Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Repairing of isoaspartyl residues by PCMT1 alleviates renal fibrosis through the repression of TGF-β1/TGFBR2/Smad signaling pathway

ABSTRACT: Repairing of isoaspartyl residues by PCMT1 alleviates renal fibrosis through the repression of TGF-β1/TGFBR2/Smad signaling pathway

PROVIDER: PRJNA1043803 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26908864_1.fastq.gz	Fastqsanger.gz
	SRR26908864_2.fastq.gz	Fastqsanger.gz
	SRR26908865_1.fastq.gz	Fastqsanger.gz
	SRR26908865_2.fastq.gz	Fastqsanger.gz
	SRR26908866_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 64

Similar Datasets

Repairing of isoaspartyl residues by PCMT1 alleviates renal fibrosis through the repression of TGF-β1/TGFBR2/Smad signaling pathway

Project description:Protein L-isoaspartyl/D-aspartyl Methyltransferase (PCMT1) plays a pivotal role in repairing a spontaneous post-translational modification (PTM) of L-isoaspartyl residues resulted from asparagine deamidation or aspartate isomerization. This PTM is particularly important for extracellular matrix (ECM) proteins because their low turnover rate and are susceptible to factors that could accelerate such modification. Therefore, it becomes imperative to comprehensively investigate the impact of PCMT1 on ECM homeostasis and its associated pathological alterations. In this study, we revealed that secreted PCMT1 repairs the isoaspartyl residues of the TGFBR2 protein on the cell membrane to suppress TGF-β1/Smad pathway. Through this novel PTM regulation, PCMT1 played essential roles in combating renal fibrosis, as lack of PCMT1 worsened tubular injury, collagen deposition, myofibroblast activation, and macrophage infiltration in total kidney and tubular contexts in a mouse model of chronic kidney disease. Moreover, PCMT1 level decreased in fibrotic kidney tissues and inversely related to kidney function in mice and in humans. Our study highlights the important function of PCMT1 in modifying proteins in the extracellular space and identified a novel role of PCMT1 in regulating TGF-β1 pathway in renal fibrosis. This study holds the potential of innovative therapeutic avenue for the mitigation of renal fibrosis.

2024-01-01 | GSE248435 | GEO

Repairing of isoaspartyl residues by PCMT1 alleviates renal fibrosis through the repression of TGF-β1/TGFBR2/Smad signaling pathway

2025-03-18 | PXD047057 | Pride

The TGF-β/SMAD pathway upregulates SRC

Project description:The non-receptor tyrosine kinase SRC is upregulated in various human cancers and plays crucial roles in cancer progression by promoting invasion and metastasis. We show that the transforming growth factor beta (TGF-β/SMAD pathway directly upregulates SRC during the epithelial-mesenchymal transition. In human epithelial MCF10A cells, TGF-β1 treatment markedly upregulated mRNA expression of SRC. Knockout of SMAD4 suppressed upregulation of SRC by TGF-β1. ChIP-sequencing analysis revealed that SRC was transcribed from the SRC1A promoter, which interacted with SMAD2 and SMAD4, in response to TGF-β1. These findings demonstrate that a direct interaction of the activated SMAD complex with the SRC1A promoter directly upregulates SRC and suggest that TGF-β contributes to SRC upregulation in the tumor microenvironment, where TGF-β-mediated tumor progression takes place.

2023-11-20 | GSE122913 | GEO

TGF-β1 promotes wound healing after ionizing radiation through the TGFβ-SMAD canonical signaling pathway

Project description:Objective: Ionizing radiation (IR) therapy, commonly used in cancer treatment, has detrimental effects on the skin. When combined with surgical resection, IR leads to persistent wounds and forms a significant side effect, making wound healing difficult. This study aimed to understand the mechanisms underlying IR-induced wound damage and develop treatment methods. Approach: A mouse model of IR was created by exposing mice to 7Gy of radiation after skin excision. The temporal changes of epidermal stem cells (EPSCs) and wound healing were examined. RNA-seq analysis was performed on skin tissues to investigate regulatory mechanisms during the healing process. Topical application of TGFβ was used to assess its impact on wound healing. Results: Mice in the IR group exhibited prolonged wound healing time, and the healing rate was significantly reduced. IR exposure decreased Ki67+/K14+ cells (proliferating EPSCs), reduced the expression levels of K14 and K15. The RNA-seq results revealed a significant decrease in epidermal stem cell-related genes following IR. Additionally, the TGFβ-SMAD pathway exhibited temporal changes during the wound healing process, while pre-treatment with TGFβ1 significantly promotes the healing of IR-induced wounds. Innovation: TGF-β1 activated the TGFβ-SMAD pathway and promotes wound healing after ionizing radiation. Conclusions: These findings indicate that IR diminishes the population of epidermal stem cells (EPSCs), thereby impeding the healing process by disrupting the TGFβ-Smad pathway. However, the external application of TGFβ1 to the wound area effectively improves IR-induced skin damage and exhibits promising therapeutic effects. These findings provide intervention targets and agents for the clinical applications.

