Overexpression of vasostatin‐1 protects hypoxia/reoxygenation injuries in cardiomyocytes–endothelial cells transwell co‐culture system

Liu, Jian; Yang, Dongjian; Shi, Sheng; Lei, Lin; Xiao, Mengli; Zhang, Yuan; Yu, Min

doi:10.1002/cbin.10166

Cited by 8 publications

(3 citation statements)

References 26 publications

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“…At this regard Cappello et al [304] showed that in the isolated rat heart exposed to I/R, VS-1 simulated PreC through two different pathways: the first one mediated by A1 receptors activation and the other by NO release. Moreover, VS-1 exerted protective effects on neonatal rat cardiomyocytes, both cultured alone and in the presence of aortic endothelial cells, suggesting the involvement of direct and endothelial dependent mechanisms [305,306].…”

Section: Agents With Unknown Membrane Target Chromogranin A-derived Pmentioning

confidence: 95%

Endogenous Cardioprotective Agents: Role in Pre and Postconditioning

Penna¹,

Granata²,

Tocchetti³

et al. 2015

CDT

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Cardiovascular diseases (CVD) are the leading cause of death, chronic illness and disability in Western countries. The most common cause of CVD derives from the harmful effects of acute myocardial ischemia and subsequent reperfusion injury. Cardioprotection against acute ischemia/ reperfusion injury is made possible by the "conditioning protocols." Conditioning is obtained by applying a few periods of brief ischemia and reperfusion in the event of prolonged (index) ischemia that may cause myocardial infarction. Whilst the conditioning stimulus is applied before the index ischemia in ischemic pre-conditioning, it is applied after the event in post-conditioning. Pre and post- conditioning stimuli can be applied in a different/remote organ (remote pre- and post-conditioning); in this case conditioning stimulus can also be applied during the index event, in the so called remote per-conditioning. All these endogenous cardioprotective strategies recruit endogenous cytoprotective agents and factors that elicit specific cardioprotective pathways. Here, we discuss many of these cardioprotective factors compared to literature and highlight their main characteristics and mechanisms of action. Enphasis is given to endogenous cardioprotective agents acting or not on surface receptors, including chromogranin A derivatives, ghrelin-associated peptides, growth factors and cytokines, and to microvesicles and exosomes. Moreover the cardioprotective effects of gasotransmitters nitric oxide, hydrogen sulphide and carbon monoxide are reviewed. The possible clinical translation of these knowledge for future successful therapies is briefly and critically discussed.

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Section: Agents With Unknown Membrane Target Chromogranin A-derived Pmentioning

confidence: 95%

Endogenous Cardioprotective Agents: Role in Pre and Postconditioning

Penna¹,

Granata²,

Tocchetti³

et al. 2015

CDT

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“…This may indicate that the adaptive evolution of the immune system is involved in adaptation to high altitudes [57,58]. Of the two cell types with strongest communication with other cells, endothelial cells can exert a protective effect on cardiomyocytes in a hypoxic environment [59]. The more studied vascular endothelial cells in their subpopulation are involved in responding to the regulation of vascular function of mechanical stimulation and in immune regulatory mechanisms [60].…”

Section: Discussionmentioning

confidence: 99%

Single‐cell transcriptomic survey of cell diversity and functional changes in yak hearts at different altitude

et al. 2023

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The yak (Bos grunniens) is a species adapted to the hypoxic environment in the plateau area. The heart is a hypoxia-sensitive organ involved in this adaptation. Herein, we used single-cell RNA-seq technology and clustering to determine the presence of 11 cell populations in the yak heart. We analyzed gene expression differences and expression patterns in each cell subpopulation at different altitudes. The cells related to altitude changes are mainly smooth muscle cells and vascular endothelial cells. Of the four transcription factors (TFs, MEF2B, FOXP4, ARID5A, and HES4) found in smooth muscle cells, only MEF2B was specifically expressed in vascular smooth muscle cells. Three key TFs (HNF1B, DMRTA1, and ARNTL2) were also found in the cardiomyocyte module. Compared with data extracted from low-altitude yak, we observed that the high altitude yak has enhanced contraction and relaxation of vascular smooth muscle cells and an increased metabolic level of cardiomyocytes. These may be strategies for the yak to adapt to high-altitude hypoxia environments.

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“…For Western blot detection of Parp, the treatments of the Jurkat T cells used different concentrations of GW (0, 5, 10, or 20 μg/mL), different concentrations of AM630 (0, 5, 10, or 20 μg/mL), or GW (20 μg/mL) plus AM630 (2 μg/mL). The L02 liver cells were cocultured with Jurkat cells using a Transwell coculture system [20] to research the immune injury of the hepatocytes with 10% fetal bovine serum in 1640 medium for the coculture. Con A at 5 μg/mL was used to stimulate the Jurkat cells to release cytotoxic cytokines.…”

Section: Cell Experiments the Jurkat T-cell Line Was Used As The T-celmentioning

confidence: 99%

Protective effects of specific cannabinoid receptor 2 agonist GW405833 on concanavalin A-induced acute liver injury in mice

Huang

Zheng

et al. 2019

Acta Pharmacol Sin

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Cannabinoid receptor 2 (CB2R) is highly expressed in immune cells and plays an important role in regulating immune responses. In the current study, we investigated the effects of GW405833 (GW), a specific CB2R agonist, on acute liver injury induced by concanavalin A (Con A). In animal experiments, acute liver injury was induced in mice by injection of Con A (20 mg/kg, i.v.). The mice were treated with GW (20 mg/kg, i.p., 30 min after Con A injection) or GW plus the selective CB2R antagonist AM630 (2 mg/kg, i.p., 15 min after Con A injection). We found that Con A caused severe acute liver injury evidenced by significantly increased serum aminotransferase levels, massive hepatocyte apoptosis, and necrosis, as well as lymphocyte infiltration in liver tissues. Treatment with GW significantly ameliorated Con A-induced pathological injury in liver tissue, decreased serum aminotransferase levels, and decreased hepatocyte apoptosis. The therapeutic effects of GW were prevented by AM630. In cell experiments, we showed that CB2Rs were highly expressed in Jurkat T cells, but little expression in L02 liver cells. Treatment with GW (10−40 μg/mL) dosedependently decreased the viability of Jurkat T cells and induced cell apoptosis, which was reversed by AM630. In the coculture of Jurkat T cells with L02 liver cells, GW dose-dependently protected L02 cells from apoptosis induced by Con A (5 μg/mL). The protective effect of GW was reversed by AM630 (1 μg/mL). Our results suggest that GW protects against Con A-induced acute liver injury in mice by inhibiting Jurkat T-cell proliferation through the CB2Rs.

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Overexpression of vasostatin‐1 protects hypoxia/reoxygenation injuries in cardiomyocytes–endothelial cells transwell co‐culture system

Cited by 8 publications

References 26 publications

Endogenous Cardioprotective Agents: Role in Pre and Postconditioning

Endogenous Cardioprotective Agents: Role in Pre and Postconditioning

Single‐cell transcriptomic survey of cell diversity and functional changes in yak hearts at different altitude

Protective effects of specific cannabinoid receptor 2 agonist GW405833 on concanavalin A-induced acute liver injury in mice

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