Influence of overexpression of SOCS2 on cells of DN rat

Bao, Nana; Kong, Deyang; Zhu, Dan; Hao, Lirong

doi:10.1016/j.apjtm.2015.06.006

Cited by 13 publications

(10 citation statements)

References 14 publications

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“…TAK-242 and PDTC both conspicuously suppressed apoptosis and inflammatory cytokines production in HG-stimulated podocytes; moreover, either TAK-242 or PDTC strengthened the inhibitory influence of SOCS2 overexpression on apoptosis and inflammatory cytokines, indicating that SOCS2 overexpression repressed apoptosis and inflammatory cytokines production by inhibiting the TLR4/NF-κB signaling pathway in HG-stimulated podocytes. Additionally, upregulation of SOCS2 has been demonstrated to suppress JAK/STAT and EPK signaling pathways induced by STZ in rat kidneys [ 9 , 24 ], consistent with our present results. Our study demonstrated that SOCS2 overexpression showed a stronger inhibitory effect on the TLR4/NF-κB pathway than the JAK/STAT pathway in HG-stimulated podocytes.…”

Section: Discussionsupporting

confidence: 92%

“…Zhou et al reported that SOCS2 attenuated STZ-induced renal lesions including renal/glomerular hypertrophy, glomerular hyperfiltration, aberrant inflammation and fibrosis and reduced the levels of proinflammatory proteins (TGF-β, collagen IV and fibronectin) in DN [ 25 ]. Bao et al found that SOCS2 overexpression decreased the increased expressions of inflammatory cytokines (MCP-1, TNF-α and IL-6) and fibrosis related protein in STZ-induced DN rats [ 9 ]. Consistently, our study showed that SOCS2 overexpression significantly increased the body weight and dramatically decreased the 24-h proteinuria which is a significant clinical hallmark of early stage DN, blood glucose level, serum creatinine and blood urea nitrogen in DN rats, alleviating diabetic renal injury.…”

Section: Discussionmentioning

confidence: 99%

“…As another member of SOCS family, SOCS2 was initially characterized for its role in the periphery as a negative regulator of growth hormone (GH) signaling [ 8 ]. SOCS2 was reported to inhibit the activation of the JAK/STAT signaling pathway and reduce the expression of inflammatory cytokines and fibrosis associated proteins in DN [ 9 ]. However, its underlying mechanism remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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SOCS2 overexpression alleviates diabetic nephropathy in rats by inhibiting the TLR4/NF-κB pathway

et al. 2017

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Suppressor of cytokine signaling 2 (SOCS2) was reported to be involved in the development of Diabetic Nephropathy (DN). However, its underlying mechanism remains undefined. Western blot was carried out to determine the expressions of SOCS2, Toll-like receptors 4 (TLR4) and nuclear factor kappa B (NF-κB) pathwayrelated proteins in DN patients, streptozotocin (STZ)-induced DN rats and high glucose (HG)-stimulated podocytes. The effects of SOCS2 overexpression on renal injury, the inflammatory cytokines production, renal pathological changes, apoptosis and the TLR4/NF-κB pathway in DN rats or HG-stimulated podocytes were investigated. TLR4 antagonist TAK-242 and NF-κB inhibitor PDTC were used to confirm the functional mechanism of SOCS2 overexpression in HG-stimulated podocytes. SOCS2 was downregulated, while TLR4 and NF-κB were up-regulated in renal tissues of DN patients and DN rats. Ad-SOCS2 infection alleviated STZ-induced renal injury and pathological changes and inhibited STZ-induced IL-6, IL-1β and MCP-1 generation and activation of the TLR4/NF-κB pathway in DN rats. SOCS2 overexpression attenuated apoptosis, suppressed the inflammatory cytokines expression, and inactivated the TLR4/NF-κB pathway in HG-stimulated podocytes. Suppression of the TLR4/NF-κB pathway enhanced the inhibitory effect of SOCS2 overexpression on apoptosis and inflammatory cytokines expressions in HG-stimulated podocytes. SOCS2 overexpression alleviated the development of DN by inhibiting the TLR4/NF-κB pathway, contributing to developing new therapeutic strategies against DN.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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SOCS2 overexpression alleviates diabetic nephropathy in rats by inhibiting the TLR4/NF-κB pathway

et al. 2017

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“…e overexpression of SOCS2 could decrease the expression of inflammatory cytokines [26,27]. SOCS2 knockout or deficiency led to increasing nuclear factor κB (NF-κB) activity as well as elevated expression of genes for the inflammatory cytokines [25,28].…”

