CTRP3 inhibits high glucose–induced human glomerular mesangial cell dysfunction

Hu, Tian‐ying; Lamei, LI; Pan, Yan‐zi

doi:10.1002/jcb.27859

Cited by 23 publications

(17 citation statements)

References 37 publications

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“…reported a protective role for CTRP3 in high glucose-induced glomerular mesangial cell dysfunction that was suggested as a cellular model of diabetic nephropathy [20]. CTRP3 exert its protective role via inactivation of janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) in high glucose-induced glomerular mesangial cell [20]. The association between CTRP3 and Cr as well as eGFR are in vivo evidence for association of CTRP3 with diabetic nephropathy that confirm previous study by Hu et.…”

Section: Discussionmentioning

confidence: 99%

“…The association between CTRP3 and Cr as well as eGFR are in vivo evidence for association of CTRP3 with diabetic nephropathy that confirm previous study by Hu et. al [20].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, CTRP3 inhibits vascular cell adhesion molecule-1 (VCAM-1) expression and could be a potential biomarker for diabetic retinopathy [19]. Recently, a study by Hu et al, reported a protective role for CTRP3 in cellular model of diabetic nephropathy, they show that CTRP3 attenuates high glucose-induced glomerular mesangial cell dysfunction [20]. Several line of evidence suggested a possible role for CTRP3 in diabetes complications, especially diabetes nephropathy.…”

Section: Introductionmentioning

confidence: 99%

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Serum levels of CTRP3 in diabetic nephropathy and its relationship with insulin resistance and kidney function

et al. 2019

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Background C1q TNF related protein 3 (CTRP3) is an adipokine secreted from adipose tissue. Previous studies have suggested that CTRP3 improves insulin sensitivity and reduces inflammation. Human studies have evaluated circulating levels of this adipokine in patients with diabetes mellitus (DM), diabetic retinopathy, metabolic syndrome, and coronary artery diseases. However, circulating levels of this adipokine in patients with diabetic nephropathy have not been evaluated. The present study aimed to assess serum levels of CTRP3 in patients with type 2 diabetes mellitus (T2DM) and diabetic nephropathy (T2DM-NP) and its relationship with metabolic and inflammatory markers. Methods This cross-sectional study was performed on 55 controls, 54 patients with T2DM, and 55 patients with T2DM-NP. Serum levels of CTRP3, adiponectin, TNF-α, and IL-6 were measured by ELISA technique. Results Serum levels of CTRP3 were significantly lower in patients with T2DM (257.61 ± 69.79 ng/mL, p < 0.001) and T2DM-NP (222.03 ± 51.99 ng/mL, p < 0.001) compared to controls (328.17 ± 80.73 ng/mL), and those with T2DM-NP compared to T2DM group. CTRP3 was independently associated with HOMA-IR (r = -0.327, p < 0.05) and adiponectin (r = 0.436, p < 0.01) in T2DM group. In T2DM-NP patients, CTRP3 independently was associated with eGFR (r = 0.428, p < 0.01) and HOMA-IR (r = -0.436, p < 0.01). Furthermore, CTRP3 revealed a ability to differentiate T2DM-NP patients from controls (area under curve (95% confidence interval): 0.881 (0.820–0.943) and p < 0.001). Conclusion Decreased serum levels of CTRP3 in patients with T2DM and diabetic nephropathy and its association with pathologic mechanism in these patients suggested a possible role for CTRP3 in pathogenesis of diabetic nephropathy; nevertheless, further studies are required in this regard.

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Section: Discussionmentioning

confidence: 99%

“…The association between CTRP3 and Cr as well as eGFR are in vivo evidence for association of CTRP3 with diabetic nephropathy that confirm previous study by Hu et. al [20].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Serum levels of CTRP3 in diabetic nephropathy and its relationship with insulin resistance and kidney function

et al. 2019

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“…C1q/tumor necrosis factor-related protein 3 (CTRP3), a novel adipokine, belongs to the highly conserved CTRP superfamily of adiponectin paralogs [ 17 , 18 ]. Previous studies have demonstrated that CTRP3 is an endogenous antagonist of lipopolysaccharide [ 19 ] and that aberrant CTRP3 expression is related to multiple types of human disorders, such as arthritis [ 20 ], sepsis [ 21 ] and myocardiac dysfunction [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

