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Proteolysis of Extracellular Matrix in Human Disease 2.0
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Proteolysis of Extracellular Matrix in Human Disease 2.0

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

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 19085

Special Issue Editor

Dr. Hironobu Yamashita

E-Mail Website
Guest Editor
Department of Pathology and Laboratory Medicine, The Pennsylvania State University, Hershey, PA 17033, USA
Interests: transcription factor; extracellular matrix; tumor plasticity; tumor heterogeneity; matrix proteases; urological cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue "Proteolysis of Extracellular Matrix in Human Disease".

The extracellular matrix (ECM) is a three-dimensional molecular network complex including growth factors and ECM molecules such as collagens, laminins, and proteoglycans. ECM not only serves as a scaffold to support various biological structures but also implicates multiple biological processes (cell migration, invasion, proliferation, differentiation, and survival). More importantly, there is accumulating evidence that ECM is a dynamic microenvironment. In particular, ECM is processed by matrix proteases during disease initiation and progression, such as viral infection and malignancy. Thus, ECM proteolysis plays a significant role in many human diseases. In this Special Issue on “Proteolysis of Extracellular Matrix in Human Disease 2.0”, therefore, research and review manuscripts regarding the link between ECM and matrix proteases are collected. Moreover, manuscripts in terms of epigenetics and transcription factors in these topics are also welcome.

Dr. Hironobu Yamashita
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. 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

  • extracellular matrix
  • matrix proteases
  • proteolysis
  • tumor microenvironment
  • gene regulation
  • transcription factor

Related Special Issue

Published Papers (6 papers)

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Research

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18 pages, 4153 KiB  
Article
Increased Risk of Aortic Dissection with Perlecan Deficiency
by Risa Nonaka, Takafumi Iesaki, Aurelien Kerever and Eri Arikawa-Hirasawa
Int. J. Mol. Sci. 2022, 23(1), 315; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010315 - 28 Dec 2021
Cited by 5 | Viewed by 1997
Abstract
Perlecan (HSPG2), a basement membrane-type heparan sulfate proteoglycan, has been implicated in the development of aortic tissue. However, its role in the development and maintenance of the aortic wall remains unknown. Perlecan-deficient mice (Hspg2−/−-Tg: Perl KO) have been found to [...] Read more.
Perlecan (HSPG2), a basement membrane-type heparan sulfate proteoglycan, has been implicated in the development of aortic tissue. However, its role in the development and maintenance of the aortic wall remains unknown. Perlecan-deficient mice (Hspg2−/−-Tg: Perl KO) have been found to show a high frequency (15–35%) of aortic dissection (AD). Herein, an analysis of the aortic wall of Perl KO mice revealed that perlecan deficiency caused thinner and partially torn elastic lamina. Compared to the control aortic tissue, perlecan-deficient aortic tissue showed a significant decrease in desmosine content and an increase in soluble tropoelastin levels, implying the presence of immature elastic fibers in Perl KO mice. Furthermore, the reduced expression of the smooth muscle cell contractile proteins actin and myosin in perlecan-deficient aortic tissue may explain the risk of AD. This study showed that a deficiency in perlecan, which is localized along the elastic lamina and at the interface between elastin and fibrillin-1, increased the risk of AD, largely due to the immaturity of extracellular matrix in the aortic tissue. Overall, we proposed a new model of AD that considers the deficiency of extracellular molecule perlecan as a risk factor. Full article
(This article belongs to the Special Issue Proteolysis of Extracellular Matrix in Human Disease 2.0)
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17 pages, 2287 KiB  
Article
MT1-MMP Cooperates with TGF-β Receptor-Mediated Signaling to Trigger SNAIL and Induce Epithelial-to-Mesenchymal-like Transition in U87 Glioblastoma Cells
by Souad Djediai, Narjara Gonzalez Suarez, Layal El Cheikh-Hussein, Sahily Rodriguez Torres, Loraine Gresseau, Sheraz Dhayne, Zoé Joly-Lopez and Borhane Annabi
Int. J. Mol. Sci. 2021, 22(23), 13006; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222313006 - 30 Nov 2021
Cited by 16 | Viewed by 3133
Abstract
Epithelial-to-mesenchymal transition (EMT) recapitulates metastasis and can be induced in vitro through transforming growth factor (TGF)-β signaling. A role for MMP activity in glioblastoma multiforme has been ascribed to EMT, but the molecular crosstalk between TGF-β signaling and membrane type 1 MMP (MT1-MMP) [...] Read more.
Epithelial-to-mesenchymal transition (EMT) recapitulates metastasis and can be induced in vitro through transforming growth factor (TGF)-β signaling. A role for MMP activity in glioblastoma multiforme has been ascribed to EMT, but the molecular crosstalk between TGF-β signaling and membrane type 1 MMP (MT1-MMP) remains poorly understood. Here, the expression of common EMT biomarkers, induced through TGF-β and the MT1-MMP inducer concanavalin A (ConA), was explored using RNA-seq analysis and differential gene arrays in human U87 glioblastoma cells. TGF-β triggered SNAIL and fibronectin expressions in 2D-adherent and 3D-spheroid U87 glioblastoma cell models. Those inductions were antagonized by the TGF-β receptor kinase inhibitor galunisertib, the JAK/STAT inhibitors AG490 and tofacitinib, and by the diet-derived epigallocatechin gallate (EGCG). Transient gene silencing of MT1-MMP prevented the induction of SNAIL by ConA and abrogated TGF-β-induced cell chemotaxis. Moreover, ConA induced STAT3 and Src phosphorylation, suggesting these pathways to be involved in the MT1-MMP-mediated signaling axis that led to SNAIL induction. Our findings highlight a new signaling axis linking MT1-MMP to TGF-β-mediated EMT-like induction in glioblastoma cells, the process of which can be prevented by the diet-derived EGCG. Full article
(This article belongs to the Special Issue Proteolysis of Extracellular Matrix in Human Disease 2.0)
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Review

