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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

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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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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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Hormones and Bone Tissue01:17

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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.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
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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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Exosomes are stable, lipid bilayer-enclosed vesicles capable of crossing biological barriers. They can carry a wide range of molecules required for intercellular communication. Once exosomes are released from the cell where they originated, they enter a recipient cell through various pathways such as fusion, receptor-mediated endocytosis, macropinocytosis, and phagocytosis.
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  1. Home
  3. Osteoclast-derived Exosomes Influence Osteoblast Differentiation In Osteoporosis Progression Via The Lncrna Aw011738/ Mir-24-2-5p/ Trem1 Axis.
  1. Home
  3. Osteoclast-derived Exosomes Influence Osteoblast Differentiation In Osteoporosis Progression Via The Lncrna Aw011738/ Mir-24-2-5p/ Trem1 Axis.

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Osteoclast-derived exosomes influence osteoblast differentiation in osteoporosis progression via the lncRNA AW011738/

Jingcheng Liu1, Binyu Wang1, Hongtao Chen2

  • 1Department of Orthopedics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu 210029, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|August 2, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Osteoclast-derived exosomes carrying lncRNA AW011738 worsen osteoporosis by inhibiting osteoblast differentiation via the AW011738/miR-24-2-5p/TREM1 pathway. Reducing AW011738 in exosomes improves bone density in osteoporosis models.

Keywords:
AW011738ExosomesOsteogenic DifferentiationOsteoporosisTREM1

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Area of Science:

  • Molecular biology
  • Cell biology
  • Biochemistry

Background:

  • Osteoporosis is a metabolic bone disease characterized by decreased bone mass and increased fracture risk.
  • Osteoclast-derived exosomes play a role in bone remodeling and disease pathogenesis.
  • Understanding the molecular mechanisms of these exosomes is crucial for developing novel therapeutic strategies for osteoporosis.

Purpose of the Study:

  • To elucidate the molecular mechanism by which osteoclast-derived exosomes contribute to osteoporosis.
  • To investigate the role of long non-coding RNA (lncRNA) AW011738 within these exosomes.
  • To identify the specific molecular axis involved in exosome-mediated regulation of osteogenesis.

Main Methods:

  • Whole RNA sequencing identified differentially expressed lncRNAs and mRNAs in a RANKL-induced osteoclast model.
  • Exosome characterization involved electron microscopy, western blotting, and nanosight analysis.
  • Functional studies utilized overexpression/knockdown of AW011738, dual luciferase reporter assays, and in vivo osteoporosis models (OVX mice).

    • Main Results:

    • Osteoclast-derived exosomes containing lncRNA AW011738 were found to decrease osteogenesis markers and accelerate bone loss in ovariectomized (OVX) mice.
    • Knockdown of AW011738 in osteoclast-derived exosomes significantly increased osteoblast differentiation markers in vitro.
    • In vivo, tail vein injection of exosomes with reduced AW011738 ameliorated osteoporosis in OVX mice, indicating a protective effect.

    Conclusions:

    • Osteoclast-derived exosomes harboring lncRNA AW011738 inhibit osteogenesis in MC3T3-E1 cells.
    • This inhibition occurs through the lncRNA AW011738/microRNA-24-2-5p (miR-24-2-5p)/TREM1 signaling axis.
    • Targeting this axis offers a potential therapeutic strategy for exacerbating osteoporosis in OVX mice.