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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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 bone...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
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Bone Remodeling01:40

Bone Remodeling

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.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

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Endocytosis
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Related Experiment Videos

Glucocorticoids and osteocyte autophagy.

Wei Yao1, Weiwei Dai, Jean X Jiang

  • 1Department of Medicine, University of California at Davis Medical Center Sacramento, CA 95818, USA.

Bone
|January 30, 2013
PubMed
Summary

Glucocorticoids (GCs) cause bone loss by affecting bone cells. This study shows GCs induce autophagy at low doses and apoptosis at high doses in osteocytes, explaining fracture risk.

Area of Science:

  • Bone biology
  • Endocrinology
  • Cellular biology

Background:

  • Glucocorticoids (GCs) are vital for treating inflammatory and autoimmune conditions.
  • GC therapy is associated with significant bone loss and increased fracture risk.
  • Previous research implicated GCs in osteoclast and osteoblast dysfunction.

Purpose of the Study:

  • To investigate the specific effects of glucocorticoids (GCs) on osteocytes.
  • To elucidate the cellular mechanisms underlying GC-induced bone loss.

Main Methods:

  • Exposure of osteocytes to varying doses and durations of GCs.
  • Microscopic and biochemical analysis of osteocyte responses.

Main Results:

  • Low-dose GC exposure induced autophagy in osteocytes.

Related Experiment Videos

  • High-dose or prolonged GC exposure led to osteocyte apoptosis.
  • These findings highlight a dose-dependent and time-dependent effect of GCs on osteocyte viability.

    • Conclusions:

    • Osteocyte autophagy and apoptosis are key mechanisms mediating GC-induced bone loss.
    • Targeting osteocyte responses to GCs may mitigate skeletal side effects.
    • Understanding these cellular pathways is crucial for managing patients on long-term GC therapy.