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Special Issue "Non-coding RNAs: Promising Targets in Regenerative Medicine and Cell Therapies"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editors

Dr. Stephana Carelli
E-Mail Website
Guest Editor
1. Department of Biomedical and Clinical Sciences "L. Sacco", University of Milan, Milan, Italy
2. Pediatric Research Center "Romeo ed Enrica Invernizzi", University of Milan, Milan, Italy
Interests: cell therapies for neurodegenerative disease (Spinal cord injury, Parkinson’s disease); molecular mechanisms of neuronal degeneration and regeneration (epigenetic and non-coding RNA); organoids; 3D culture systems; mechanotransduction and pluripotency; neural stem cells; mesenchymal stem cells; lncRNAs in stemness and differentiation
Special Issues and Collections in MDPI journals
Dr. Federica Rey
E-Mail Website
Guest Editor
Department of Biomedical and Clinical Sciences "L. Sacco", University of Milan, Milan, Italy.Pediatric Research Center "Romeo ed Enrica Invernizzi", University of Milan, Milan, Italy
Interests: lncRNAs; stem cells biology; neurodegenerative diseases; molecular mechanisms of neuronal degeneration and regeneration (epigenetics and non-coding RNA); transcriptional profiling of diseases conditions

Special Issue Information

Dear Colleagues,

Long non-coding RNAs (lncRNAs) are RNA molecules longer than 200 bp, with multiple functions in both physiological and diseases-related processes. These molecules present gene expression regulatory abilities, although their role is not limited to this function. Several well-studied examples of lncRNAs suggest that they can operate through distinct modes, including working as signals, scaffolds for protein–protein interactions, molecular decoys, and guides to target elements in the genome or transcriptome. Extensive research is now focused on the full characterization of lncRNAs in multiple biological processes, as they require interdisciplinary studies due to their numerous possible functions. More and more evidence is highlighting fundamental roles for lncRNAs in stem cells renewal and differentiation, along with their potential disruption when these processes are impaired. LncRNAs could thus become new key targets in regenerative medicine and cell therapies, and their study in stem cells is thus fundamental. Moreover, lncRNAs are being investigated and evaluated for clinical use as possible innovative pharmacological treatments. In this Special Issue, we expect to collect both original research and review articles aimed at assessing key advancements in lncRNA’s role as potential therapeutic targets.

Dr. Stephana Carelli
Dr. Federica Rey
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Long non-coding RNAs
  • Stem cells
  • Neurodegenerative diseases
  • Regeneration
  • Cellular transcriptome
  • Regenerative medicine
  • Cell differentiation
  • Pluripotency
  • Drug development

Published Papers (1 paper)

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Research

Article
Irradiation Activates MZF1 to Inhibit miR-541-5p Expression and Promote Epithelial-Mesenchymal Transition (EMT) in Radiation-Induced Pulmonary Fibrosis (RIPF) by Upregulating Slug
by , , , , , , , , , , , and
Int. J. Mol. Sci. 2021, 22(21), 11309; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111309 - 20 Oct 2021
Abstract
Understanding miRNAs regulatory roles in epithelial-mesenchymal transition (EMT) would help establish new avenues for further uncovering the mechanisms underlying radiation-induced pulmonary fibrosis (RIPF) and identifying preventative and therapeutic targets. Here, we demonstrated that miR-541-5p repression by Myeloid Zinc Finger 1 (MZF1) [...] Read more.
Understanding miRNAs regulatory roles in epithelial-mesenchymal transition (EMT) would help establish new avenues for further uncovering the mechanisms underlying radiation-induced pulmonary fibrosis (RIPF) and identifying preventative and therapeutic targets. Here, we demonstrated that miR-541-5p repression by Myeloid Zinc Finger 1 (MZF1) promotes radiation-induced EMT and RIPF. Irradiation could decrease miR-541-5p expression in vitro and in vivo and inversely correlated to RIPF development. Ectopic miR-541-5p expression suppressed radiation-induced-EMT in vitro and in vivo. Knockdown of Slug, the functional target of miR-541-5p, inhibited EMT induction by irradiation. The upregulation of transcription factor MZF1 upon irradiation inhibited the expression of endogenous miR-541-5p and its primary precursor (pri-miR-541-5p), which regulated the effect of the Slug on the EMT process. Our finding showed that ectopic miR-541-5p expression mitigated RIPF in mice by targeting Slug. Thus, irradiation activates MZF1 to downregulate miR-541-5p in alveolar epithelial cells, promoting EMT and contributing to RIPF by targeting Slug. Our observation provides further understanding of the development of RIPF and determines potential preventative and therapeutic targets. Full article
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