CTRP3 ameliorates cerulein-induced severe acute pancreatitis in mice via SIRT1/NF-κB/p53 axis

Wei

et al. 2020

Bioscience Reports

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Severe acute pancreatitis (SAP) is a common and life-threatening clinical acute abdominal disease. C1q/tumor necrosis factor-related protein 3 (CTRP3), a novel paralog of adiponectin, has been identified as a crucial regulator in multiple types of inflammatory disorders. However, the biological role of CTRP3 in SAP remains poorly understood. This study aimed to characterize the role of CTRP3 in SAP and illuminate the potential mechanisms involved. In the current study, SAP mouse models were induced by seven hourly intraperitoneal injection of cerulein (50 μg/kg) and an immediate intraperitoneal injection of lipopolysaccharide (10 mg/kg) after the last cerulein administration. Histological examination and serological analysis demonstrated that SAP mouse models were successfully established. Herein, we found that CTRP3 expression was significantly decreased in the pancreatic tissues of SAP mice compared with normal control mice. Furthermore, we explored the effects of CTRP3 rescue in SAP mice and discovered that CTRP3 over-expression attenuated pathological lesions, inhibited inflammatory mediator release and repressed acinar cell apoptosis. Notably, mechanistic studies revealed that CTRP3 over-expression suppressed NF-κB p65 phosphorylation and p53 acetylation to alleviate cerulein-induced SAP in mouse models through activation of silent information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide-dependent protein deacetylase. Collectively, our data indicate that CTRP3 may exert its protective effects in SAP mice via regulation of SIRT1-mediated NF-κB and p53 signaling pathways, implying a promising therapeutic strategy against SAP.

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“…Glomerular mesangial cells (GMCs) are groups of cells that function as key regulators in the renal system, and over-proliferation of GMCs was also considered as an important reason for the incidence and development of TIF [3][4][5] . Nevertheless, at the current stage, the roles of GMCs in the pathogenesis of TIF as well as the possible mechanism has not yet been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Calycosin may Alleviate Ang II-Induced Pro-proliferative Effects on Glomerular Mesangial Cells <i>via</i> Partially Inhibiting Autophagy and ERK Signaling Pathway

Ding

Luan

et al. 2020

Biological & Pharmaceutical Bulletin

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Over-expression of angiotensin II (Ang II) is an important reason for the development of chronic kidney disease. Calycosin is the active component of traditional Chinese medicine astragali radix. The present work aims to explore whether calycosin could affect the growth and apoptosis ability of the Ang II treated glomerular mesangial cells and the underlying mechanism. Human glomerular mesangial cells (GMCs) were cultured and treated by Ang II and 0, 0.1, 1 or 10 μM calycosin, and the viability and proliferation of the cells were determined by MTT and EdU staining; moreover, the apoptosis of the cells was examined by flow cytometry assay; furthermore, the expression levels of ERK, pERK , anti-apoptotic factor Bcl-2, as well as pro-apoptotic factor Bax have been examined by western blot methods; finally, the expression of autophagic markers in each group was examined by WB and immunocytochemistry methods. We found that Ang II increased viability and proliferation, meanwhile inhibited apoptosis of the GMCs; furthermore, 1 and 10 μM calycosin significantly inhibited the growth and promoted the apoptosis of the GMCs treated by Ang II; moreover, calycosin also inhibited ERK signaling in mesangial cells activated by Ang II treatment; Finally, calycosin could inhibit Ang II induced autophagy of GMCs in a dose-dependent manner. In conclusion, calycosin may alleviate Ang II-induced pro-proliferative and anti-apoptotic effects on glomerular mesangial cells at least partially via inhibiting autophagy and ERK signaling pathway, suggesting that calycosin may function as a potential alternative medication for the management of chronic kidney diseases.

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CTRP3 inhibits high glucose–induced human glomerular mesangial cell dysfunction

Cited by 23 publications

References 37 publications

Serum levels of CTRP3 in diabetic nephropathy and its relationship with insulin resistance and kidney function

Serum levels of CTRP3 in diabetic nephropathy and its relationship with insulin resistance and kidney function

CTRP3 ameliorates cerulein-induced severe acute pancreatitis in mice via SIRT1/NF-κB/p53 axis

Calycosin may Alleviate Ang II-Induced Pro-proliferative Effects on Glomerular Mesangial Cells <i>via</i> Partially Inhibiting Autophagy and ERK Signaling Pathway

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