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Extracellular Matrix01:26

Extracellular Matrix

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Unlike epithelial tissue, which is composed of cells closely packed with little or no extracellular space in between, connective tissue cells are dispersed in a matrix. This extracellular matrix (ECM) is composed of fibrous proteins like collagen, elastin, and fibronectin in a ground substance consisting of interstitial fluid, cell adhesion proteins, and proteoglycans. The proteoglycans form a gel-like material in the spaces between cells and provide hydration, buffering, binding, and force...
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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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ECM Modifications Driven by Age and Metabolic Stress Directly Promote Vascular Smooth Muscle Cell Osteogenic

Meredith Whitehead1, Maria Faleeva1, Rafael Oexner1

  • 1British Heart Foundation Centre of Research Excellence, School of Cardiovascular and Metabolic Medicine & Sciences (M.W., M.F., R.O., L.S., M.M., C.M.S.), King's College London, United Kingdom.

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Changes in the extracellular matrix (ECM) due to aging and disease directly trigger vascular smooth muscle cell (VSMC) osteogenic differentiation. This study introduces a new model to investigate ECM

Keywords:
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Area of Science:

  • Biomedical Engineering
  • Cell Biology
  • Vascular Biology

Background:

  • The extracellular matrix (ECM) is crucial for vascular smooth muscle cell (VSMC) function.
  • Aging and metabolic diseases alter ECM composition and properties, impacting VSMC phenotype.
  • The specific effects of these ECM changes on VSMC phenotype are not well understood.

Purpose of the Study:

  • To develop and utilize a novel in vitro model system to investigate how ECM modifications associated with aging and metabolic disease affect VSMC phenotype.
  • To analyze the mechanisms by which altered ECM induces VSMC osteogenic differentiation.

Main Methods:

  • Synthesized endogenous ECM using primary human VSMCs, modifying it during culture or after decellularization.
  • Characterized ECM integrity, stiffness, and composition using superresolution microscopy, atomic force microscopy, and proteomics.
  • Assessed VSMC viability and osteogenic differentiation on modified ECM.

Main Results:

  • Mineral-stressed ECM showed hydroxyapatite deposition and altered collagen, inducing VSMC osteogenic gene expression via Runx2 (Runt-related transcription factor 2) and increased reactive oxygen species.
  • Senescent ECM also promoted Runx2-mediated osteogenic gene expression and accelerated calcification.
  • Glycated ECM induced alkaline phosphatase (ALP) activity dependent on RAGE (receptor for advanced glycation end products) signaling, which was attenuated by inhibiting ALP or RAGE.

Conclusions:

  • ECM modifications in aging and metabolic disease directly induce VSMC osteogenic differentiation through distinct pathways.
  • The ECM microenvironment is a critical factor in VSMC phenotypic modulation, accelerating vascular pathologies.
  • This study provides a novel model for investigating vascular calcification mechanisms.