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Cellular and Molecular Mechanisms of Fibrosis: From Wound Healing Studies...
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Cellular and Molecular Mechanisms of Fibrosis: From Wound Healing Studies to Clinical Management of Fibrotic Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Motility and Adhesion".

Deadline for manuscript submissions: closed (15 August 2022) | Viewed by 8291

Special Issue Editor

Prof. Dr. Jingwu Xie

E-Mail Website
Guest Editor
Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA
Interests: hedgehog pathway; cancer drug resistance; cancer stem cells; fibrosis; cholesterol metabolism; metastasis

Special Issue Information

Dear Colleagues,

Fibrosis is often regarded as a pathological wound healing process, developed in response to chronic injury in nearly all organs. However, how chronic damage in epithelial cells triggers a cascade of events leading to fibrosis remains unclear. Fibrosis contributes to nearly half of human mortality. Currently, there are no effective treatments for fibrosis. Thus, strategies to slow down fibrosis represent an urgent medical need. In contrast to fibrosis, wound healing is better understood at the molecular and cellular levels, including the origin of myofibroblasts and the functions of cytokines, chemokines, and immune cells that participate in this process. How can we utilize this knowledge in fibrosis research? 

For this Special Issue, we invite scientists to contribute original research articles, reviews, or shorter “Perspective” articles on all aspects related to the “Cellular and Molecular Mechanisms of Fibrosis: From Wound Healing Studies to Clinical Management of Fibrotic Diseases”. We hope to highlight current trends and novel models with functional insights from a cellular and molecular perspective.

Prof. Dr. Jingwu Xie
Guest Editor

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 submissions that pass pre-check are 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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • wound healing
  • fibrosis
  • mesenchymal stem cells
  • inflammation
  • cytokines
  • chemokines
  • growth factors

Published Papers (3 papers)

