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Vol. 12, No. 7, pp. 982-995, April 1, 1998
1 Skirball Institute of Biomolecular Medicine, the
Departments of Medicine, Cell Biology, and the Kaplan Cancer Center,
New York University (NYU) Medical Center, New York, New York 10016 USA;
2 Adirondack Biomedical Research Facility, Lake Placid, New
York 12946 USA;
3 Department of Pathology, Cornell University
Medical Center, New York, New York 10021 USA
Cellular stress, particularly in response to toxic and metabolic
insults that perturb function of the endoplasmic reticulum (ER stress),
is a powerful inducer of the transcription factor CHOP. The role of
CHOP in the response of cells to injury associated with ER stress was
examined in a murine deficiency model obtained by homologous
recombination at the chop gene. Compared with the wild type,
mouse embryonic fibroblasts (MEFs) derived from chop 
/ animals exhibited significantly less programmed
cell death when challenged with agents that perturb ER function. A
similar deficit in programmed cells death in response to ER stress was also observed in MEFs that lack CHOP's major dimerization partner, C/EBP
, implicating the CHOP-C/EBP
pathway in programmed cell death. An animal model for studying the
effects of chop on the response to ER stress was developed. It
entailed exposing mice with defined chop genotypes to a single
sublethal intraperitoneal injection of tunicamycin and resulted in a
severe illness characterized by transient renal insufficiency. In
chop +/+ and chop
+/ mice this was associated with the early
expression of CHOP in the proximal tubules followed by the development
of a histological picture similar to the human condition known as acute
tubular necrosis, a process that resolved by cellular regeneration. In
the chop / animals, in spite of the
severe impairment in renal function, evidence of cellular death in the
kidney was reduced compared with the wild type. The proximal tubule
epithelium of chop / animals exhibited
fourfold lower levels of TUNEL-positive cells (a marker for programmed
cell death), and significantly less evidence for subsequent
regeneration. CHOP therefore has a role in the induction of cell death
under conditions associated with malfunction of the ER and may also
have a role in cellular regeneration under such circumstances.
[Key Words: Cell injury; gene targeting; animal model; nephrotoxicity; renal failure]
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