Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequencing in healthy controls, intermittent claudicant, and CLI patient skeletal muscle

ABSTRACT: Gastrocnemius muscle biopsies were obtained from 15 health older adults without peripheral artery disease (PAD), 20 PAD patients with intermittent claudication, and 16 patients with critical limb ischemia undergoing limb amputation. Gene expression analysis was performed using RNA sequencing analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE120642 | GEO | 2018/11/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Muscle Proteome of Critical Limb Ischemia Patients

Project description:This is a TMT-labeled proteomics analysis of human skeletal muscle specimens obtained from the following groups: older adult controls, critical limb ischemia patients undergoing surgical intervention, and critical limb ischemia patients undergoing limb amputation.

2021-10-06 | PXD021849 | JPOST Repository

Transcriptomic profile of ischemic and non-ischemic skeletal muscle tissue from peripheral artery disease patients

Project description:Peripheral artery disease (PAD) can cause limb pain and ulcers that won't heal. It is a leading cause of amputation, yet the moleculer mechanims that drive disease are poorly understood. To gain insights into mechanims of PAD at the transcriptome level, we performed sc-RNA-seq on non-ischemic and ischemic tissue from a male PAD patient who had undergone a below knee amputation.

2024-08-19 | GSE266788 | GEO

Single Nuclei RNA Sequencing of the Gastrocnemius Muscle Reveals Unique Transcriptomic Signatures of Peripheral Artery Disease

Project description:This study examines the transcriptional profile at the single-nuclei resolution human gastrocnemius skeletal muscle from 20 patients with Peripheral artery disease (PAD) and 12 non-PAD controls. In all libraries, muscle specimens were pooled prior to nuclei isolations were performed.

2023-10-10 | GSE233882 | GEO

Proteomic analysis of vascular tissue from critical limb ischemia mouse models treated with Etrinabdione

Project description:Vasculogenic therapies have been investigated for the treatment of peripheral artery disease (PAD) with very limited success in clinical trials. The isoform PP2A (protein phosphatase 2)/B55alpha inhibits the activity of the prolyl hydroxylase 2 (PHD2) and activates the hypoxia inducing factor-1alpha (HIF-1alpha), playing a key role in in vessel remodeling. Thus, PP2A/B55alpha activators may have the potential to induce angiogenesis and arteriogenesis. Herein we investigated the pharmacological attributes of VCE-004.8 (Etrinabdione) and its effectiveness in a murine model of critical limb ischemia.

2024-04-03 | PXD050360 | Pride

Interventional- and amputation-stage muscle proteomes in the chronically threatened ischemic limb

Project description:Background: Despite improved surgical approaches for chronic limb threatening ischemia (CLTI), amputation rates remain high and contributing tissue-level factors remain unknown. Objective: The purpose of this study was twofold: 1) to identify differences between the healthy adult and CLTI limb muscle proteome, and 2) to identify differences in the limb muscle proteome of CLTI patients prior to surgical intervention or at the time of amputation. Methods: Gastrocnemius muscle was collected from non-ischemic control (n=26) and either pre-interventional surgery (n=10) or at amputation outcome (n=29) CLTI patients. All samples were subjected to isobaric tandem-mass-tag-assisted quantitative proteomics. Results: The mitochondrion was the primary classification of downregulated proteins (>70%) in CLTI limb muscles and paralleled robust functional mitochondrial impairment. Upregulated proteins (>38%) were largely from the extracellular matrix. Across the two independent sites, 39 proteins were downregulated and 20 upregulated uniformly. Pre-interventional CLTI muscles revealed a robust upregulation of mitochondrial proteins but modest functional impairments in fatty acid oxidation as compared with controls. Comparison of pre-intervention and amputation CLTI limb muscles revealed mitochondrial proteome and functional deficits similar to that between amputation and healthy controls. Interestingly, these observed changes occurred despite 50% of the amputation CLTI patients having undergone a prior surgical intervention. Conclusions: The CLTI proteome supports failing mitochondria as a mechanism contributing to amputation outcomes. The signature of pre-intervention CLTI muscle reveals stable mitochondrial protein abundance that is insufficient to uniformly prevent functional impairments. Taken together, our findings support the investigation of mitochondrial functional therapeutics as both adjuvant and independent therapies for CLTI.

2022-04-21 | PXD025810 | JPOST Repository

Unique metabolomic profile of skeletal muscle in chronic limb threatening ischemia (HR-MAS study)

Project description:This project is focused on a cross-sectional analysis of non-PAD controls and CLTI patients undergoing either a vascular intervention or undergoing limb amputation was performed and involved a detailed assessment of the limb muscle metabolome using HR-MAS and solution state NMR spectroscopy. It was hypothesized that patients undergoing limb amputation would present with altered muscle metaolite features compared with non-PAD controls.

2020-11-30 | ST001617 | MetabolomicsWorkbench

Unique metabolomic profile of skeletal muscle in chronic limb threatening ischemia (aqueous phase samples )

2020-11-30 | ST001616 | MetabolomicsWorkbench

Unique metabolomic profile of skeletal muscle in chronic limb threatening ischemia (organic phase samples)

2020-11-30 | ST001615 | MetabolomicsWorkbench

Circadian Dysfunction in Skeletal Muscle Impairs Limb Perfusion and Muscle Regeneration in Peripheral Artery Disease [Myotube-ATACseq]

Project description:Peripheral arterial disease (PAD), caused by atherosclerosis, leads to limb ischemia, muscle damage, and impaired mobility in the lower extremities. Recent studies suggest that circadian rhythm disruptions can hinder vascular repair during ischemia, but the specific tissues involved and the impact on muscle health remain unclear. This study investigates the role of the skeletal muscle circadian clock in muscle adaptation to ischemic stress using a surgical mouse model of hindlimb ischemia. We used mice with specific genetic loss of the circadian clock activator, BMAL1, in adult skeletal muscle tissues (Bmal1muscle). Bmal1muscle mice and controls underwent femoral artery ligation surgery to induce hindlimb ischemia. Laser doppler imaging was used to assess limb perfusion at various time points after the surgery. Muscle tissues were analyzed with RNA sequencing and histological examination to investigate PAD-related muscle pathologies. Additionally, we studied the role of BMAL1 in muscle fiber adaptation to hypoxia using RNA and ATAC sequencing analyses in primary myotube culture model. Disrupted expression of circadian rhythm-related genes was observed in existing RNA-seq datasets from PAD patient-derived endothelial cells and ischemic limb skeletal muscles. Genetic loss of Bmal1 specifically in adult mouse skeletal muscle tissues delayed reperfusion recovery following induction of hindlimb ischemia. Histological examination of muscle tissues showed reduced regenerated myofiber number and a decreased proportion of type IIB fast-twitch myofibers in Bmal1musc mouse muscles in the ischemic limbs, but not in their contralateral non-ischemic limbs. Transcriptomic analysis revealed abrogated metabolic, angiogenic, and myogenic pathways relevant to hypoxia-adaptation in Bmal1musc mouse muscles. These changes were corroborated in Bmal1-deficient cultured primary myotubes cultured under hypoxic conditions.

2024-09-02 | GSE275893 | GEO

Circadian Dysfunction in Skeletal Muscle Impairs Limb Perfusion and Muscle Regeneration in Peripheral Artery Disease

2024-09-01 | GSE275811 | GEO