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Glucocorticoid-Induced Autophagy Protects Osteocytes Against Oxidative Stress Through Activation of MAPK/ERK

Rekha Kar1, Manuel A Riquelme1, Rui Hua1

  • 1Department of Biochemistry and Structural Biology University of Texas Health Science Center San Antonio TX USA.

JBMR Plus
|May 3, 2019
PubMed

Insights

Autophagy protects osteocytes from cell death, particularly under oxidative stress. Glucocorticoids like dexamethasone enhance this protective autophagy, preconditioning cells against various insults.

Area of Science:

  • Cell Biology
  • Bone Biology
  • Autophagy Research

Background:

  • Autophagy's role in cell survival is context-dependent.
  • Osteocyte cell death is implicated in bone diseases.
  • Oxidative stress is a known factor in osteocyte apoptosis.

Purpose of the Study:

  • To investigate the role of autophagy in oxidative stress-induced osteocyte death.
  • To determine the effect of glucocorticoids on osteocyte autophagy and survival.
  • To elucidate the signaling pathways involved in autophagy-mediated osteocyte protection.

Main Methods:

  • Utilized MLO-Y4 osteocytic cell line and SOD1-deficient mice.
  • Administered oxidative stress inducers and autophagy inhibitors (e.g., chloroquine).
  • Assessed cell death, autophagy markers (autophagosome formation), and MAPK/ERK pathway activity.

Main Results:

  • Decreased autophagy correlated with increased oxidative stress-induced osteocyte death.
  • Autophagy inhibition worsened cell death, while dexamethasone pretreatment conferred protection.
  • Inhibition of MAPK/ERK signaling reduced autophagosome formation and increased cell death.

Conclusions:

  • Basal autophagy levels protect osteocytes against oxidative stress-induced cell death.
  • Glucocorticoids induce protective autophagy, preconditioning osteocytes against cell death.
  • Autophagy represents a novel therapeutic target for preserving osteocyte viability.
Keywords:
APOPTOSISAUTOPHAGYCELL PROTECTIONMAPK/ERKOSTEOCYTE

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