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Life
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UPR Regulated Noncoding RNAs in Diseases
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UPR Regulated Noncoding RNAs in Diseases

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Biochemistry, Biophysics and Computational Biology".

Deadline for manuscript submissions: closed (15 November 2020) | Viewed by 13681

Special Issue Editor

Dr. Sanjeev Gupta

E-Mail Website
Guest Editor
School of Medicine, National University of Ireland Galway, University Road, Galway H91 TK33, Ireland
Interests: endoplasmic reticulum stress; unfolded protein response; tumour microenvironment; XBP1; endocrine resistance; microRNAs

Special Issue Information

Dear Colleagues,

Several pathophysiological stresses cause accumulation of misfolded proteins in the endoplasmic reticulum (ER) and induce an evolutionarily conserved pathway termed the unfolded protein response (UPR). The ER senses both extracellular and intracellular stimuli that can compromise its ability to handle the maturation of ER-resident and secretory proteins. UPR activation contributes to cell adaptation by reducing the production of client protein load while increasing the synthesis of chaperones. UPR aims to restore protein homeostasis in the ER but can trigger cell death if ER homeostasis cannot be restored and the damage is prolonged. Several studies have revealed the role of ER stress and UPR in regulation of tissue physiology and human diseases.

Although we have gained considerable insight into the mechanisms that regulate gene expression and certain aspects of protein translation, the contribution of noncoding RNAs to UPR-dependent activities has only recently been investigated. This Special Issue provides diverse aspects of UPR-regulated noncoding RNAs in various physiological and pathological contexts. We invite authors to submit original research and review articles related to the role of noncoding RNAs in ER stress and UPR signalling.

Dr. Sanjeev Gupta
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • microRNAs
  • long non-coding RNAs
  • Piwi-interacting RNAs (piRNAs)
  • Circular RNAs
  • Cancer
  • Unfolded protein response
  • biomarkers
  • ER stress
  • Tumour microenvironment

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Published Papers (2 papers)

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Research

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15 pages, 3009 KiB  
Article
Downregulation of miR-17-92 Cluster by PERK Fine-Tunes Unfolded Protein Response Mediated Apoptosis
by Danielle E. Read, Ananya Gupta, Karen Cawley, Laura Fontana, Patrizia Agostinis, Afshin Samali and Sanjeev Gupta
Life 2021, 11(1), 30; https://doi.org/10.3390/life11010030 - 6 Jan 2021
Cited by 5 | Viewed by 2922
Abstract
An important event in the unfolded protein response (UPR) is activation of the endoplasmic reticulum (ER) kinase PERK. The PERK signalling branch initially mediates a prosurvival response, which progresses to a proapoptotic response upon prolonged ER stress. However, the molecular mechanisms of PERK-mediated [...] Read more.
An important event in the unfolded protein response (UPR) is activation of the endoplasmic reticulum (ER) kinase PERK. The PERK signalling branch initially mediates a prosurvival response, which progresses to a proapoptotic response upon prolonged ER stress. However, the molecular mechanisms of PERK-mediated cell death are not well understood. Here we show that expression of the primary miR-17-92 transcript and mature miRNAs belonging to the miR-17-92 cluster are decreased during UPR. We found that miR-17-92 promoter reporter activity was reduced during UPR in a PERK-dependent manner. Furthermore, we show that activity of the miR-17-92 promoter is repressed by ectopic expression of ATF4 and NRF2. Promoter deletion analysis mapped the region responding to UPR-mediated repression to a site in the proximal region of the miR-17-92 promoter. Hypericin-mediated photo-oxidative ER damage reduced the expression of miRNAs belonging to the miR-17-92 cluster in wild-type but not in PERK-deficient cells. Importantly, ER stress-induced apoptosis was inhibited upon miR-17-92 overexpression in SH-SY5Y and H9c2 cells. Our results reveal a novel function for ATF4 and NRF2, where repression of the miR-17-92 cluster plays an important role in ER stress-mediated apoptosis. Mechanistic details are provided for the potentiation of cell death via sustained PERK signalling mediated repression of the miR-17-92 cluster. Full article
(This article belongs to the Special Issue UPR Regulated Noncoding RNAs in Diseases)
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Review

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27 pages, 1792 KiB  
Review
The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis
by Mahmoud Aghaei, Sanaz Dastghaib, Sajjad Aftabi, Mohamad-Reza Aghanoori, Javad Alizadeh, Pooneh Mokarram, Parvaneh Mehrbod, Milad Ashrafizadeh, Ali Zarrabi, Kielan Darcy McAlinden, Mathew Suji Eapen, Sukhwinder Singh Sohal, Pawan Sharma, Amir A. Zeki and Saeid Ghavami
Life 2021, 11(1), 1; https://doi.org/10.3390/life11010001 - 22 Dec 2020
Cited by 30 | Viewed by 10171
Abstract
Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the [...] Read more.
Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the increased functional demands. Cells are able to induce a highly conserved adaptive mechanism, known as the unfolded protein response (UPR), to manage such stresses. UPR dysregulation and ER stress are involved in numerous human illnesses, such as metabolic syndrome, fibrotic diseases, and neurodegeneration, and cancer. Therefore, effective and specific compounds targeting the UPR pathway are being considered as potential therapies. This review focuses on the impact of both external and internal stressors on the ER in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) and discusses the role of the UPR signaling pathway activation in the control of cellular damage and specifically highlights the potential involvement of non-coding RNAs in COPD. Summaries of pathogenic mechanisms associated with the ER stress/UPR axis contributing to IPF and COPD, and promising pharmacological intervention strategies, are also presented. Full article
(This article belongs to the Special Issue UPR Regulated Noncoding RNAs in Diseases)
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