The Use of Targeted Next Generation Sequencing to Explore Candidate Regulators of TGF-β1’s Impact on Kidney Cells

Wang, Bo; Ji, Guanyu; Naeem, Haroon; Wang, Junwen; Kantharidis, Phillip; Powell, David R.; Ricardo, Sharon D.

doi:10.3389/fphys.2018.01755

Cited by 8 publications

(6 citation statements)

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“…Uniquely mapped reads were used to analyze the DNA methylation differential peaks based on a defined model of ChIP-Seq data (MACS2) ( Liu, 2014 ). Peaks were identified by the Poisson test with p -value < 0.01; then, we modified results by FDR < 0.01 for further analysis, and all the other parameters were used as the default ( Wang et al, 2018 ).…”

Section: Methodsmentioning

confidence: 99%

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The Profiling of DNA Methylation and Its Regulation on Divergent Tenderness in Angus Beef Cattle

Zhao

Ji²,

Carrillo

et al. 2020

Front. Genet.

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Beef is an essential food source in the world. Beef quality, especially tenderness, has a significant impact on consumer satisfaction and industry profit. Many types of research to date have focused on the exploration of physiological and developmental mechanisms of beef tenderness. Still, the role and impact of DNA methylation status on beef tenderness have yet to be elucidated. In this study, we exhaustively analyzed the DNA methylation status in divergent tenderness observed in Angus beef. We characterized the methylation profiles related to beef tenderness and explored methylation distributions on the whole genome. As a result, differentially methylated regions (DMRs) associated with tenderness and toughness of beef were identified. Importantly, we annotated these DMRs on the bovine genome and explored bio-pathways of underlying genes and methylation biomarkers in beef quality. Specifically, we observed that the ATP binding cassette subfamily and myosin-related genes were highly methylated gene sets, and generation of neurons, regulation of GTPase activity, ion transport and anion transport, etc. , were the significant pathways related with beef tenderness. Moreover, we explored the relationship between DNA methylation and gene expression in DMRs. Some methylated genes were identified as candidate biomarkers for beef tenderness. These results provide not only novel epigenetic information associated with beef quality but offer more significant insights into meat science, which will further help us explore the mechanism of muscle biology.

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Section: Methodsmentioning

confidence: 99%

“…The values of each bin were used to determine the read density or read distribution on the gene element regions. All the details on data analysis can be found in a previous publication ( Wang et al, 2018 ).…”

Section: Methodsmentioning

confidence: 99%

The Profiling of DNA Methylation and Its Regulation on Divergent Tenderness in Angus Beef Cattle

Zhao

Ji²,

Carrillo

et al. 2020

Front. Genet.

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“…Moreover, after treatment of MCs with TGF-β1, 5140 genes with significant differences were identified by Next-Generation Sequencing (NGS) identification. Among these genes, Tnfrsf11b , Rxfp3 , MMP9 , Syn1 , IL6 , and Megf6 are known to be involved in the regulation of fibrosis and inflammatory pathway [ 53 ].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, the hypomethylation of TIMP-2 and AKR1B1 genes is associated with proteinuria in patients with early DKD, and TIMP-2 methylation levels are associated with increased fibronectin expression and ECM accumulation [ 58 ]. TGF-β1 stimulation also plays a regulatory role in renal fibrosis by regulating DNA methylation of various genes [ 53 ]. When TGF-β1 is stimulated, DNMT1-mediated hypermethylation of RASAL1 can lead to increased fibroblast activation and fibrosis [ 59 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of metabolic memory on inflammation and fibrosis associated with diabetic kidney disease: an epigenetic perspective

