MiRNA expression profiling and identification of a miRNA regulator for muscle regeneration in the ischemic limb with proanthocyanidins treatment of adult mice
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ABSTRACT:
PROVIDER: PRJNA611933 | ENA |
REPOSITORIES: ENA
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Project description:Using the highly sensitive miRNA array, we screened 411 differentially expressed genes microRNAs in the ischemic muscle with proanthocyanidins treatment and we explored the functions of these miRNAs in the ischemic muslce by Gene Ontology and Kyoto Encyclopedia of Genes annotation. The enrichment results indicated that these miRNAs mainly participated in the muscle regeneration process. Furthermore, the quantitative real-time polymerase chain reaction, immunohistochemistry and dual luciferase reporter assay results showed that miR-133b-3p is a specific regulator of MKP1/ p38-MAPK signal axis, offering a novel therapeutic opportunity for limb ischemic injury.
2023-03-01 | GSE146772 | GEO
Project description:The initial factor in the occurrence, development, and prognosis of cerebral ischemia is vascular dysfunction in the brain, and vascular remodeling of the brain is the key therapeutic target and strategy for ischemic tissue repair. Limb remote ischemic preconditioning exhibits potential pleiotropic protective effects in many brain-related diseases, including stroke.Whether limb remote ischemic preconditioning has other effects such as vascular protective effects and the detailed mechanism by which limb remote ischemic preconditioning improves pathology and angiogenesis in cerebral ischemia remains to be further elucidated. The present study was designed to investigate whether limb remote ischemic preconditioning protects vascular structure and promotes angiogenesis in cerebral ischemic rats.
2024-06-05 | PXD052843 |
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
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.
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Project description:The influence of cranberry proanthocyanidins on the transcriptomic responses of Streptococcus mutans during biofilm formation was investigated. Treatment regimens simulating topical exposures experienced clinically (twice-daily, 60 s each) were used over saliva-coated hydroxyapatite biofilm model. Cranberry proanthocyanidins (1.5 mg/ml) in 15% ethanol was used to treat the biofilms. Four biological replicates each for the treatment and vehicle control were used for RNA extraction and microarray.
2012-08-22 | E-GEOD-40172 | biostudies-arrayexpress
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
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.
2024-09-01 | GSE275812 | GEO
Project description:The difference of circulating miRNA expressions by the presence of atherosclerosis in intra- and extra-cranial vessels were evaluated using serum of ischemic stroke patients.
2017-03-16 | GSE96621 | GEO
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
Project description:The influence of cranberry proanthocyanidins on the transcriptomic responses of Streptococcus mutans during biofilm formation was investigated.
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