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15 pages, 10953 KiB  
Review
The Proteolysis of ECM in Intervertebral Disc Degeneration
by Huaizhen Liang, Rongjin Luo, Gaocai Li, Weifeng Zhang, Yu Song and Cao Yang
Int. J. Mol. Sci. 2022, 23(3), 1715; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031715 - 02 Feb 2022
Cited by 50 | Viewed by 3179
Abstract
Intervertebral disc (IVD) degeneration (IDD) is a pathological process that commonly occurs throughout the human life span and is a major cause of lower back pain. Better elucidation of the molecular mechanisms involved in disc degeneration could provide a theoretical basis for the [...] Read more.
Intervertebral disc (IVD) degeneration (IDD) is a pathological process that commonly occurs throughout the human life span and is a major cause of lower back pain. Better elucidation of the molecular mechanisms involved in disc degeneration could provide a theoretical basis for the development of lumbar disc intervention strategies. In recent years, extracellular matrix (ECM) homeostasis has received much attention due to its relevance to the mechanical properties of IVDs. ECM proteolysis mediated by a variety of proteases is involved in the pathological process of disc degeneration. Here, we discuss in detail the relationship between the IVD as well as the ECM and the role of ECM proteolysis in the degenerative process of the IVD. Targeting ECM proteolysis-associated proteases may be an effective means of intervention in IDD. Full article
(This article belongs to the Special Issue Proteolysis of Extracellular Matrix in Human Disease 2.0)
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24 pages, 872 KiB  
Review
The Role of Matrix Proteins in Cardiac Pathology
by Katie Trinh, Sohel M. Julovi and Natasha M. Rogers
Int. J. Mol. Sci. 2022, 23(3), 1338; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031338 - 25 Jan 2022
Cited by 10 | Viewed by 3317
Abstract
The extracellular matrix (ECM) and ECM-regulatory proteins mediate structural and cell-cell interactions that are crucial for embryonic cardiac development and postnatal homeostasis, as well as organ remodeling and repair in response to injury. These proteins possess a broad functionality that is regulated by [...] Read more.
The extracellular matrix (ECM) and ECM-regulatory proteins mediate structural and cell-cell interactions that are crucial for embryonic cardiac development and postnatal homeostasis, as well as organ remodeling and repair in response to injury. These proteins possess a broad functionality that is regulated by multiple structural domains and dependent on their ability to interact with extracellular substrates and/or cell surface receptors. Several different cell types (cardiomyocytes, fibroblasts, endothelial and inflammatory cells) within the myocardium elaborate ECM proteins, and their role in cardiovascular (patho)physiology has been increasingly recognized. This has stimulated robust research dissecting the ECM protein function in human health and disease and replicating the genetic proof-of-principle. This review summarizes recent developments regarding the contribution of ECM to cardiovascular disease. The clear importance of this heterogeneous group of proteins in attenuating maladaptive repair responses provides an impetus for further investigation into these proteins as potential pharmacological targets in cardiac diseases and beyond. Full article
(This article belongs to the Special Issue Proteolysis of Extracellular Matrix in Human Disease 2.0)
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38 pages, 2659 KiB  
Review
The Heparanase Regulatory Network in Health and Disease
by Alyce J. Mayfosh, Tien K. Nguyen and Mark D. Hulett
