Hypoxia-induced miR-210 modulates gene expression in response to acute peripheral ischemia.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE43340 | GEO | 2015/10/23
SECONDARY ACCESSION(S): PRJNA185485
REPOSITORIES: GEO
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Project description:Peripheral Artery Disease is caused by the restriction or occlusion of arteries supplying the leg. Better understanding of the molecular mechanisms underpinning tissue response to acute and chronic ischemia is urgently needed to improve therapeutic options. The aim of this study is understanding miR-210 regulation and role in a mouse model of hindlimb ischemia. To investigate miR-210 function, mice were injected with a miR-210 complementary LNA-oligonucleotide (anti-miR-210). Then, the left femoral artery was dissected in order to induce unilateral hindlimb ischemia. Mice were sacrified 3 days later and gene expression profiles of gastrocnemius muscles were obatained.
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Project description:The aim of this study was to identify angiogenic microRNAs (miRNAs) that could be used in the treatment of hindlimb ischemic tissues. miRNAs contained in extracellular vesicles (EVs) deriving from the plasma were analyzed in C57BL/6 mice, which have ischemia tolerance, and in BALB/c mice without ischemia tolerance as part of a hindlimb ischemia model; as a result 43 angiogenic miRNA candidates were identified. An aortic ring assay was employed by using femoral arteries isolated from BALC/c mice and EVs containing miRNA; as a result, the angiogenic miRNA candidates were limited to 14. The blood flow recovery was assessed after injecting EVs containing miRNA into BALB/c mice with hindlimb ischemia, and miR-709 was identified as a promising angiogenic miRNA. miR-709-encapsulating EVs were found to increase the expression levels of the fibroblast growth factor 2 (FGF2) mRNA in the thigh tissues of hindlimb ischemia model BALB/c mice. miR-709 was also found to bind to the 3’UTR of glycogen synthase kinase 3 beta (GSK3B) in three places. GSK3B-knockdown human artery-derived endothelial cells were found to express high levels of FGF2, and were characterized by increased cell proliferation. These findings indicate that miR-709 induces an upregulation of FGF2 through the downregulation of GSK3B.
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Project description:Arterial occlusive diseases are major causes of morbidity and mortality. Blood flow to the affected tissue must be restored quickly if viability and function are to be preserved. Collaterals are artery-to-artery or arteriole-to-arteriole interconnections that can bypass an occlusion by providing an alternative route for blood flow to the affected tissue. The increased flow and sheer stress initiate processes that result in the remodeling (arteriogenesis) of these vessels into efficient conductance arteries. Here we report that the mixed-lineage kinase (MLK) pathway activates cJun NH2-terminal kinase (JNK) in endothelial cells. Disruption of Mlk2/3 or Jnk1/2 genes caused severe blockade of blood flow and failure to recover in the femoral artery ligation model of hindlimb ischemia because of abnormal collateral arteries. We show that the MLK-JNK pathway is essential for patterning and maturation of collateral arteries during development, but this pathway is not required for angiogenesis or arteriogenesis in adults. JNK in endothelial cells promotes Delta-like 4-induced Notch signaling and suppresses excessive sprouting angiogenesis during development. This function of the MLK-JNK pathway contributes to normal formation of native collateral arteries. The MLK-JNK pathway is therefore a key regulatory mechanism for vascular development. These data highlight the crucial importance of the collateral circulation in the response to arterial occlusive diseases. RNA-seq analysis of mouse lung endothelial cells (MLEC) of the following genotypes Cdh5-Cre+ Jnk1+/+ Jnk2+/+ Jnk3-/-(ECtrl), Cdh5-Cre- Jnk1LoxP/LoxP Jnk2LoxP/LoxP Jnk3-/- (EfCtrl), and Cdh5-Cre+ Jnk1LoxP/LoxP Jnk2LoxP/LoxP Jnk3-/- (E3KO). Three separate samples from mouse lung endothelial cells of each genotype were analyzed.
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Project description:MicroRNAs are small non-coding RNA species, some of which are playing important roles in malignancies. However, roles of miR-210 in cancer have yet to be unknown and controversial. Here, we found the expression level of miR-210 is downregulated in human esophageal squamous cell carcinoma and its cell lines. Additionally, we demonstrate that miR-210 inhibits cancer cell survival and proliferation through upregulation of cell death and induction of cell cycle arrest at G1/G0 and G2/M phases. However, candidate target mRNAs of miR-210 and the mechanism behind observed phenomena is uncertain. Then, we performed comprehensive gene expression analysis to identify candidate target mRNAs and understand their mechanisms.
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Project description:Peripheral Artery Disease (PAD) is a disease characterized by atherosclerosis of the arteries supplying the lower extremities. In PAD, atherosclerotic occlusions restrict the delivery of blood to the skeletal muscles of affected extremities. As a result, the muscles which are supplied by the affected arteries can experience ischemia/reperfusion (I/R) injuries. This can lead to an altered metabolomics profile, increased oxidative damage to those muscles, and the degeneration of myofibers. In our study, we modeled I/R injuries by culturing differentiated skeletal muscle derived cells (skMDCs), also known as myotubes, under cyclic conditions of hypoxia and hyperoxia. These conditions mimic those that PAD patient muscles experience. Our results show an altered transcriptomic profile in PAD patient derived myotubes and explore the contribution of I/R injuries to those transcriptomic changes.
2022-03-04 | GSE197727 | GEO
Project description:MicroRNAs are small non-coding RNA species, some of which are playing important roles in malignancies. However, roles of miR-210 in cancer have yet to be unknown and controversial. Here, we found the expression level of miR-210 is downregulated in human esophageal squamous cell carcinoma and its cell lines. Additionally, we demonstrate that miR-210 inhibits cancer cell survival and proliferation through upregulation of cell death and induction of cell cycle arrest at G1/G0 and G2/M phases. However, candidate target mRNAs of miR-210 and the mechanism behind observed phenomena is uncertain. Then, we performed comprehensive gene expression analysis to identify candidate target mRNAs and understand their mechanisms. KYSE-170 cells were transfected with oligoribonucleotides for miR-210 or ncRNA (Ambion, Austin, TX) using Hiperfect (Qiagen, Valencia, CA) according to the provider’s protocol for overexpression. Total RNA was extracted by the acid guanidinium thiocyanate-phenol-chloroform method and was labeled and prepared for hybridization to human Oligo chip 25k (Toray, Kamakura, Japan) using standard methods.
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