CTRP3 Protects against High Glucose-Induced Cell Injury in Human Umbilical Vein Endothelial Cells

Wang, Fang; Zhao, Linlin; Shan, Yingguang; Li, Ran; Qin, Guijun

doi:10.1155/2019/7405602

Cited by 10 publications

(4 citation statements)

References 27 publications

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“…According to the previous studies, CTRP3 executed its roles via multiple mechanisms, such as regulation of p38 MAPK, 24 c-Jun NH-terminal kinase (JNK), 24 extracellular signal-regulated kinase (ERK1/2), 25 Nrf2/HO-1, 20 AKT/mTOR, 26 Notch, 27 and AMPK. 19 Among these signaling pathways, AMPK is a heterotrimeric complex that plays an important role in maintaining energy homeostasis in eukaryotic cells.…”

Section: Discussionmentioning

confidence: 99%

CTRP3 protects hippocampal neurons from oxygen-glucose deprivation-induced injury through the AMPK/Nrf2/ARE pathway

2021

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Objective: C1q/TNF-related protein 3 (CTRP3), a member of CTRP family, has been found to have neuroprotective effect. In the current study, we investigated the protective role of CTRP3 in hippocampal neurons exposed to oxygen-glucose deprivation/reperfusion (OGD/R). Materials and methods: The mRNA and protein levels of CTRP3 in OGD/R-stimulated hippocampal neurons were measured using qRT-PCR and western blot analysis, respectively. CCK-8 assay was performed to assess cell viability. ROS production was measured using the fluorescence probe 2′,7′-dichlorofluorescein diacetate (H2DCFDA). The activities of SOD and GPx were determined using ELISA. Cell apoptosis was assessed. Luciferase reporter assay was carried out to assess the activation of ARE). The levels of p-AMPK and Nrf2 were measured using western blot. Results: Our results showed that the expression of CTRP3 was significantly downregulated in hippocampal neuronal cells exposed to OGD/R. Overexpression of CTRP3 improved cell viability of OGD/R-induced hippocampal neurons. In addition, overexpression of CTRP3 attenuated the OGD/R-caused oxidative stress with decreased ROS production and increased activities of SOD and GPx. Moreover, CTRP3 caused a significant increase in bcl-2 expression and decreases in bax expression and caspase-3 activity. Furthermore, CTRP3 overexpression significantly upregulated the levels of p-AMPK and Nrf2, as well induced the activation of ARE in OGD-R-induced hippocampal neurons. CTRP3 upregulated the mRNA expression levels of HO-1, NQO-1 and GPx-3. Additionally, treatment with the inhibitor of AMPK partially reversed the neuroprotective effect of CTRP3 in OGD/R-exposed neurons. Conclusion: CTRP3 exerted protective effect on OGD/R-induced cerebral injury, which was regulated by AMPK/Nrf2/ARE pathway.

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Section: Discussionmentioning

confidence: 99%

CTRP3 protects hippocampal neurons from oxygen-glucose deprivation-induced injury through the AMPK/Nrf2/ARE pathway

2021

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“…19 In addition, there were several studies indicating the antiapoptotic effects of CTRP3 on HUVECs and mouse aortic endothelial cells stimulated with oxidized low-density lipoprotein (ox-LDL) 19 or high glucose. 20 However, there are little data regarding the role of CTRP3 in endothelial injury induced by high uric acid. Our study showed that, for rats with hyperuricemia, CTRP3 increased eNOS mRNA expression in the thoracic aortas.…”

Section: Discussionmentioning

confidence: 99%

CTRP3 protects against uric acid-induced endothelial injury by inhibiting inflammation and oxidase stress in rats

Zhang

Lin

et al. 2021

Exp Biol Med (Maywood)