2025-08-15 | GSE241297 | GEO

Expression changes in respiratory epithelial cells when treated with TGF-β1

Project description:TGF-β1 is involved in various biological processes through downstream signals including SMAD, Akt, Erk, etc. TGF-β1 overexpressed by harmful stimuli can act as a causative factor in diseases such as accumulation of extracellular matrix and development of cancerous characteristics. Therefore, we sought to compare changes in expression of intracellular miRNAs to study diseases caused by TGF-β1. In our study, we aimed to discover therapeutic targets for TGF-β1-induced disease by investigating changes in miRNA expression and identifying the correlation between genes that can be regulated by miRNA.

2024-07-24 | GSE267490 | GEO

TGF-β1 promotes wound healing after ionizing radiation through the TGFβ-SMAD canonical signaling pathway

Project description:TGF-β1 promotes wound healing after ionizing radiation through the TGFβ-SMAD canonical signaling pathway

| PRJNA1007660 | ENA

Defining the molecular properties of the repairing epithelium during DSS induced colitis

Project description:In order to understand the molecular changes associated with the establishment of the repairing epithelium following dextran sulfate sodium (DSS) induced injury of the colon we have isolated Epcam+Sca1+ expressing epithelial cells from repairing tissue and Epcam+ homeostatic intestine. Cells isolated by flow cytometry were subjected to RNA extraction and analysed by expression analysis

2017-11-30 | E-MTAB-5249 | biostudies-arrayexpress

The effect of Schisandra chinensis fruit extract (SCE) and Schisandrin B (SchB) on gene expression profile in TGF-β1-treated A7r5 rat aortic smooth muscle cell

Project description:Schisandra chinensis fruit extract (SCE) and its active ingredient Schisandrin B (SchB), which are effective in the treatment of vascular diseases, have been known to suppress transforming growth factor β1 (TGF-β1)-mediated Smad activation and myosin light chain (MLC) phosphorylation in vascular smooth muscle cells (VSMCs). However, it is still largely unknown about the pharmacologic effects and mechanisms of SCE and SchB on TGF-β1-induced intracellular signaling pathways in vascular smooth muscle cells (VSMCs).

2017-12-20 | GSE87439 | GEO

Vericiguat reduces atrial fibrillation recurrence by alleviating myocardial fibrosis via the TGF-β1/Smad2/3 pathway

Project description:Atrial fibrillation (AF) and heart failure (HF) are mutually reinforcing, and the prognosis for both diseases is poor. Vericiguat is the first oral soluble guanylate cyclase (sGC) stimulator to be approved for the treatment of symptomatic, ejection fraction-reduced chronic heart failure (HFrEF) in adults. It exerts a general therapeutic effect on cardiovascular diseases, with a particular efficacy in the treatment of HF. However, the mechanism of vericiguat treatment of atrial fibrillation remains unclear. The objective of this study was to investigate the potential mechanism of vericiguat in the treatment of atrial fibrillation. A retrospective analysis was conducted to investigate the effects of vericiguat on patients with heart failure and paroxysmal AF. Furthermore, the effects of vericiguat on AF and the degree of myocardial fibrosis in rat AF models and cells were observed. It was found that vericiguat can control the recurrence of AF in clinical studies and can control the fibrosis of AF rats in vivo and in vitro experiments. RNA-Seq sequencing revealed that the TGF-β1/Smad pathway in cells treated with vericiguat was significantly enriched. In vitro validation demonstrated that the anti-fibrotic effect of Vericiguat was weakened by the TGF-β1/Smad pathway when Protein Kinase G (PKG) was knocked down. The findings indicate that vericiguat can inhibit myocardial fibroblast activation and collagen synthesis via the TGF-β1/Smad pathway, thereby exerting a controlling effect on the recurrence of atrial fibrillation.

2025-07-23 | GSE278356 | GEO

Transcriptomic Changes in TGF-β1 Differentiated and PGE2 Dedifferentiated Myofibroblasts

Project description:These data show that the genes that distinguish myofibroblasts from fibroblasts are myriad, and that some genes not traditionally associated with myofibroblast differentiation may serve as novel therapeutic targets for fibrosing disorders. Gene expression levels were assessed from total RNA on the Affymetrix U219 microarray. Here, we use transforming growth factor-β1 (TGF-β1) and prostaglandin E2 (PGE2), which has recently been shown to reverse myofibroblast differentiation, to investigate the transcriptomic changes that occur during TGF-β1-induced differentiation and PGE2-induced de-differentiation of myofibroblasts.

2015-06-30 | E-GEOD-63659 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data