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RNA-expression analysis on smooth muscle cells of diabetic donors after empagliflozin treatment

ABSTRACT: RNA-expression analysis on smooth muscle cells of diabetic donors after empagliflozin treatment

PROVIDER: PRJNA783346 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17032292_1.fastq.gz	Fastqsanger.gz
	SRR17032292_2.fastq.gz	Fastqsanger.gz
	SRR17032293_1.fastq.gz	Fastqsanger.gz
	SRR17032293_2.fastq.gz	Fastqsanger.gz
	SRR17032294_1.fastq.gz	Fastqsanger.gz

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RNA-expression analysis on smooth muscle cells of diabetic donors after empagliflozin treatment

Project description:Purpose: We report vascular effects of empagliflozin stimulation. Results: Gene set enrichment analysis of RNA-Seq showed negative regulation of vascular smooth muscle cell proliferation. Gene set overlapped by the vasoactive peptide apelin, being upregulated by empagliflozin treatment.

2021-11-27 | GSE189538 | GEO

Empagliflozin alleviates atherosclerotic calcification by inhibiting osteogenic differentiation of vascular smooth muscle cells

Project description:SGLT-2 inhibitors, such as empagliflozin, have been shown to reduce the occurrence of cardiovascular events and delay the progression of atherosclerosis. However, its role in atherosclerotic calcification remains unclear. In this research, ApoE-/- mice were fed with western diet and empagliflozin was added to the drinking water for 24 weeks. Empagliflozin treatment significantly alleviated arterial calcification assessed by alizarin red and von kossa staining in aortic roots and reduced the lipid levels, while had little effect on body weight and blood glucose levels in ApoE-/- mice. In vitro studies, empagliflozin significantly inhibits calcification of primary vascular smooth muscle cells (VSMCs) and aortic rings induced by osteogenic media (OM) or inorganic phosphorus (Pi). RNA sequencing of VSMCs cultured in OM with or without empagliflozin showed that empagliflozin negatively regulated the osteogenic differentiation of VSMCs. And further studies confirmed that empagliflozin significantly inhibited osteogenic differentiation of VSMCs via qRT-PCR. Our study demonstrates that empagliflozin alleviates atherosclerotic calcification by inhibiting osteogenic differentiation of VSMCs, which addressed a critical need for the discovery of a drug-based therapeutic approach in the treatment of atherosclerotic calcification.

2023-11-22 | GSE243752 | GEO

RNA seq analysis of human macrophages after treatment of glimepiride versus empagliflozin.

Project description:Purpose: The goal of this study is to compare NGS-derived macrophage transcriptome profiling (RNA-seq) between diabetic patients treated with glimepiride versus empagliflozin. Methods: Macrophage mRNA profiles of 7 patients treated with either glimepiride or empagliflozin were generated by deep sequencing using Illumina HiSeq 4000 system. The sequence reads that passed quality filters were analyzed at the transcript isoform level using CLC Genomics Workbench v.9.0.1 software (CLC Bio, Cambridge, USA). Conclusion: A total of 64 genes were differentially expressed in the glimepiride treated patients compared to those of the empagliflozin treated patients, with 47 genes increased and 17 genes decreased in the glimepiride group. Most of these genes were related to immune-related receptor signaling pathway.

2019-07-17 | GSE134329 | GEO

Empagliflozin alleviates atherosclerotic calcification by inhibiting osteogenic differentiation of vascular smooth muscle cells

Project description:Empagliflozin alleviates atherosclerotic calcification by inhibiting osteogenic differentiation of vascular smooth muscle cells

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Effect of TGF-B treatment on human vascular smooth muscle cells

Project description:The authors did a microarray analysis to investigate the effect of TGF-B treatment on cultured smooth muscle cells from the human aorta. In particular, the authors were interested to see which cell types were upregulated or downregulated after treatment with TGF-B. Human Smooth muscle cells from 4 different donors in triplicates were analyzed. The cells were either untreated (n=12) or were treated with TGF-B (1 ng/ml)

