follow-up, 228 individuals experienced a primary cardiovascular event (myocardial infarction, stroke or cardiovascular death). After comprehensive adjustment for age, sex, BMI, metabolic and lifestyle factors and medication use, HRs (95% CIs) for the 2nd and 3rd tertile of omentin compared with the 1st tertile were: 1.24 (95% CI 0.86, 1.79) and 1.63 (1.15, 2.32) (p trend = 0.005) for the composite cardiovascular endpoint; 1.39 (0.78, 2.47) and 1.71 (0.98, 2.99) (p trend = 0.065) for incident myocardial infarction; 1.40 (0.78, 2.53) and 2.05 (1.17, 3.58) (p trend = 0.010) for incident stroke; and 1.43 (0.85, 2.40) and 1.72 (1.04, 2.83) (p trend = 0.040) for cardiovascular death. Effect estimates and p values were almost unaltered after additional adjustment for adiponectin. Conclusions/interpretation Higher omentin concentrations are associated with an increased risk for cardiovascular events in individuals with diabetes after adjustment for multiple cardiovascular risk factors. Given data from preclinical studies, it appears possible that this association reflects a compensatory, but insufficient upregulation of omentin concentrations as a response to stimuli that increase cardiovascular risk.

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Section: Association Between Omentin and Cardiovascular Outcomesmentioning

confidence: 99%

Higher circulating omentin is associated with increased risk of primary cardiovascular events in individuals with diabetes

et al. 2019

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“…1 Cerebral ischemia is found to trigger programmed neuronal death via induction of parthanatos, as well as apoptosis. 2,3 As a new modality of programmed cell death, parthanatos is characterized by a series of choreographed biochemical events including overactivation of poly (ADP-ribose) synthetase 1 (PARP-1), intracellular accumulation of PAR polymer, mitochondrial depolarization, and nuclear translocation of apoptosis-inducing factor (AIF). 4 The nuclear AIF would cause cell death via induction of chromatolysis or chromatin condensation.…”

Section: Introductionmentioning

confidence: 99%

Endoplasmic reticulum stress regulates oxygen‐glucose deprivation‐induced parthanatos in human SH‐SY5Y cells via improvement of intracellular ROS

Wang

Ding

et al. 2017

CNS Neurosci Ther

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“…Stroke is a life-threatening cerebrovascular disease caused by the reduction of bloodstream to an area of the brain, leading to neurological failure and fatality [ 1 , 2 ] . Following cerebral ischemia, two zones are distinguishable in the brain.…”

Section: Introductionmentioning

confidence: 99%

Extracellular Vesicles Derived from Human Umbilical Cord Perivascular Cells Improve Functional Recovery in Brain Ischemic Rat via the Inhibition of Apoptosis

Seifali

Hassanzadeh

Mahdavipour

et al. 2020

ibj

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Background: Ischemic stroke, as a health problem caused by the reduced blood supply to the brain, can lead to the neuronal death. The number of reliable therapies for stroke is limited. MSCs exhibit therapeutic achievement. A major limitation of MSC application in cell therapy is the short survival span. MSCs affect target tissues through the secretion of many paracrine agents including EVs. This study aimed to investigate the effect of HUCPVCs-derived EVs on apoptosis, functional recovery, and neuroprotection. Methods: Ischemia was induced by MCAO in male Wistar rats. Animals were classified into sham, MCAO, MCAO + HUCPVC, and MCAO + EV groups. Treatments began at two hours after ischemia. Expressions of apoptotic-related proteins (BAX/BCl-2 and caspase-3 and -9), the amount of TUNEL-positive cells, neuronal density (MAP2), and dead neurons (Nissl staining) were assessed on day seven post MCAO. Results: Administration of EVs improved the sensorimotor function ( p < 0.001) and reduced the apoptotic rate of Bax/Bcl-2 ratio ( p < 0.001), as well as caspases and TUNEL-positive cells ( p < 0.001) in comparison to the MCAO group. EV treatment also reduced the number of dead neurons and increased the number of MAP2 + cells in the IBZ ( p < 0.001), as compared to the MCAO group. Conclusion: Our findings showed that HUCPVCs-derived EVs are more effective than their mother’s cells in improving neural function, possibly via the regulation of apoptosis in the ischemic rats. The strategy of cell-free extracts is, thus, helpful in removing the predicaments surrounding cell therapy in targeting brain diseases.

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Anti-apoptotic and angiogenic effects of intelectin-1 in rat cerebral ischemia

Cited by 25 publications

References 37 publications

Higher circulating omentin is associated with increased risk of primary cardiovascular events in individuals with diabetes

Higher circulating omentin is associated with increased risk of primary cardiovascular events in individuals with diabetes

Endoplasmic reticulum stress regulates oxygen‐glucose deprivation‐induced parthanatos in human SH‐SY5Y cells via improvement of intracellular ROS

Extracellular Vesicles Derived from Human Umbilical Cord Perivascular Cells Improve Functional Recovery in Brain Ischemic Rat via the Inhibition of Apoptosis

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