更新于：2024-11-01

MIR133

更新于：2024-11-01

基本信息

别名

miR-133 family

简介-

关联

100 项与 MIR133 相关的临床结果

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100 项与 MIR133 相关的转化医学

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0 项与 MIR133 相关的专利（医药）

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832

项与 MIR133 相关的文献（医药）

2024-12-31·Annals of Medicine

Combined miRNA transcriptome and proteome analysis of extracellular vesicles in urine and blood from the Pompe mouse model

Article

作者: Melber, Andrew ; Moore, Simon W. ; Li, Bin ; Palmieri, Kathleen ; Su, Zhenqiang ; Moreland, Rodney ; Merberg, David ; Makhija, Mahindra ; Carey, Galen ; Crooker, Bob ; Boyanapalli, Ruby

INTRODUCTIONAcid α-glucosidase (GAA) is a lysosomal enzyme that hydrolyzes glycogen to glucose. Deficiency of GAA causes Pompe disease (PD), also known as glycogen storage disease type II. The resulting glycogen accumulation causes a spectrum of disease severity ranging from infantile-onset PD to adult-onset PD. Additional non-invasive biomarkers of disease severity are needed to monitor response to therapeutic interventions.METHODSWe measured protein and miRNA abundance in exosomes from serum and urine from the PD mouse model (B6;129-GaaTm1Rabn/J), wild-type mice, and PD mice treated with a candidate gene therapy.RESULTSThere were significant differences in the abundance of 113 miRNA in serum exosomes from Pompe versus healthy mice. Levels of miR-206, miR-133, miR-1a, miR-486, and other important regulators of muscle development and maintenance were altered in the Pompe samples. The serum and urine exosome proteomes of healthy and Pompe mice also differed broadly. Several of the dysregulated proteins are encoded by genes with potential target sites for affected miRNA.CONCLUSIONExosomes derived from urine or serum are a potential source of biomarkers for Pompe Disease. Further study of the differences in the miRNA transcriptome and proteome content of exosomes may yield new insights into disease mechanisms.

2024-12-01·Cytotechnology

MiR-133 promotes the multidrug resistance of acute myeloid leukemia cells (HL-60/ADR) to daunorubicin

Article

作者: Wei, Yueping ; Tao, Wei ; Yu, Jingxing ; Yu, Kun ; Liu, Lin

This study aimed to explore the role and molecular mechanism of miR-133 in multidrug resistance in acute myeloid leukemia (AML) and provide a new theoretical basis for the treatment and prognosis of AML patients. We performed experiments at the cellular level. RT‒qPCR and Western blotting were used to detect gene and protein expression; cell viability was measured with CCK-8 assays; apoptosis was detected via flow cytometry; and a dual-luciferase reporter gene assay was used to verify the binding between miR-133 and CXCL12. In this study, we found that miR-133 was upregulated in HL-60/ADR multidrug-resistant cells. Functionally, the inhibition of miR-133 alleviated the resistance of HL-60/ADR cells to daunorubicin (DNR). After inhibiting miR-133 in HL-60/ADR cells treated with DNR, the expression of the intracellular drug resistance-related proteins MRP562 and P-gp was inhibited, cell proliferation decreased, and apoptosis increased. Mechanistically, the NF-κB signaling pathway regulates the expression of miR-133 in HL-60/ADR cells, and the targeting of CXCL12 by miR-133 enhances the resistance of HL-60/ADR cells to DNR. In conclusion, the NF-κB signaling pathway regulates the expression of miR-133, and inhibiting miR-133 expression can target CXCL12 to increase the sensitivity of HL-60/ADR cells to DNR.

2024-10-01·Annals of Clinical and Translational Neurology

miR‐133b as a potential regulator of a synaptic NPTX2 protein in Alzheimer's disease

Article

作者: Bennett, David A. ; Saykin, Andrew J. ; Nho, Kwangsik ; Park, Young Ho ; Han, Sang‐Won ; Kim, SangYun ; Bice, Paula J

AbstractA synaptic protein, Neuronal Pentraxin 2 (NPTX2), has emerged as a pivotal biomarker for Alzheimer's dementia (AD). We identified candidate miRNAs targeting NPTX2 and performed association and mediation analyses using multi‐omics data (N = 702). Among 44 candidate miRNAs, miR‐133b was significantly associated with AD and Braak positivity. Higher miR‐133b expression was also associated with higher NPTX2 gene expression and better cognition. Mediation analysis showed that miR‐133b partially influences AD and cognition through the NPTX2 protein. Our integrated approach suggests a potential role of miR‐133b in synaptic integrity and offers new insights into AD pathogenesis.