Last update 01 Nov 2024

MIR29B2

Last update 01 Nov 2024

Basic Info

Synonyms

hsa-mir-29b-2, microRNA 29b-2, MIR29B2

+ [1]

Introduction-

Drugs associated with MIR29B2

AAV-miR-29b

Target

MIR29B1 x MIR29B2

Mechanism

MIR29B1 inhibitors [+1]

Active Org.

Jichi Medical University

Originator Org.

Jichi Medical University

Active Indication

Stomach Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MIR29B2

100 Translational Medicine associated with MIR29B2

0 Patents (Medical) associated with MIR29B2

Literatures (Medical) associated with MIR29B2

01 Oct 2024·Brain Research

The potential of five c-miRNAs as serum biomarkers for Late-Onset Alzheimer’s disease diagnosis: miR-10a-5p, miR-29b-2-5p, miR-125a-5p, miR-342-3p, and miR-708-5p

Article

Author: Tureck, Luciane Viater ; Furtado-Alle, Lupe ; Coutinho de Almeida, Rodrigo ; Lehtonen Rodrigues Souza, Ricardo ; Monteiro de Almeida, Sergio ; de Lourdes Signorini-Souza, Isadora ; Batistela, Meire Silva

The nervous system is rich in miRNAs, indicating an important role of these molecules in regulating processes associated with cognition, memory, and others. Therefore, qualitative and quantitative imbalances involving such miRNAs may be involved in dementia contexts, including Late-Onset Alzheimer's Disease (LOAD). To test the viability of circulating miRNAs (c-miRNAs) as biomarkers for LOAD, we proceed accordingly to the following reasoning. The first stage was to discover and identify profile of c-miRNAs by RNA sequencing (RNA-Seq). For this purpose, blood serum samples were used from LOAD patients (n = 5) and cognitively healthy elderly control group (CTRL_CH) (n = 5), all over 70 years old. We identified seven c-miRNAs differentially expressed (p ≤ 0.05) in the serum of LOAD patients compared to CTRL_CH (miR-10a-5p; miR-29b-2-5p; miR-125a-5p; miR-342-3p, miR-708-5p, miR-380-5p and miR-340-3p). Of these, five (p ≤ 0.01) were selected for in silico analysis (miR-10a-5p; miR-29b-2-5p; miR-125a-5p; miR-342-3p, miR-708-5p), for which 44 relevant target genes were found regulated by these c-miRNAs and related to LOAD. Through the analysis of these target genes in databases, it was possible to observe that they have functions related to the development and progress of LOAD, directly or indirectly connecting the different Alzheimer's pathways. Thus, this work found five promising serum c-miRNAs as options for biomarkers contributing to LOAD diagnosis. Our study shows the complex network between these molecules and LOAD, supporting the relevance of studies using c-miRNAs in dementia contexts.

19 Jun 2023·Cells

Silencing of circCacna1c Inhibits ISO-Induced Cardiac Hypertrophy through miR-29b-2-5p/NFATc1 Axis.

Article

Author: Lu, Peilei ; Ma, Jialu ; Zhao, Meimi ; Ding, Fan ; Zhang, Danyu ; Xiang, Yang K

Pathological cardiac hypertrophy is one of the notable causes of heart failure. Circular RNAs (circRNAs) have been studied in association with cardiac hypertrophy; however, the mechanisms by which circRNAs regulate cardiac hypertrophy remain unclear. In this study, we identified a new circRNA, named circCacna1c, in cardiac hypertrophy. Adult male C57BL/6 mice and H9c2 cells were treated with isoprenaline hydrochloride (ISO) to establish a hypertrophy model. We found that circCacna1c was upregulated in ISO-induced hypertrophic heart tissue and H9c2 cells. Western blot and quantitative real-time polymerase chain reaction showed that silencing circCacna1c inhibited hypertrophic gene expression in ISO-induced H9c2 cells. Mechanistically, circCacna1c competitively bound to miR-29b-2-5p in a dual-luciferase reporter assay, which was downregulated in ISO-induced hypertrophic heart tissue and H9c2 cells. MiR-29b-2-5p inhibited the nuclear factor of activated T cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) to control hypertrophic gene expression. After silencing circCacna1c, the expression of miR-29b-2-5p increased, which reduced hypertrophic gene expression by inhibiting NFATc1 expression. Together, these experiments indicate that circCacna1c promotes ISO-induced pathological hypertrophy through the miR-29b-2-5p/NFATc1 axis.

01 Feb 2022·BioengineeredQ4 · BIOLOGY

Identification of circular RNAs and functional competing endogenous RNA networks in human proximal tubular epithelial cells treated with sodium-glucose cotransporter 2 inhibitor dapagliflozin in diabetic kidney disease

Q4 · BIOLOGY

ArticleOA

Author: Zhao, Lin ; Liu, Yifan ; Qin, Guijun ; Fan, Xunjie ; Guo, Feng ; Huang, Fengjuan ; Song, Yi

Diabetic kidney disease (DKD) is a serious diabetes complication. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are novel anti-diabetes drugs that confer clinical renal protection. However, the molecular mechanisms involved remain unclear. Here, human proximal tubular epithelial cells (PTECs) were treated with normal glucose, high glucose, and anti-diabetes agents, including SGLT2i (dapagliflozin), metformin, and dipeptidyl peptidase-4 inhibitor (DPP-4i, vildagliptin) and microarray analysis was performed. Firstly, a total of 2,710 differentially expressed circular RNAs (circRNAs) were identified. Secondly, network pharmacology and transcriptomics analyses showed that the effects of dapagliflozin on PTECs primarily involved lipid metabolism, Rap1, and MAPK signaling pathways. Metformin mainly affected the AMPK and FOXO signaling pathways, whereas vildagliptin affected insulin secretion and the HIF-1 signaling pathway. Furthermore, circRNA-miRNA-mRNA networks, real-time reverse transcription-polymerase chain reaction (RT-PCR), and fluorescence in situ hybridization (FISH) assay revealed that the expression of hsa_circRNA_012448 was increased in PTECs treated with high glucose, whereas its expression was reversed by dapagliflozin. Finally, the hsa_circRNA_012448-hsa-miR-29b-2-5p-GSK3β pathway, involved in the oxidative stress response, was identified as an important pathway mediating the action of dapagliflozin against DKD. Overall, our study provides novel insights into the molecular mechanisms underlying the effects of dapagliflozin on DKD.

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MIR29B2

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