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others in ECM Proteins Background

The formation of extracellular matrix (ECM) requires the cell to secrete ECM proteins. Assembly is achieved by following a strict layered assembly pattern that begins with the deposition of fibronectin filaments on the cell surface, a process known as fibril formation. Cells continue to remodel ECM through degradation and recombination mechanisms, and the dynamics of ECM are particularly pronounced in development, wound healing, and certain disease states. It is estimated that more than 300 proteins contain mammalian ECM or "core matrix" and do not include a large number of ECM-related proteins. Cells interact with ECM through receptors such as integrins and synthetic decane, resulting in the transduction of a variety of signals, thereby modulating key cellular processes such as cell differentiation, proliferation, survival and movement. It has also been shown that ECM binds to growth factors such as VEGF (Figure 1), HGF and BMP, which are thought to produce a growth factor gradient that regulates pattern formation during development. Many ECM-regulated cellular processes work through the reorganization of actin and microtubule cytoskeleton.

Structure of protein VEGF Figure 1. Structure of protein VEGF

Stiffness and elasticity

From soft brain tissue to hard bone tissue, ECM can exist with varying degrees of stiffness and elasticity. The elasticity of ECM may differ by several orders of magnitude. This property is mainly determined by the concentration of collagen and elastin, and has recently been shown to play an important role in regulating numerous cellular functions. The cells can sense the mechanical properties of the surrounding environment by applying a force and measuring the resulting recoil. This plays an important role because it helps regulate many important cellular processes, including cell contraction, cell migration, cell proliferation, differentiation (Figure 2), and cell death (apoptosis). Inhibition of non-muscle myosin II can prevent most of these effects, suggesting that they are indeed related to the mechanical properties of perceived ECM, which has become a new focus of research in the past decade.

Stem cell differentiation into various tissue types. Figure 2. Stem cell differentiation into various tissue types.

The biological effects of extracellular matrix are as follows:

1. Affect the survival and death of cells.
2. Determine the shape of the cell.
3. Regulate the proliferation of cells.
4. Control the differentiation of cells.
5. Participate in the migration of cells.

Clinical significance

Extracellular matrices have been found to cause tissue regeneration and healing. Although the mechanism by which extracellular matrix promotes structural remodeling of tissues remains unknown, researchers now believe that matrix-bound nanovesicles (MBV) are a key player in the healing process. For example, in a human fetus, the extracellular matrix grows with stem cells and regenerates all parts of the body, and the fetus can regenerate anything damaged in the uterus. Scientists have long believed that the matrix will stop functioning when fully developed. It has been used in the past to help horses repair ligament tears, but it is being further studied as a device for human tissue regeneration.

Extracellular matrices have been found to cause tissue regeneration and healing. Although the mechanism by which extracellular matrices promote tissue remodeling remains unknown, researchers now believe that matrix-bound nanovesicles (MBV) are a key player in the healing process. For example, in a human fetus, the extracellular matrix grows with the stem cells and regenerates all parts of the body, and the fetus can regenerate anything damaged in the uterus. Scientists have long believed that the matrix will stop functioning after it has fully developed. It has been used in the past to help horses repair ligament tears, but it is being further studied as a device for tissue regeneration in humans.

References:

1. Liotta LA.; et al. Metastatic potential correlates with enzymatic degradation of basement membrane collagen. Nature. 1980.284 (5751): 67–8.

2. Wang JH.; et al. Mechanoregulation of gene expression in fibroblasts. Gene. 2007,391 (1–2): 1–15.

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