CHOP is involved in neuronal apoptosis induced by neurotrophic factor deprivation

• Published in: FEBS letters 2006-06, Vol.580 (14), p.3462-3468
• Main Authors: Tajiri, Seiji, Yano, Shigetoshi, Morioka, Motohiro, Kuratsu, Jun-ichi, Mori, Masataka, Gotoh, Tomomi
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Base Sequence; C/EBP homologues protein; Cells, Cultured; CHOP; Corpus Striatum - cytology; Corpus Striatum - metabolism; DNA Primers; Endoplasmic reticulum; Endoplasmic reticulum stress; GAPDH; glyceraldehyde 3-phosphate dehydrogenase; Immunohistochemistry; In Situ Nick-End Labeling; lactate dehydrogenase; LDH; MAP2; Mice; microtubule associated protein 2; nerve growth factor; Nerve Growth Factors - physiology; Neurons - cytology; Neurons - metabolism; Neurotrophic factor; NGF; PC12 Cells; Rats; Reverse Transcriptase Polymerase Chain Reaction; Subventricular zone; SVZ; terminal transferase-mediated dUTP-biotin nick end labeling; Transcription Factor CHOP - physiology; TUNEL
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/j.febslet.2006.05.021

Neurotrophic factors are essential for the survival of neurons. We found that the endoplasmic reticulum (ER) stress-C/EBP homologues protein (CHOP) pathway to be activated during neurotrophic factor deprivation-induced apoptosis in PC12 neuronal cells and in primary cultured neurons, and this apoptosis was suppressed in the neurons from chop −/− mice. In addition, we found that CHOP is expressed in the subventricular zone (SVZ) and striatum of the young adult mouse brain. The number of apoptotic cells in the SVZ decreased in chop −/− mice. These results indicate that the ER stress-CHOP pathway plays a role in neuronal apoptosis during the development of the brain.