International Journal of Molecular Sciences

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Dear Colleagues,

In recent years a great deal of research has demonstrated the important role of the extracellular matrix in supporting cells, but also in modifying cellular signals and activity. This knowledge is important above all for the fascial system, since the extracellular matrix is its key element and defines many of its mechanical properties. The synthesis of the extracellular matrix can be stimulated and regulated by sex hormones, drugs, cannabinoids, mechanical stimulation and many other factors. At the same time, temperature, pH, nutrition, aging and movement can also alter the properties of the loose connective tissue, changing the gliding capacity of the fascial layers. The cells of the fasciae respond differently to two-dimensional substrates and three-dimensional environments, activating distinct signaling pathways for each. The characterization of how various stimuli and conditions can modify the fascial tissue and its properties plays a crucial role in the analysis of the fasciae microanatomy and functionality, and for the investigation of pathological phenomena. Direct integrin signaling and indirect integrin modulation of growth factor and other intracellular signaling pathways regulate ECM remodeling and control subsequent cell behavior and tissue organization.

This Special Issue aims to publish the latest research about the composition of the extracellular matrix, with a special focus on the ECM of the fasciae, and about the mechanisms of ECM synthesis and proteolytic degradation, as well as the roles of integrins and tension in ECM remodeling. Original research papers, brief reports, and review articles are invited.

Prof. Dr. Carla Stecco
Guest Editor

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Keywords

extracellular matrix
intracellular signaling pathways
fasciae
ECM remodeling

Published Papers (2 papers)

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Research

21 pages, 3848 KiB

Open AccessArticle

Potentiation of Collagen Deposition by the Combination of Substance P with Transforming Growth Factor Beta in Rat Skin Fibroblasts

by Brendan A. Hilliard, Mamta Amin, Steven N. Popoff and Mary F. Barbe

Int. J. Mol. Sci. 2024, 25(3), 1862; https://doi.org/10.3390/ijms25031862 - 03 Feb 2024

Viewed by 739

Abstract

A role for substance P has been proposed in musculoskeletal fibrosis, with effects mediated through transforming growth factor beta (TGFβ). We examined the in vitro effects of substance P on proliferation, collagen secretion, and collagen deposition in rat primary dermal fibroblasts cultured in medium containing 10% fetal bovine serum, with or without TGFβ. In six-day cultures, substance P increased cell proliferation at concentrations from 0.0002 to 100 nM. TGFβ increased proliferation at concentrations from 0.0002 to 2 pg/mL, although higher concentrations inhibited proliferation. Substance P treatment alone at concentrations of 100, 0.2, and 0.00002 nM did not increase collagen deposition per cell, yet when combined with TGFβ (5 ng/mL), increased collagen deposition compared to TGFβ treatment alone. Substance P treatment (100 nM) also increased smooth muscle actin (SMA) expression at 72 h of culture at a level similar to 5 ng/mL of TGFβ; only TGFβ increased SMA at 48 h of culture. Thus, substance P may play a role in potentiating matrix deposition in vivo when combined with TGFβ, although this potentiation may be dependent on the concentration of each factor. Treatments targeting substance P may be a viable strategy for treating fibrosis where both substance P and TGFβ play roles. Full article

(This article belongs to the Special Issue Extracellular Matrix Remodeling: Recent Progress)

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27 pages, 15650 KiB

Open AccessArticle

Blocking CCN2 Reduces Established Palmar Neuromuscular Fibrosis and Improves Function Following Repetitive Overuse Injury

by Alex G. Lambi, Robert J. DeSante, Parth R. Patel, Brendan A. Hilliard, Steven N. Popoff and Mary F. Barbe

Int. J. Mol. Sci. 2023, 24(18), 13866; https://doi.org/10.3390/ijms241813866 - 08 Sep 2023

Viewed by 941

Abstract

The matricellular protein cell communication factor 2/connective tissue growth factor (CCN2/CTGF) is critical to development of neuromuscular fibrosis. Here, we tested whether anti-CCN2 antibody treatment will reduce established forepaw fibro-degenerative changes and improve function in a rat model of overuse injury. Adult female rats performed a high repetition high force (HRHF) task for 18 weeks. Tissues were collected from one subset after 18 wks (HRHF-Untreated). Two subsets were provided 6 wks of rest with concurrent treatment with anti-CCN2 (HRHF-Rest/anti-CCN2) or IgG (HRHF-Rest/IgG). Results were compared to IgG-treated Controls. Forepaw muscle fibrosis, neural fibrosis and entheseal damage were increased in HRHF-Untreated rats, compared to Controls, and changes were ameliorated in HRHF-Rest/anti-CCN2 rats. Anti-CCN2 treatment also reduced phosphorylated-β-catenin (pro-fibrotic protein) in muscles and distal bone/entheses complex, and increased CCN3 (anti-fibrotic) in the same tissues, compared to HRHF-Untreated rats. Grip strength declines and mechanical sensitivity observed in HRHF-Untreated improved with rest; grip strength improved further in HRHF-Rest/anti-CCN2. Grip strength declines correlated with muscle fibrosis, entheseal damage, extraneural fibrosis, and decreased nerve conduction velocity, while enhanced mechanical sensitivity (a pain-related behavior) correlated with extraneural fibrosis. These studies demonstrate that blocking CCN2 signaling reduces established forepaw neuromuscular fibrosis and entheseal damage, which improves forepaw function, following overuse injury. Full article

(This article belongs to the Special Issue Extracellular Matrix Remodeling: Recent Progress)

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