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Research

17 pages, 2494 KiB  
Article
Dysregulated Cell–Cell Communication Characterizes Pulmonary Fibrosis
by Jonathan S. Kurche, Ian T. Stancil, Jacob E. Michalski, Ivana V. Yang and David A. Schwartz
Cells 2022, 11(20), 3319; https://doi.org/10.3390/cells11203319 - 21 Oct 2022
Cited by 4 | Viewed by 2819
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive disease of older adults characterized by fibrotic replacement of functional gas exchange units in the lung. The strongest risk factor for IPF is a genetic variantin the promoter region of the gel-forming mucin, MUC5B. To [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a progressive disease of older adults characterized by fibrotic replacement of functional gas exchange units in the lung. The strongest risk factor for IPF is a genetic variantin the promoter region of the gel-forming mucin, MUC5B. To better understand how the MUC5B variant influences development of fibrosis, we used the NicheNet R package and leveraged publicly available single-cell RNA sequencing data to identify and evaluate how epithelia participating in gas exchange are influenced by ligands expressed in control, MUC5B variant, and fibrotic environments. We observed that loss of type-I alveolar epithelia (AECI) characterizes the single-cell RNA transcriptome in fibrotic lung and validated the pattern of AECI loss using single nuclear RNA sequencing. Examining AECI transcriptomes, we found enrichment of transcriptional signatures for IL6 and AREG, which we have previously shown to mediate aberrant epithelial fluidization in IPF and murine bleomycin models. Moreover, we found that the protease ADAM17, which is upstream of IL6 trans-signaling, was enriched in control MUC5B variant donors. We used immunofluorescence to validate a role for enhanced expression of ADAM17 among MUC5B variants, suggesting involvement in IPF pathogenesis and maintenance. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Fibrosis: From Wound Healing Studies to Clinical Management of Fibrotic Diseases)
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22 pages, 63610 KiB  
Article
Long Non-Coding RNA H19 Prevents Lens Fibrosis through Maintaining Lens Epithelial Cell Phenotypes
by Lang Xiong, Yan Sun, Jingqi Huang, Pengjuan Ma, Xiaoran Wang, Jiani Wang, Baoxin Chen, Jieping Chen, Mi Huang, Shan Huang and Yizhi Liu
Cells 2022, 11(16), 2559; https://doi.org/10.3390/cells11162559 - 17 Aug 2022
Cited by 4 | Viewed by 1762
Abstract
The integrity of lens epithelial cells (LECs) lays the foundation for lens function and transparency. By contrast, epithelial-mesenchymal transition (EMT) of LECs leads to lens fibrosis, such as anterior subcapsular cataracts (ASC) and fibrotic forms of posterior capsule opacification (PCO). However, the underlying [...] Read more.
The integrity of lens epithelial cells (LECs) lays the foundation for lens function and transparency. By contrast, epithelial-mesenchymal transition (EMT) of LECs leads to lens fibrosis, such as anterior subcapsular cataracts (ASC) and fibrotic forms of posterior capsule opacification (PCO). However, the underlying mechanisms remain unclear. Here, we aimed to explore the role of long non-coding RNA (lncRNA) H19 in regulating TGF-β2-induced EMT during lens fibrosis, revealing a novel lncRNA-based regulatory mechanism. In this work, we identified that lncRNA H19 was highly expressed in LECs, but downregulated by exposure to TGF-β2. In both human lens epithelial explants and SRA01/04 cells, knockdown of H19 aggravated TGF-β2-induced EMT, while overexpressing H19 partially reversed EMT and restored lens epithelial phenotypes. Semi-in vivo whole lens culture and H19 knockout mice demonstrated the indispensable role of H19 in sustaining lens clarity through maintaining LEC features. Bioinformatic analyses further implied a potential H19-centered regulatory mechanism via Smad-dependent pathways, confirmed by in vitro experiments. In conclusion, we uncovered a novel role of H19 in inhibiting TGF-β2-induced EMT of the lens by suppressing Smad-dependent signaling, providing potential therapeutic targets for treating lens fibrosis. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Fibrosis: From Wound Healing Studies to Clinical Management of Fibrotic Diseases)
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18 pages, 2603 KiB  
Article
Pathologic Proteolytic Processing of N-Cadherin as a Marker of Human Fibrotic Disease
by Paul Durham Ferrell, Kristianne Michelle Oristian, Everett Cockrell and Salvatore Vincent Pizzo
Cells 2022, 11(1), 156; https://doi.org/10.3390/cells11010156 - 04 Jan 2022
Cited by 7 | Viewed by 2880
Abstract
Prior research has implicated the involvement of cell adhesion molecule N-cadherin in tissue fibrosis and remodeling. We hypothesize that anomalies in N-cadherin protein processing are involved in pathological fibrosis. Diseased tissues associated with fibrosis of the heart, lung, and liver were probed for [...] Read more.
Prior research has implicated the involvement of cell adhesion molecule N-cadherin in tissue fibrosis and remodeling. We hypothesize that anomalies in N-cadherin protein processing are involved in pathological fibrosis. Diseased tissues associated with fibrosis of the heart, lung, and liver were probed for the precursor form of N-cadherin, pro-N-cadherin (PNC), by immunohistochemistry and compared to healthy tissues. Myofibroblast cell lines were analyzed for cell surface pro-N-cadherin by flow cytometry and immunofluorescent microscopy. Soluble PNC products were immunoprecipitated from patient plasmas and an enzyme-linked immunoassay was developed for quantification. All fibrotic tissues examined show aberrant PNC localization. Cell surface PNC is expressed in myofibroblast cell lines isolated from cardiomyopathy and idiopathic pulmonary fibrosis but not on myofibroblasts isolated from healthy tissues. PNC is elevated in the plasma of patients with cardiomyopathy (p ≤ 0.0001), idiopathic pulmonary fibrosis (p ≤ 0.05), and nonalcoholic fatty liver disease with cirrhosis (p ≤ 0.05). Finally, we have humanized a murine antibody and demonstrate that it significantly inhibits migration of PNC expressing myofibroblasts. Collectively, the aberrant localization of PNC is observed in all fibrotic tissues examined in our study and our data suggest a role for cell surface PNC in the pathogenesis of fibrosis. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Fibrosis: From Wound Healing Studies to Clinical Management of Fibrotic Diseases)
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