2011-06-16 | E-GEOD-30004 | biostudies-arrayexpress

Nuclear factor 90 isoform of vascular smooth muscle cells accelerates diabetic arteriosclerotic calcification by mediating FBXW7-AGER1-AGEs axis

Project description:Hyperglycemia accelerates calcification of atherosclerotic plaques in diabetic patients, and the prolonged accumulation of advanced glycation end products (AGEs) induced by hyperglycemia may be closely related to the pathogenesis of aortic calcification. However, the mechanisms underlying this association remain unclear. In the current study, we investigated the role of vascular smooth muscle cell nuclear factor 90/110 (NF90/110) in mediating AGEs accumulation and accelerating diabetic atherosclerotic calcification. Using vascular smooth muscle cells (VSMCs), human samples, and mouse models, we found that hyperglycemia-mediated AGEs markedly increased VSMC NF90/110 activation both in human and mouse atherosclerotic calcified tissues with diabetes. Silencing of NF90/110 in vitro and genetic deletion of VSMC NF90/110 in mice decreased obviously AGEs-induced arteriosclerotic calcification. Mechanistically, AGEs increased the activity of NF90, which then enhanced ubiquitination and degradation of AGE receptor 1 (AGER1) by stabilizing the mRNA of E3 ubiquitin ligase, F-box, and WD repeat domain 7 (FBXW7), thus causing the accumulation of more AGEs. Furthermore, AGEs accumulation accelerated diabetic atherosclerotic calcification by inducing VSMC phenotypic changes to osteoblast-like cells, apoptosis, and matrix vesicle release. Collectively, our study demonstrated the effects of VSMC NF90 in mediating the metabolic imbalance of AGEs to accelerate diabetic arteriosclerotic calcification. These novel findings elucidate a pivotal mechanism underlying AGE-induced diabetic atherosclerotic calcification and provide a framework for potential interventions against diabetic vascular complications.

2024-04-02 | GSE253682 | GEO

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Project description:Hybrid insulin peptides (HIPs) result from the linkage of an insulin C-peptide fragment and another peptide via a traditional peptide bond to generate a sequence that is not encoded in the genome. Here, we sought to identify HIPs naturally present in the pancreatic islets of non-obese diabetic (NOD) mice, BALB/c mice, and non-diabetic human donors by mass spectrometry.

2019-01-07 | PXD011606 | Pride

Fatal Asthma and Non-Asthma Donor-Derived Airway Smooth Muscle Transcriptome Response to Glucocorticoid Treatment

Project description:Asthma is a chronic inflammatory respiratory disease affecting over 300 million people around the world. Some asthma patients remain poorly controlled by conventional therapies and experience more life-threatening exacerbations. While patients with severe, refractory disease represent a heterogeneous group, a feature shared by most includes glucocorticoid insensitivity. We sought to characterize differences in the airway smooth muscle transcriptome response to glucocorticoids in fatal asthma vs. non-asthma donors. RNA-Seq was used to measure airway smooth muscle transcript expression differences between 9 donors with fatal asthma and 8 non-asthma donors. Cells from each donor were treated with budesonide or with vehicle control. Poly(A)-selected RNA-Seq libraries were prepared with the Illumina TruSeq method. An Illumina HiSeq 2500 instrument was used to generate 125 base pair paired-end reads.

2018-12-31 | GSE94335 | GEO

Single Cell Gene Expression Profiling of CD45+ Cells in Mouse Liver with or without Empagliflozin (EMPA) Treatment

Project description:Single-Cell Sequencing Reveals Immune Cell Subtype Differences in Mouse Liver Between MCD and MCD+Empagliflozin (EMPA) Treatment.

2024-10-01 | GSE271786 | GEO

RNA-seq of cardiomyocytes exposed to glucose deprivation with or without empagliflozin treatment

Project description:Glucose-lowering drugs sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of serious heart failure events, regardless of diabetes status, but the underling mechanism of this cardioprotective benefit is unknown. Here, we performed RNA-seq screening in cardiomyocytes to determine the potential cardioprotective mechanism of empagliflozin (EMPA).

2022-12-12 | GSE200598 | GEO

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