Characterization of the hsp110/sse gene family response to
hyperosmolality and other stresses.
Santos, Bento C., Alejandro Chevaile, Ryoji Kojima, Steven R. Gullans.
Department of Medicine, Renal Division, Brigham and Women's
Hospital and Harvard Institutes of Medicine, Boston, MA 02115 and
Department of Pharmacology, Faculty of Pharmacy, Meijo University,
Nagoya 468, Japan
APStracts 5:0041F, 1998.
Hsp110, Osp94, and Hsp70RY are members of the recently described
Hsp110/SSE subfamily of stress proteins whose members are
structurally related to the Hsp70/BiP gene superfamily. To date,
little is known concerning the response of this gene family to
stresses in vitro or in vivo. In this study, an analysis of mRNA
expression showed that Hsp110 and Osp94, like Hsp70, are induced in
renal mIMCD3 epithelial cells by heat shock, hyperosmotic NaCl, and
cadmium; whereas low pH had a suppressive effect on Osp94. Hydrogen
peroxide decreased expression of Osp94, while inducing levels of
Hsp110 and Hsp70 message. Tunicamycin, hypertonic urea and TNF[alpha]
had no effects. Hsp70RY was responsive exclusively to cadmium
chloride. Moreover, enhanced expression of Hsp110 and Osp94 was
subsequent to induction of Hsp70 and was suppressed by inhibition of
protein synthesis by cycloheximide. RT-PCR analysis showed Hsp110,
Osp94, and Hsp70RY are ubiquitously expressed in mouse tissues. In
murine kidney, there was a cortico-medullary gradient of expression
of Hsp110, Osp94, Hsp70RY, and Hsp70, but not Hsc70 or BiP. Further,
dehydration increased inner medullary expression of Hsp110 and Osp94.
An analysis of stress tolerance in mIMCD3 cells showed that heat
shock and hyperosmotic NaCl stress are cross-tolerant stresses
suggesting hyperosmolality is a physiological correlate of heat shock
in mammalian kidney. Thus, Hsp110 and Osp94 behave as heat shock
proteins though they are regulated differently than Hsp70.
Received 10 June 1997; accepted in final form 17 February 1998.
APS Manuscript Number F188-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 19 February 1998