2021

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Diabetic kidney disease (DKD) is one of the most common microvascular complication of both type 1 (T1DM) and type 2 diabetes mellitus (T2DM), and the leading cause of end-stage renal disease (ESRD) worldwide. Persistent inflammation and subsequent chronic fibrosis are major causes of loss of renal function, which is associated with the progression of DKD to ESRD. In fact, DKD progression is affected by a combination of genetic and environmental factors. Approximately, one-third of diabetic patients progress to develop DKD despite intensive glycemic control, which propose an essential concept “metabolic memory.” Epigenetic modifications, an extensively studied mechanism of metabolic memory, have been shown to contribute to the susceptibility to develop DKD. Epigenetic modifications also play a regulatory role in the interactions between the genes and the environmental factors. The epigenetic contributions to the processes of inflammation and fibrogenesis involved in DKD occur at different regulatory levels, including DNA methylation, histone modification and non-coding RNA modulation. Compared with genetic factors, epigenetics represents a new therapeutic frontier in understanding the development DKD and may lead to therapeutic breakthroughs due to the possibility to reverse these modifications therapeutically. Early recognition of epigenetic events and biomarkers is crucial for timely diagnosis and intervention of DKD, and for the prevention of the progression of DKD to ESRD. Herein, we will review the latest epigenetic mechanisms involved in the renal pathology of both type 1 (T1DN) and type 2 diabetic nephropathy (T2DN) and highlight the emerging role and possible therapeutic strategies based on the understanding of the role of epigenetics in DKD-associated inflammation and fibrogenesis.

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“…In our study, the elevation of KLF7 confers protection against fibrosis in a TGF-β1-induced cell model of renal fibrosis. KLF7 expression has also been revealed to be negatively correlated with the TGF-β1-regulated DNA methylation via integrative analysis [38]. Interestingly, KLF7 was targeted by lncRNA LINC00668, thereby promoting tumor migration and invasion in non-small cell lung cancer [39].…”

Section: Discussionmentioning

confidence: 99%

Elevation of LncRNA ENST00000453774.1 Prevents Renal Fibrosis by Upregulating FBN1, IGF1R, and KLF7

Yuan

Tang

Peng

et al. 2021

Kidney Blood Press Res

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Introduction: Transforming growth factor-β (TGF-β), a common outcome of various progressive chronic kidney diseases, can regulate and induce fibrosis. Objective: The study aimed to identify downstream targets of lncRNA ENST00000453774.1 (lnc453774.1) and outline their functions on the development of renal fibrosis. Methods: HK-2 cells were induced with 5 ng/mL TGF-β1 for 24 h to construct a renal fibrosis cell model. Differentially expressed genes (DEGs) targeted by lnc453774.1 in TGF-β1-induced renal fibrosis were identified using RNA sequencing. The dataset GSE23338 was employed to identify DEGs in 48-h TGF-β1-stimulated human kidney epithelial cells, and these DEGs were intersected with genes in the key module using weighted gene co-expression network analysis to generate key genes associated with renal fibrosis. MicroRNAs (miRs) that had targeting relationship with keys genes and lnc453774.1 were predicted by using Miranda software, and important genes were intersected with key genes that had targeting relationship with these miRs. Key target genes by lnc453774.1 were identified in a protein-protein interaction network among lnc453774.1, important genes, and reported genes related to autophagy, oxidative stress, and cell adhesion. Results: Key genes in the key module (turquoise) were intersected with DEGs in the dataset GSE23338 and yielded 20 key genes regulated by lnc453774.1 involved in renal fibrosis. Fourteen miRs had targeting relationship with lnc453774.1 and key genes, and 8 important genes targeted by these 14 miRs were identified. Fibrillin-1 (FBN1), insulin-like growth factor 1 receptor (IGF1R), and Kruppel-like factor 7 (KLF7) were identified to be involved in autophagy, oxidative stress, and cell adhesion and were elevated in the lnc453774.1-overexpressing TGF-β1-induced cells. Conclusion: These results show FBN1, IGF1R, and KLF7 serve as downstream targets of lnc453774.1, and that lnc453774.1 may protect against renal fibrosis through competing endogenous miRs which target FBN1, IGF1R, and KLF7 mRNAs.

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The Use of Targeted Next Generation Sequencing to Explore Candidate Regulators of TGF-β1’s Impact on Kidney Cells

Cited by 8 publications

References 58 publications

The Profiling of DNA Methylation and Its Regulation on Divergent Tenderness in Angus Beef Cattle

The Profiling of DNA Methylation and Its Regulation on Divergent Tenderness in Angus Beef Cattle

Effects of metabolic memory on inflammation and fibrosis associated with diabetic kidney disease: an epigenetic perspective

Elevation of LncRNA ENST00000453774.1 Prevents Renal Fibrosis by Upregulating FBN1, IGF1R, and KLF7

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