Molecular regulation of the expression of leptin by hypoxia in human coronary artery smooth muscle cells

Chiu, Chiung-Zuan; Wang, Baowei; Shyu, Kou‐Gi

doi:10.1186/s12929-014-0109-8

Cited by 17 publications

(10 citation statements)

References 44 publications

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“…However, the specific mechanism underlying NAC involvement in the HG-induced injury in vascular endothelial cells is still not clear. Previous studies found that NAC could reduce the expression level of leptin to some extent [26] and inhibit angiogenesis by inhibiting the expression of leptin [9] . Therefore, it was speculated that NAC might be able to antagonize HG-induced multiple injuries in vascular endothelial cells through inhibiting the expression of leptin/LEPR, which was also confirmed in this study.…”

Section: Discussionmentioning

confidence: 96%

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

Wang¹,

Lian

Liao

et al. 2020

Preprint

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Baclground The present study aimed to investigate whether N- acetylcysteine (NAC) protects human umbilical vein endothelial cells (HUVECs) against high glucose (HG)-induced injury by inhibiting leptin/leptin receptor (LEPR).Methods HUVECs were treated with 40 mmol/L glucose for 24 h to establish a model of HG-induced endothelial cell injury; The cell viability was examined by cell counter kit-8(CCK-8) assay; The expression levels of leptin, LEPR, cleaved caspase-3 and endothelial nitric oxide synthase (eNOS) were detected by western blot. The intracellular levels of reactive oxygen species (ROS) were tested by DCFH-DA staining followed by photofluorography. Tumor necrosis factor-α (TNF-α)、nuclear factor-kappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) were detected by enzyme-linked immunosorbent assay (ELISA). The number of apoptotic cells was observed by photofluorograph with Hoechst 33258 nuclear staining. Mitochondrial membrane potential (MMP) was obtained using JC-1. Results The expression of leptin and LEPR began to significantly increase after exposure to 40 mmol/L HG for 24 h. Pretreatment of HUVECs with 7 mmol/L NAC or 50 ng/mL leptin antagonists (LA) for 30min inhibited the increased expression of leptin and LEPR induced by HG in HUVECs. Furthermore, pretreatment with 7 mmol/L NAC or 50 ng/mL LA for 30 min also inhibited HG-induced injury, by increasing the cell viability and eNOS expression, and decreasing the inflammatory response and cleaved caspase-3 expression, the apoptotic cells and generation of intracellular ROS and a loss of MMP. Conclusions NAC protects the HUVECs against HG-induced injury by inhibiting leptin/LEPR.

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Section: Discussionmentioning

confidence: 96%

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

Wang¹,

Lian

Liao

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…However, the specific mechanism underlying NAC involvement in the HG-induced injury in vascular endothelial cells is still not clear. Previous studies found that NAC could reduce the expression level of leptin to some extent [28] and inhibit angiogenesis by inhibiting the expression of leptin [9] . Therefore, it was speculated that NAC might be able to antagonize HG-induced multiple injuries in vascular endothelial cells through inhibiting the expression of leptin/LEPR, which was also confirmed in this study.…”

Section: Discussionmentioning

confidence: 96%

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

Wang¹,

Lian

Liao

et al. 2020

Preprint

View full text Add to dashboard Cite

Background The present study aimed to investigate whether N-acetylcysteine (NAC) protects human umbilical vein endothelial cells (HUVECs) against high glucose (HG)-induced injury by inhibiting leptin/leptin receptor (LEPR).Methods HUVECs were treated with 40 mmol/L glucose for 24 h to establish a model of HG-induced endothelial cell injury; The cell viability was examined by cell counter kit-8 (CCK-8) assay; The expression levels of leptin, LEPR, cleaved caspase-3 and endothelial nitric oxide synthase (eNOS) were detected by western blot. The intracellular levels of reactive oxygen species (ROS) were tested by DCFH-DA staining followed by photofluorography. Tumor necrosis factor-α (TNF-α) nuclear factorkappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) were detected by enzyme-linked immunosorbent assay (ELISA). The number of apoptotic cells was observed by photofluorograph with Hoechst 33258 nuclear staining. Mitochondrial membrane potential (MMP) was obtained using JC-1. ResultsThe expression of leptin and LEPR began to significantly increase after exposure to 40 mmol/L HG for 24 h. Pretreatment of HUVECs with 7 mmol/L NAC or 50 ng/mL leptin antagonists (LA) for 30min inhibited the increased expression of leptin and LEPR induced by HG in HUVECs.Furthermore, pretreatment with 7 mmol/L NAC or 50 ng/mL LA for 30 min also inhibited HG-induced injury, by increasing the cell viability and eNOS expression, and decreasing the inflammatory response and cleaved caspase-3 expression, the apoptotic cells and generation of intracellular ROS and a loss of MMP.Conclusions NAC protects the HUVECs against HG-induced injury by inhibiting leptin/LEPR.

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“…HIF-1α is a protein that regulates hypoxia-regulated gene expression to mediate cell adaption to low oxygen circumstances [ 60 , 61 ]. ISO injections in rats have been shown to increase HIF-1α expression [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

Caffeic acid ethanolamide prevents cardiac dysfunction through sirtuin dependent cardiac bioenergetics preservation

Lee

Kuo

et al. 2015

J Biomed Sci

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BackgroundCardiac oxidative stress, bioenergetics and catecholamine play major roles in heart failure progression. However, the relationships between these three dominant heart failure factors are not fully elucidated. Caffeic acid ethanolamide (CAEA), a synthesized derivative from caffeic acid that exerted antioxidative properties, was thus applied in this study to explore its effects on the pathogenesis of heart failure.ResultsIn vitro studies in HL-1 cells exposed to isoproterenol showed an increase in cellular and mitochondria oxidative stress. Two-week isoproterenol injections into mice resulted in ventricular hypertrophy, myocardial fibrosis, elevated lipid peroxidation, cardiac adenosine triphosphate and left ventricular ejection fraction decline, suggesting oxidative stress and bioenergetics changes in catecholamine-induced heart failure. CAEA restored oxygen consumption rates and adenosine triphosphate contents. In addition, CAEA alleviated isoproterenol-induced cardiac remodeling, cardiac oxidative stress, cardiac bioenergetics and function insufficiency in mice. CAEA treatment recovered sirtuin 1 and sirtuin 3 activity, and attenuated the changes of proteins, including manganese superoxide dismutase and hypoxia-inducible factor 1-α, which are the most likely mechanisms responsible for the alleviation of isoproterenol-caused cardiac injuryConclusionCAEA prevents catecholamine-induced cardiac damage and is therefore a possible new therapeutic approach for preventing heart failure progression.

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Molecular regulation of the expression of leptin by hypoxia in human coronary artery smooth muscle cells

Cited by 17 publications

References 44 publications

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

N-acetylcysteine resists high-glucose-induced injury of human umbilical vein endothelial cells by inhibiting the leptin/leptin receptor

Caffeic acid ethanolamide prevents cardiac dysfunction through sirtuin dependent cardiac bioenergetics preservation

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