Section: Discussionmentioning

confidence: 99%

Circulating Exosomal SOCS2-AS1 Acts as a Novel Biomarker in Predicting the Diagnosis of Coronary Artery Disease

Liang

Zhang

Lian

et al. 2020

BioMed Research International

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Background and Aims. Critical roles of circulating exosomal long noncoding RNAs (lncRNAs) have been implicated in multiple diseases. However, little is known about their roles in coronary artery disease (CAD). The aim of the present study was to investigate the relationships between circulating exosomal lncRNAs and CAD and identify the aberrantly expressed disease-related lncRNAs as biomarkers in diagnosing CAD. Methods. The aberrantly expressed lncRNAs in plasma exosomes from CAD patients and controls were identified by microarray analysis and verified by quantitative real-time PCR (qRT-PCR). Then, the correlation between the expression level of candidate biomarker and clinic features in CAD patients, mild coronary artery stenosis (mCAS) patients, and controls was analyzed. Finally, we used the receiver operating characteristic (ROC) curve to examine the diagnosis value of candidate biomarkers. Results. The downregulated SOCS2-AS1 was determined by microarray analysis and verified by qRT-PCR in plasma from CAD patients in contrast to controls. The SOCS2-AS1 expression level in plasma exosomes was negatively correlated with PLT and Lpa. Moreover, CAD patients with elevated levels of plasma exosome-encapsulated SOCS2-AS1 were susceptible to multicoronary artery lesions. Additionally, the area under ROC (AUC) of SOCS2-AS1 was 0.704 (95% CI = 0.607–0.801, P<0.001) for diagnosis of CAD. Conclusions. Plasma exosome-encapsulated SOCS2-AS1 was an independent protective factor against CAD and could be potentially used as a novel biomarker for the diagnosis of CAD.

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“…SOCS2 was involved in hyperglycaemia and glucose intolerance caused by the abnormal regulation of proinsulin processing and insulin secretion in beta cells [13]. The overexpression of SOCS2 possess the protective function in the development of diabetic nephropathy by reducing the expression of in ammatory cytokines and suppressing the activation of JAK/STAT pathway [14]. These physiological studies proposed that SOCS2 might play an important role in diabetes, but the role of genetic polymorphism within SOCS2 gene for T2DM predisposition has been less studied.…”

Section: Introductionmentioning

confidence: 99%

The Effect of SOCS2 Polymorphisms on Type 2 Diabetes Mellitus Susceptibility and Diabetic Complications in the Chinese Han Population

Pan

Tong

Deng

et al. 2020

Preprint

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Abstract Propose: We explored the effect of SOCS2 polymorphisms on the development of type 2 diabetes mellitus (T2DM) and diabetic complications.Methods: The subjects consisted of 500 T2DM patients and 501 healthy volunteers. Five variants in SOCS2 were genotyped by Agena MassARRAY system. Logistic regression analysis was utilized to calculate the odds ratio (OR) and 95% confidence intervals (95% CI).Results: Rs3825199 (OR = 1.44, p = 0.007), rs11107116 (OR = 1.39, p = 0.014) and rs10492321 (OR = 1.48, p = 0.004) had the increased T2DM risk. Moreover, the contribution of SOCS2 polymorphisms to T2DM risk was associated with age, gender, smoking and drinking and BMI. SOCS2 variants also had the reduced risk for T2DM patients with diabetic nephropathy, diabetic retinopathy and coronary heart disease.Conclusions: This study firstly reported that rs3825199, rs11107116 and rs10492321 in SOCS2 conferred to the increased risk for T2DM occurrence in the Chinese Han population.

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Influence of overexpression of SOCS2 on cells of DN rat

Abstract: The overexpression of SOCS2 can decrease the expression of inflammatory cytokines and fibrosis related proteins in DN rats and cells, and meanwhile suppress the activation of JAK/STAT signaling pathway mediated by DN.

Cited by 13 publications

References 14 publications

SOCS2 overexpression alleviates diabetic nephropathy in rats by inhibiting the TLR4/NF-κB pathway

SOCS2 overexpression alleviates diabetic nephropathy in rats by inhibiting the TLR4/NF-κB pathway

Circulating Exosomal SOCS2-AS1 Acts as a Novel Biomarker in Predicting the Diagnosis of Coronary Artery Disease

The Effect of SOCS2 Polymorphisms on Type 2 Diabetes Mellitus Susceptibility and Diabetic Complications in the Chinese Han Population

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