scholarly journals The ECM-Cell Interaction of Cartilage Extracellular Matrix on Chondrocytes

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Yue Gao ◽  
Shuyun Liu ◽  
Jingxiang Huang ◽  
Weimin Guo ◽  
Jifeng Chen ◽  
...  

Cartilage extracellular matrix (ECM) is composed primarily of the network type II collagen (COLII) and an interlocking mesh of fibrous proteins and proteoglycans (PGs), hyaluronic acid (HA), and chondroitin sulfate (CS). Articular cartilage ECM plays a crucial role in regulating chondrocyte metabolism and functions, such as organized cytoskeleton through integrin-mediated signaling via cell-matrix interaction. Cell signaling through integrins regulates several chondrocyte functions, including differentiation, metabolism, matrix remodeling, responses to mechanical stimulation, and cell survival. The major signaling pathways that regulate chondrogenesis have been identified as wnt signal, nitric oxide (NO) signal, protein kinase C (PKC), and retinoic acid (RA) signal. Integrins are a large family of molecules that are central regulators in multicellular biology. They orchestrate cell-cell and cell-matrix adhesive interactions from embryonic development to mature tissue function. In this review, we emphasize the signaling molecule effect and the biomechanics effect of cartilage ECM on chondrogenesis.

2009 ◽  
Vol 79 (4) ◽  
pp. 652-659 ◽  
Author(s):  
Tanapan Wattanachai ◽  
Ikuo Yonemitsu ◽  
Sawa Kaneko ◽  
Kunimichi Soma

Abstract Objective: To test the hypothesis that the effects of mechanical stress from a functional lateral shift of the mandible have no effect on the expression of two main condylar cartilage extracellular matrix components, type II collagen and aggrecan, in rats from early puberty to young adulthood. Materials and Methods: Functional lateral shift of the mandible was induced in experimental groups of 5-week-old male Wistar rats, using guiding appliances. The rats were sacrificed at 3, 7, 14, and 28 days post appliance attachment. The condyles were immunohistochemically evaluated for type II collagen and aggrecan (the immunoreactive areas were quantified). Results: As compared with the control group, on the contralateral condyles, the immunoreactivity of the experimental groups was significantly increased from 7 to 14 days. While on the ipsilateral condyles, the immunoreactive areas were significantly decreased throughout the experimental period. Conclusion: A functional lateral shift of the mandible modulated the condylar cartilage extracellular matrix differently on each side of the condyle, which affected condylar morphology, growth, biomechanical properties, and even the susceptibility of the condylar cartilage to pathogenesis.


PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0241040
Author(s):  
T. A. Russo ◽  
A. M. M. Banuth ◽  
H. B. Nader ◽  
J. L. Dreyfuss

Endothelial cells (ECs) are subjected to physical forces such as shear stress (SS) induced by blood flow that leads to significant changes in morphology, physiology and gene expression. The abnormal mechanical forces applied in the cardiovascular system can influence the development of conditions and diseases such as thrombosis, hypertension and atherosclerosis. This study investigated the expression of glycosaminoglycans (GAGs), proteoglycans and extracellular matrix molecules in ECs exposed to normal and altered SS. ECs were exposed to SS of 12 dyn/cm2 (artery physiological condition) and 4 dyn/cm2 (artery pathological condition). Subsequently, ECs were subjected to immunofluorescence, qPCR, GAG biosynthesis analyses and cell-based assays. SS induced changes in ECs morphology. There were other pathological consequences of altered SS, including inhibited adhesion, stimulation of migration and capillary-like tube formation, as well as increases of GAG synthesis. We observed higher expression of syndecan-4, perlecan, decorin, fibronectin and collagen III α1 and growth factors, including VEGF-A and TGFβ-1. ECs exposed to SS displayed extracellular matrix remodeling as well as expression of cell-matrix and cell-cell interaction molecules. This study contributes to the understanding of how vascular biology is affected by mechanical forces and how these molecules can be affected in cardiovascular diseases.


Author(s):  
B.M. Vertel

Normal cartilage function is dependent upon the unique structural properties of the extensive extracellular matrix (ECM). In final assembled form, the ECM of hyaline cartilage is composed of abundant amounts of proteoglycan (PG) and type II collagen. Additional collagens and glycoproteins may be important structural components as well. Through their concentration of negative charges, PGs confer upon the cartilage ECM the ability to retain high levels of hydration and thereby resist compression. Type II collagen fibers contribute to the tensile strength of cartilage.In the cartilage ECM, PG monomers associate with hyaluronic acid and link protein to form large aggregates. In turn, PG aggregates are associated with the fibrous meshwork of type II collagen. Interactions with other ECM molecules may occur as well. The cartilage matrix constituents are themselves large and complex. For example, the PG monomer is 1-5 x 106 daltons in size and contains a core protein of Mr >300K (comprising only 8-10% of the complete monomer).


Biomaterials ◽  
2007 ◽  
Vol 28 (2) ◽  
pp. 151-161 ◽  
Author(s):  
Leah C. Abraham ◽  
J. Fred Dice ◽  
Patrick F. Finn ◽  
Nicholas T. Mesires ◽  
Kyongbum Lee ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yanyan Zhu ◽  
Yumeng Huang ◽  
Qian Ji ◽  
Shengqiao Fu ◽  
Jia Gu ◽  
...  

The extracellular matrix (ECM) is a highly dynamic and complex network structure, which exists in almost all tissues and is the microenvironment that cells rely on for survival. ECM interacts with cells to regulate diverse functions, including differentiation, proliferation, and migration. Neutrophils are the most abundant immune cells in circulation and play key roles in orchestrating a complex series of events during inflammation. Neutrophils can also mediate ECM remodeling by providing specific matrix-remodeling enzymes (such as neutrophil elastase and metalloproteinases), generating neutrophil extracellular traps, and releasing exosomes. In turn, ECM can remodel the inflammatory microenvironment by regulating the function of neutrophils, which drives disease progression. Both the presence of ECM and the interplay between neutrophils and their extracellular matrices are considered an important and outstanding mechanistic aspect of inflammation. In this review, the importance of ECM will be considered, together with the discussion of recent advances in understanding the underlying mechanisms of the intricate interplay between ECM and neutrophils. A better comprehension of immune cell-matrix reciprocal dependence has exciting implications for the development of new therapeutic options for neutrophil-associated infectious and inflammatory diseases.


2020 ◽  
Vol 22 (1) ◽  
pp. 238
Author(s):  
Stephan Niland ◽  
Johannes A. Eble

The tumor microenvironment (TME) has become the focus of interest in cancer research and treatment. It includes the extracellular matrix (ECM) and ECM-modifying enzymes that are secreted by cancer and neighboring cells. The ECM serves both to anchor the tumor cells embedded in it and as a means of communication between the various cellular and non-cellular components of the TME. The cells of the TME modify their surrounding cancer-characteristic ECM. This in turn provides feedback to them via cellular receptors, thereby regulating, together with cytokines and exosomes, differentiation processes as well as tumor progression and spread. Matrix remodeling is accomplished by altering the repertoire of ECM components and by biophysical changes in stiffness and tension caused by ECM-crosslinking and ECM-degrading enzymes, in particular matrix metalloproteinases (MMPs). These can degrade ECM barriers or, by partial proteolysis, release soluble ECM fragments called matrikines, which influence cells inside and outside the TME. This review examines the changes in the ECM of the TME and the interaction between cells and the ECM, with a particular focus on MMPs.


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