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Cells
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Study on Extracellular Matrix Remodeling
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Study on Extracellular Matrix Remodeling

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 1074

Special Issue Editor

Dr. Luca Zammataro

E-Mail Website
Guest Editor
Kiromic Biopharma, Inc., 7707 Fannin St Suite 140, Houston, TX 77054, USA
Interests: Extra Cellular Matrix; remodeling; disease

Special Issue Information

Dear Colleagues,

The extracellular matrix (ECM) is a complex of proteins and carbohydrates that supports structural and metabolic functions, from tissue morphogenesis/development to homeostasis maintenance. Some functions encompass isolating cells from organs and affecting hydrostatic tissue pressure; each organ's ECM composition is distinct and unique. The ECM's remodeling and hardening can also occur during chronic obstructive pulmonary disease, neurodegenerative diseases, and the progression and diffusion of cancer metastasis.

 

This Special Issue will focus on ideas and methods aimed at the characterization of the ECM's composition and role in disease; identification of ECM matrix isolation in vitro; new strategies for ECM regeneration; identification of animal models for in vivo experiments; next-generation sequencing and single-cell RNA sequencing analyses, proteomic analysis, bioinformatics data analysis and extensive data integration. Mathematical models and machine-learning approaches for understanding ECM remodeling and classification are welcome.

Dr. Luca Zammataro
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.

Dr. Luca Zammataro
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

  • extracellular matrix
  • remodeling
  • disease

Published Papers (1 paper)

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Research

0 pages, 2448 KiB  
Article
Collagen VI Deficiency Impairs Tendon Fibroblasts Mechanoresponse in Ullrich Congenital Muscular Dystrophy
by Vittoria Cenni, Patrizia Sabatelli, Alberto Di Martino, Luciano Merlini, Manuela Antoniel, Stefano Squarzoni, Simona Neri, Spartaco Santi, Samuele Metti, Paolo Bonaldo and Cesare Faldini
Cells 2024, 13(5), 378; https://doi.org/10.3390/cells13050378 - 22 Feb 2024
Viewed by 970
Abstract
The pericellular matrix (PCM) is a specialized extracellular matrix that surrounds cells. Interactions with the PCM enable the cells to sense and respond to mechanical signals, triggering a proper adaptive response. Collagen VI is a component of muscle and tendon PCM. Mutations in [...] Read more.
The pericellular matrix (PCM) is a specialized extracellular matrix that surrounds cells. Interactions with the PCM enable the cells to sense and respond to mechanical signals, triggering a proper adaptive response. Collagen VI is a component of muscle and tendon PCM. Mutations in collagen VI genes cause a distinctive group of inherited skeletal muscle diseases, and Ullrich congenital muscular dystrophy (UCMD) is the most severe form. In addition to muscle weakness, UCMD patients show structural and functional changes of the tendon PCM. In this study, we investigated whether PCM alterations due to collagen VI mutations affect the response of tendon fibroblasts to mechanical stimulation. By taking advantage of human tendon cultures obtained from unaffected donors and from UCMD patients, we analyzed the morphological and functional properties of cellular mechanosensors. We found that the length of the primary cilia of UCMD cells was longer than that of controls. Unlike controls, in UCMD cells, both cilia prevalence and length were not recovered after mechanical stimulation. Accordingly, under the same experimental conditions, the activation of the Hedgehog signaling pathway, which is related to cilia activity, was impaired in UCMD cells. Finally, UCMD tendon cells exposed to mechanical stimuli showed altered focal adhesions, as well as impaired activation of Akt, ERK1/2, p38MAPK, and mechanoresponsive genes downstream of YAP. By exploring the response to mechanical stimulation, for the first time, our findings uncover novel unreported mechanistic aspects of the physiopathology of UCMD-derived tendon fibroblasts and point at a role for collagen VI in the modulation of mechanotransduction in tendons. Full article
(This article belongs to the Special Issue Study on Extracellular Matrix Remodeling)
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