MIR217

Last update 08 May 2025

Basic Info

Synonyms

hsa-mir-217, microRNA 217, miR-217

+ [2]

Introduction-

100 Clinical Results associated with MIR217

100 Translational Medicine associated with MIR217

0 Patents (Medical) associated with MIR217

440

Literatures (Medical) associated with MIR217

01 Apr 2025·Marine Biotechnology

Exploring the Fanconi Anemia Gene Expression and Regulation by MicroRNAs in Gilthead Seabream (Sparus aurata) at Different Gonadal Development Stages

Article

Author: Papadaki, Maria ; Le, Ngoc-Son ; Mylonas, Constantinos C ; Sarropoulou, Elena

AbstractFanconi anaemia (FA) is a rare autosomal recessive disease in humans that is distributed worldwide. Fanconi anemia complementation (Fanc) proteins are essential for the appropriate functioning of the FA DNA repair pathway. They are also linked to a number of other biological processes, including oxygen metabolism, cell cycle regulation, haematopoiesis and apoptosis. So far, little research has been conducted on teleosts, but evidence shows that Fanc proteins play a significant role in immune response and sex reversal. For the examination of the expression of three fanc genes (fancc, fancl, and fancd2), as well as the potential regulation of these genes by microRNAs (miRNAs) in gonadal tissues at different stages of development, the present study has selected the gilthead seabream (Sparus aurata), a significant aquaculture species that exhibits protandrous hermaphroditism. The obtained data suggested the role of fancl and fancd2 in the maturation of female gonads and the miRNAs miR-210, miR-217 and miR-10926 have been identified as putative regulators of fancd2, fancc and fancl, respectively. Overall, the data indicated the potential use of fancl and fancd2 genes as sex biomarkers in conjunction with their respective regulation by miRNAs. To the best of our knowledge, this is the first study demonstrating the importance of fanc genes, along with putative regulatory miRNAs, in the reproduction of an important marine aquaculture species.

01 Mar 2025·Journal of Molecular and Cellular Cardiology Plus

Integrated transcriptomic and regulatory RNA profiling reflects complex pathophysiology and uncovers a conserved gene signature in end stage heart failure

Article

Author: Ramarao, Manjunath ; Anand, Amit ; Udwadia, Ankita ; Nawin, Kriti ; Venkatesh, Ramya ; Dokania, Manoj ; Selvam, Sabariya ; Raghuraman, Bagirath ; Kumaran, Senthil ; Gulia, Jyoti ; Nagamalesh, U M ; Gordon, David ; Shetty, Varun ; Gunawardhana, Kushan ; Zhao, Lei ; Punnen, Julius ; Garg, Shilpa ; Bysani, Madhusudhan ; Narayan, Pradeep

BackgroundHeart failure (HF) is a complex syndrome. Despite availability of multiple treatment options, the mortality remains high and the quality of life poor. Better understanding of the underlying pathophysiological processes can lead to development of novel therapies. Multiple comparative transcriptomics studies, which revealed gene level changes in the key pathophysiological pathways in failing hearts, point towards heterogeneity from interplay of disease stage, etiologies and ethnicity. Transcriptomic characterization of HF in patients from different ethnicities can potentially help in understanding the heterogeneity imparted by various factors and the core elements in heart failure.Methods & resultsAn integrated analysis of bulk transcriptome and microRNA sequencing from the cardiac tissues of 30 South Asian (SA) patients having HF with reduced ejection fraction (HFrEF) and 19 control subjects was conducted. Plasma miRNAs from a subset of HFrEF and control patients were also sequenced to understand their biomarker potential. The altered transcriptome from the myocardium of SA HFrEF patients reflected cardiac muscle contraction, cellular energetics, altered immune signaling and extracellular matrix remodelling as predominant pathophysiological mechanisms. The SA HFrEF patients also showed dysregulation of multiple microRNAs in cardiac tissue like miR-216, miR-217, miR-184 and miR-9983. Many of these miRNAs, such as miR184 and few others, showed altered levels in both the plasma and cardiac tissue of HFrEF patients suggesting their biomarker potential. The diversity in the HFrEF transcriptomes from published studies led us to examine the core HF genes in our cohort. A gene signature generated using machine learning (ML) from the top dysregulated genes in SA HFrEF cohort stratified HF from controls in other cohorts. The sensitivity of the HF gene signature was further improved when union of two cohorts was used as a training set. Our ML analyses developed a core HF gene signature consisting of 21 genes that can stratify HF patients from controls with 98 % sensitivity in all the tested cohorts.ConclusionsThis study reveals molecular changes underlying the pathophysiology as reflected by coding and regulatory non-coding components of transcriptome from South Asian patients and uncovers a conserved gene signature for HF.

01 Mar 2025·Journal of Biological Chemistry

Staufen2 dysregulation in neurodegenerative disease

Article

Author: Paul, Sharan ; Dansithong, Warunee ; Hivare, Pravin ; Scoles, Daniel R ; Figueroa, Karla P ; Pulst, Stefan M ; Gandelman, Mandi

Staufen2 (STAU2) is an RNA-binding protein that controls mRNA trafficking and expression. Previously, we showed that its paralog, Staufen1 (STAU1), was overabundant in cellular and mouse models of neurodegenerative diseases and amyotrophic lateral sclerosis (ALS) patient spinal cord. Here, we investigated features of STAU2 that might parallel STAU1. STAU2 protein, but not mRNA, was overabundant in spinocerebellar ataxia type 2 (SCA2), ALS/frontotemporal dementia patient fibroblasts, ALS patient spinal cord tissues, and in central nervous system tissues from SCA2 and ALS animal models. Exogenous expression of STAU2 in human embryonic kidney 293 cells activated mechanistic target of rapamycin (mTOR) and stress granule formation. Targeting STAU2 by RNAi normalized mTOR in SCA2 and C9ORF72 cellular models. The microRNA miR-217, previously identified as downregulated in SCA2 mice, targets the STAU2 3'-UTR. We now demonstrate that exogenous expression of miR-217 significantly reduced STAU2 and mTOR levels in cellular models of neurodegenerative disease. These results suggest a functional link between STAU2 and mTOR signaling and identify a major role for miR-217 that could be exploited in therapeutic development.

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MIR217

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