Role of upstream stimulatory factor 2 in diabetic nephropathy

Wang, Shuxia

doi:10.1007/s11515-015-1359-x

Cited by 7 publications

(4 citation statements)

References 105 publications

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“…Moreover, Ang II can stimulate the expression and activation of oxidative stress protein p66Shc in tubular epithelial cells (TECs) and participate in the oxidative damage of tubular cells through induces the overproduction of ROS in tubular cells mitochondria. In addition, high glucose can up-regulate Ang II expression in various renal cells, which can induce the accumulation of ECM and promoting the renal fibrosis of DN (Wang 2015). Generally, the mechanism of Ang II-induced renal fibrosis includes the promotion of hypertrophy and proliferation of MCs through the TGF-β signaling pathway (Meng et al 2012).…”

Section: Angiotensin IImentioning

confidence: 99%

A Glimpse of the Mechanisms Related to Renal Fibrosis in Diabetic Nephropathy

Zeng

Xiao

Sun

2019

Advances in Experimental Medicine and Biology

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Diabetic nephropathy (DN) is a common kidney disease in people with diabetes, which is also a serious microvascular complication of diabetes and the main cause of end-stage renal disease (ESRD) in developed and developing countries. Renal fibrosis is a finally pathological change in DN. Nevertheless, the relevant mechanism of cause to renal fibrosis in DN is still complex. In this review, we summarized that the role of cell growth factors, epithelial-mesenchymal transition (EMT) in the renal fibrosis of DN, we also highlighted the miRNA and inflammatory cells, such as macrophage, T lymphocyte, and mastocyte modulate the progression of DN. In addition, there are certain other mechanisms that may yet be conclusively defined. Recent studies demonstrated that some of the new signaling pathways or molecules, such as Notch, Wnt, mTOR, Epac-Rap-1 pathway, may play a pivotal role in the modulation of ECM accumulation and renal fibrosis in DN. This review aims to elucidate the mechanism of renal fibrosis in DN and has provided new insights into possible therapeutic interventions to inhibit renal fibrosis and delay the development of DN. Keywords Renal fibrosis • Diabetic nephropathy • TGF-β • Epithelial-mesenchymal transition • miRNA Ling-Feng Zeng and Ying Xiao contributed equally to this work.

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Section: Angiotensin IImentioning

confidence: 99%

A Glimpse of the Mechanisms Related to Renal Fibrosis in Diabetic Nephropathy

Zeng

Xiao

Sun

2019

Advances in Experimental Medicine and Biology

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“…The dysregulation of FOXC1 is involved in skeletal abnormalities [30]. The USF2 is also involved in diabetic nephropathy [31]. Dysregulation of YY1 in the liver causes insulin resistance, dyslipidemia etc and has also been proposed as targeting hepatic YY1 an important target for insulin-resistant diabetes [32].…”

Section: Discussionmentioning

confidence: 99%

Network-Based Computational Approach to Identify Delineating Common Cell Pathways Influencing Type 2 Diabetes and Diseases of Bone and Joints

