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  • Endoplasmic reticulum stress-induced CHOP activation mediates the down-regulation of leptin in human neuroblastoma SH-SY5Y cells treated with the oxysterol 27-hydroxycholesterol
  • Marwarha G; Dasari B; Ghribi O
  • Cell Signal 2012[Feb]; 24 (2): 484-92
  • Epidemiological studies have suggested an inverse relationship between the adipocytokine leptin and the onset of Alzheimer's disease (AD), and leptin supplementation decreases amyloid-beta (Abeta) production and tau phosphorylation (p-tau), two major biochemical events that play a key role in the pathogenesis of AD. We have previously shown that the cholesterol oxidized product 27-hydroxycholesterol (27-OHC) inhibits leptin expression, an effect that correlated with increased levels of Abeta and p-tau. We have also shown that 27-OHC induces endoplasmic reticulum (ER) stress, a cellular response that is implicated in AD and confers leptin resistance. However the extent to which ER stress is involved in 27-OHC-induced attenuation in leptin expression has not been determined. In this study we determined the involvement of ER stress in the 27-OHC-induced attenuation of leptin expression in SH-SY5Y human neuroblastoma cells. We demonstrate that 27-OHC-induced ER stress attenuates leptin expression by activating C/EBP Homologous Protein (CHOP) which negatively regulates C/EBPalpha, a transcription factor required for leptin expression. The molecular chaperone 4-phenylbutyric acid (4-PBA) precludes 27-OHC-evoked ER stress and down-regulation of leptin. Furthermore, we demonstrate that the activation of the transcription factor CHOP in response to ER stress is pivotal in the attenuation of leptin expression as knocking-down CHOP alleviates the attenuation in leptin expression. Our study implicates ER stress as the mechanistic link in the 27-OHC-induced negative regulation of leptin, a hormone that has potential therapeutic effects in AD by reducing Abeta and phosphorylated tau accumulation.
  • |Alzheimer Disease/genetics/*metabolism/pathology[MESH]
  • |Amyloid beta-Peptides/genetics/*metabolism[MESH]
  • |Cell Line, Tumor[MESH]
  • |Electrophoretic Mobility Shift Assay[MESH]
  • |Endoplasmic Reticulum Stress[MESH]
  • |Endoplasmic Reticulum/*drug effects/genetics/metabolism[MESH]
  • |Gene Expression Regulation/drug effects[MESH]
  • |Humans[MESH]
  • |Hydroxycholesterols/*adverse effects[MESH]
  • |Leptin/antagonists & inhibitors/genetics/*metabolism[MESH]
  • |Neuroblastoma/genetics/*metabolism/pathology[MESH]
  • |Phosphorylation[MESH]
  • |RNA, Small Interfering/genetics/metabolism[MESH]
  • |Real-Time Polymerase Chain Reaction[MESH]
  • |Signal Transduction[MESH]
  • |Transcription Factor CHOP/antagonists & inhibitors/genetics/*metabolism[MESH]
  • |tau Proteins/genetics/*metabolism[MESH]





  • *{{pmid21983012}}
    *<b>[http://www.kidney.de/mlpefetch.php?search=21983012 Endoplasmic reticulum stress-induced CHOP activation mediates the down-regulation of leptin in human neuroblastoma SH-SY5Y cells treated with the oxysterol 27-hydroxycholesterol ]</b> Cell Signal 2012; 24(2) ; 484-92 Marwarha G; Dasari B; Ghribi O

        *21983012*

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    Cell Signal

    484 2.24 2012