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Hyperuricemia, which contributes to vascular endothelial damage, plays a key role in multiple cardiovascular diseases. This study was designed to investigate whether C1q/tumor necrosis factor (TNF)-related protein 3 (CTRP3) has a protective effect on endothelial damage induced by uric acid and its underlying mechanisms. Animal models of hyperuricemia were established in Sprague-Dawley (SD) rats through the consumption of 10% fructose water for 12 weeks. Then, the rats were given a single injection of Ad-CTRP3 or Ad-GFP. The animal experiments were ended two weeks later. In vitro, human umbilical vein endothelial cells (HUVECs) were first infected with Ad-CTRP3 or Ad-GFP. Then, the cells were stimulated with 10 mg/dL uric acid for 48 h after pretreatment with or without a Toll-like receptor 4 (TLR4)-specific inhibitor. Hyperuricemic rats showed disorganized intimal structures, increased endothelial apoptosis rates, increased inflammatory responses and oxidative stress, which were accompanied by reduced CTRP3 and elevated TLR4 protein levels in the thoracic aorta. In contrast, CTRP3 overexpression decreased TLR4 protein levels and ameliorated inflammatory responses and oxidative stress, thereby improving the morphology and apoptosis of the aortic endothelium in rats with hyperuricemia. Similarly, CTRP3 overexpression decreased TLR4-mediated inflammation, reduced oxidative stress, and rescued endothelial damage induced by uric acid in HUVECs. In conclusion, CTRP3 ameliorates uric acid-induced inflammation and oxidative stress, which in turn protects against endothelial injury, possibly by inhibiting TLR4-mediated inflammation and downregulating oxidative stress.

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“…CTRP3 is a most well‐studied member of CTRP family that has been found to closely related with diabetes mellitus and diabetic complications . CTRP3 exerts protective effect on diabetes‐related endothelial dysfunction via protecting human umbilical vein endothelial cells (HUVECs) from HG‐induced cell injury . CTRP3 inhibits HG‐induced oxidative stress and apoptosis in retinal pigment epithelial (RPE) cells, suggesting that CTRP3 may be a therapeutic target for the treatment of diabetic retinopathy .…”

Section: Discussionmentioning

confidence: 99%

Knockdown of CTRP6 inhibits high glucose‐induced oxidative stress, inflammation and extracellular matrix accumulation in mesangial cells through regulating the Akt/NF‐κB pathway

Chen

et al. 2020

Clin Exp Pharma Physio

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C1qTNF-related protein 6 (CTRP6) is a member of the CTRP family and exerts a key role in the progression of diabetes mellitus. However, the role of CTRP6 in diabetic nephropathy remains unknown. The present study was designed to examine the roles of CTRP6 in diabetic nephropathy and explore the potential molecular mechanisms. Our results showed that the expression level of CTRP6 was significantly increased in high glucose (HG)-stimulated glomerular mesangial cells (MCs). The following loss/gain-of-function assays demonstrated that CTRP6 knockdown significantly inhibited HG-induced reactive oxygen species (ROS) production in MCs. CTRP6 knockdown caused significant decreases in tumour necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 production levels in HG-induced MCs. Moreover, knockdown of CTRP6 inhibited HG-stimulated extracellular matrix (ECM) accumulation in MCs characterized by decreased expression and production levels of fibronectin (FN) and collagen IV (Col IV). Furthermore, CTRP6 knockdown suppressed HG-induced the activation of Akt/NF-κB pathway in MCs, while overexpression of CTRP6 exhibited the opposite effects. Treatment with LY294002, an inhibitor of Akt, reversed the induction effects of CTRP6 overexpression on ROS production, inflammation and ECM accumulation in MCs. In conclusion, these findings demonstrated that CTRP6 knockdown inhibits HG-induced ROS production, inflammation and ECM accumulation in MCs, which were mediated by the inactivation of the Akt/NF-κB pathway. The roles of CTRP6 in diabetic nephropathy provided evidence for its therapeutic potential for the treatment of diabetic nephropathy. K E Y W O R D SAkt/NF-κB pathway, C1qTNF-related protein 6 (CTRP6), diabetic nephropathy, extracellular matrix (ECM), inflammation, reactive oxygen species (ROS) How to cite this article: Xu E, Yin C, Yi X, Liu Y. Knockdown of CTRP6 inhibits high glucose-induced oxidative stress, inflammation and extracellular matrix accumulation in mesangial cells through regulating the Akt/NF-κB pathway.

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CTRP3 Protects against High Glucose-Induced Cell Injury in Human Umbilical Vein Endothelial Cells

Cited by 10 publications

References 27 publications

CTRP3 protects hippocampal neurons from oxygen-glucose deprivation-induced injury through the AMPK/Nrf2/ARE pathway

CTRP3 protects hippocampal neurons from oxygen-glucose deprivation-induced injury through the AMPK/Nrf2/ARE pathway

CTRP3 protects against uric acid-induced endothelial injury by inhibiting inflammation and oxidase stress in rats

Knockdown of CTRP6 inhibits high glucose‐induced oxidative stress, inflammation and extracellular matrix accumulation in mesangial cells through regulating the Akt/NF‐κB pathway

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