Moni

Islam

Rahman³

et al. 2020

IEEE Access

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Developing type 2 diabetes (T2D) can increase patient risk of developing other common diseases and exacerbate their severity, including diseases that affect bone and joints. Such comorbidity interactions are hard to study in detail by traditional endocrinological methods. Thus, we developed tissue transcript analytical approaches to identify common pathways through which these diseases can interact. We examined RNAseq and microarray transcript datasets from studies of T2D and chronic bone and joint diseases, namely rheumatoid arthritis (RA), osteoarthritis (OA), juvenile idiopathic arthritis (JIA) and low peak bone density, a key osteoporosis (OP) determinant. These datasets contained data from affected individuals and matched controls. Differentially expressed genes (DEGs) for each condition were compared with T2D DEG. Overlapping DEGs (i.e., those common to T2D and a bone or joint condition) were subjected to gene enrichment by pathway analyses and by gene ontology methods, and the results were evaluated by using SNP-disease linkage (dbGaP) and gene-disease association (OMIM) databases that indicate gene involvement in pathologies. By examining gene targets of transcription factors (TFs) and microRNA (miRNAs), we also constructed DEG-TF and DEG-miRNA interactions networks for analysis. We identified strong candidate genes in common pathways, notably including SYK, UCP3, ROR1, PPARG, BUB1, AKT2, ADCY2 and CCR5. The DEG-TF network and DEG-miRNA interactions network analyses revealed a number of TFs (GATA2, FOXC1, USF2, YY1, E2F1, JUN, RELA, CREB1, TFAP2A, NFB1) and miRNAs (mir-335-5p, mir-16-5p, mir-26b-5p, mir-124-3p, mir-218-5p, mir-98-5p, mir-29b-3p, mir-3135b, mir-29c-3p, mir-1-1) that can regulate the identified DEGs at the transcriptional and post-transcriptional levels. Thus this data-driven approach has enabled identification and validation of regulatory factors and cell pathways by which T2D may influence bone and joint conditions, which may suggest new ways to interfere with the pathogenic processes involved.INDEX TERMS T2 diabetes, network-based approach, joint diseases, bone diseases.

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“…As for Gdh, starvation decreased hepatic mRNA levels of Usf2 in the liver of S. aurata. In this regard, it was previously reported that high glucose levels upregulate Usf2 expression in human-derived HK-2 cells and primary rat mesangial cells (Shi et al 2008, Visavadiya et al 2011, Wang 2015. Therefore, low levels of glycemya associated to long-term starvation may be critical to downregulate Usf2 expression, which in turn may lead to decreased Gdh mRNA levels in the liver of S. aurata.…”

Section: Figurementioning

confidence: 94%

Role of upstream stimulatory factor 2 in glutamate dehydrogenase gene transcription

Gaspar

Silva-Marrero

Salgado

et al. 2018

Journal of Molecular Endocrinology

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Glutamate dehydrogenase (Gdh) plays a central role in ammonia detoxification by catalysing reversible oxidative deamination of l-glutamate into α-ketoglutarate using NAD or NADP as cofactor. To gain insight into transcriptional regulation of , the gene that codes for Gdh, we isolated and characterised the 5' flanking region of from gilthead sea bream (). In addition, tissue distribution, the effect of starvation as well as short- and long-term refeeding on Gdh mRNA levels in the liver of were also addressed. 5'-Deletion analysis of promoter in transiently transfected HepG2 cells, electrophoretic mobility shift assays, chromatin immunoprecipitation (ChIP) and site-directed mutagenesis allowed us to identify upstream stimulatory factor 2 (Usf2) as a novel factor involved in the transcriptional regulation of Analysis of tissue distribution of Gdh and Usf2 mRNA levels by reverse transcriptase-coupled quantitative real-time PCR (RT-qPCR) showed that Gdh is mainly expressed in the liver of, while Usf2 displayed ubiquitous distribution. RT-qPCR and ChIP assays revealed that long-term starvation down-regulated the hepatic expression of Gdh and Usf2 to similar levels and reduced Usf2 binding to promoter, while refeeding resulted in a slow but gradual restoration of both Gdh and Usf2 mRNA abundance. Herein, we demonstrate that Usf2 transactivates by binding to an E-box located in the proximal region of promoter. In addition, our findings provide evidence for a new regulatory mechanism involving Usf2 as a key factor in the nutritional regulation of transcription in the fish liver.

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Role of upstream stimulatory factor 2 in diabetic nephropathy

Cited by 7 publications

References 105 publications

A Glimpse of the Mechanisms Related to Renal Fibrosis in Diabetic Nephropathy

A Glimpse of the Mechanisms Related to Renal Fibrosis in Diabetic Nephropathy

Network-Based Computational Approach to Identify Delineating Common Cell Pathways Influencing Type 2 Diabetes and Diseases of Bone and Joints

Role of upstream stimulatory factor 2 in glutamate dehydrogenase gene transcription

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