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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Bones contain a relatively small number of cells entrenched in a matrix of organic and inorganic components. Although bone cells compose only a small amount of the bone volume, they are crucial to its function. Four types of cells are found within the bone tissue— osteoblasts, osteocytes, osteogenic cells, and osteoclasts.
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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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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Related Experiment Video

Updated: Aug 31, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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Periostin Augments Vascular Smooth Muscle Cell Calcification via β-Catenin Signaling.

Ioana Alesutan1, Laura A Henze2, Beate Boehme2

  • 1Institute for Physiology and Pathophysiology, Johannes Kepler University Linz, Altenberger Strasse 69, 4040 Linz, Austria.

Biomolecules
|August 26, 2022
PubMed
Summary

Periostin worsens vascular calcification in chronic kidney disease (CKD) by activating the WNT/β-catenin pathway and integrin αvβ3. Inhibiting periostin may reduce calcification in CKD patients.

Keywords:
chronic kidney diseaseperiostinphosphatevascular calcificationvascular smooth muscle cellsβ-catenin

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Area of Science:

  • Biomedical research
  • Vascular biology
  • Nephrology

Background:

  • Medial vascular calcification is prevalent in chronic kidney disease (CKD), linked to hyperphosphatemia.
  • Vascular smooth muscle cells (VSMCs) actively contribute to vascular calcification.
  • Pro-inflammatory mediators can promote VSMC calcification.

Purpose of the Study:

  • To investigate the role and mechanisms of periostin in calcifying human VSMCs.
  • To explore periostin's impact on vascular calcification markers and processes.
  • To assess the association between serum periostin levels and CKD.

Main Methods:

  • Examined periostin's effects on VSMC calcification markers and β-catenin signaling.
  • Utilized WNT/β-catenin pathway inhibitors and integrin αvβ3-blocking antibodies.
  • Assessed periostin silencing and measured serum periostin in hemodialysis patients versus controls.

Main Results:

  • Periostin induced pro-calcific marker expression and aggravated VSMC calcification, potentiating β-glycerophosphate effects.
  • Periostin increased β-catenin abundance and target gene expression, effects blocked by pathway inhibitors.
  • Integrin αvβ3 blockade and periostin silencing reduced pro-calcific effects; elevated serum periostin found in hemodialysis patients.

Conclusions:

  • Periostin acts as an augmentative factor in VSMC calcification.
  • Periostin's pro-calcific effects are mediated through integrin αvβ3 and WNT/β-catenin pathway activation.
  • Inhibiting periostin may offer a therapeutic strategy to mitigate vascular calcification in CKD.