Int. J. Mol. Sci. 2021, 22(20), 11096; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011096 - 14 Oct 2021
Cited by 21 | Viewed by 3324
Abstract
The extracellular matrix (ECM) is a structural framework that has many important physiological functions which include maintaining tissue structure and integrity, serving as a barrier to invading pathogens, and acting as a reservoir for bioactive molecules. This cellular scaffold is made up of [...] Read more.
The extracellular matrix (ECM) is a structural framework that has many important physiological functions which include maintaining tissue structure and integrity, serving as a barrier to invading pathogens, and acting as a reservoir for bioactive molecules. This cellular scaffold is made up of various types of macromolecules including heparan sulfate proteoglycans (HSPGs). HSPGs comprise a protein core linked to the complex glycosaminoglycan heparan sulfate (HS), the remodeling of which is important for many physiological processes such as wound healing as well as pathological processes including cancer metastasis. Turnover of HS is tightly regulated by a single enzyme capable of cleaving HS side chains: heparanase. Heparanase upregulation has been identified in many inflammatory diseases including atherosclerosis, fibrosis, and cancer, where it has been shown to play multiple roles in processes such as epithelial-mesenchymal transition, angiogenesis, and cancer metastasis. Heparanase expression and activity are tightly regulated. Understanding the regulation of heparanase and its downstream targets is attractive for the development of treatments for these diseases. This review provides a comprehensive overview of the regulators of heparanase as well as the enzyme’s downstream gene and protein targets, and implications for the development of new therapeutic strategies. Full article
(This article belongs to the Special Issue Proteolysis of Extracellular Matrix in Human Disease 2.0)
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17 pages, 772 KiB  
Review
Therapeutic Approaches Targeting Proteostasis in Kidney Disease and Fibrosis
by Jia-Huang Chen, Chia-Hsien Wu and Chih-Kang Chiang
Int. J. Mol. Sci. 2021, 22(16), 8674; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168674 - 12 Aug 2021
Cited by 14 | Viewed by 3329
Abstract
Pathological insults usually disturb the folding capacity of cellular proteins and lead to the accumulation of misfolded proteins in the endoplasmic reticulum (ER), which leads to so-called “ER stress”. Increasing evidence indicates that ER stress acts as a trigger factor for the development [...] Read more.
Pathological insults usually disturb the folding capacity of cellular proteins and lead to the accumulation of misfolded proteins in the endoplasmic reticulum (ER), which leads to so-called “ER stress”. Increasing evidence indicates that ER stress acts as a trigger factor for the development and progression of many kidney diseases. The unfolded protein responses (UPRs), a set of molecular signals that resume proteostasis under ER stress, are thought to restore the adaptive process in chronic kidney disease (CKD) and renal fibrosis. Furthermore, the idea of targeting UPRs for CKD treatment has been well discussed in the past decade. This review summarizes the up-to-date literature regarding studies on the relationship between the UPRs, systemic fibrosis, and renal diseases. We also address the potential therapeutic possibilities of renal diseases based on the modulation of UPRs and ER proteostasis. Finally, we list some of the current UPR modulators and their therapeutic potentials. Full article
(This article belongs to the Special Issue Proteolysis of Extracellular Matrix in Human Disease 2.0)
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