AJP - Renal Physiology, Vol 273, Issue 4 530-F537, Copyright © 1997 by American Physiological Society
Heat shock-induced protection and enhancement of Na+-glucose cotransport by LLC-PK1 monolayers
C. R. Sussman and J. L. Renfro
Department of Physiology and Neurobiology, University of Connecticut, Storrs 06269, USA.
Monolayers of the porcine-derived renal epithelial cell line, LLC-PK1, were
used to characterize the effects of heat stress on Na+-glucose cotransport.
Transepithelial current dependent on 5 mM glucose (I(Glc)),
phloridzin-sensitive current (I(phz)), and total transepithelial current
(I(total)) were measured as indicators of Na+-glucose cotransport. Severe
heat shock (SHS; 45 degrees C for 1 h, then 37 degrees C for measurements)
decreased transepithelial electrical resistance (TER), I(Glc), I(phz), and
I(total) 50-70%. Mild heat shock (MHS; 42 degrees C for 3 h, then 37
degrees C for 12 h) induced accumulation of 72-kDa heat shock protein
(HSP-72), decreased damage to TER from SHS, and prevented damage to I(Glc),
I(phz), and I(total). Kinetic analysis showed that SHS damaged and MHS
protected total Na+-glucose transport capacity (Vmax of I(Glc)). MHS alone
increased TER (50%), I(Glc) (20%), I(total) (20%), and Vmax of I(Glc)
(25%). On enhancement of the Na+ gradient by depletion of intracellular
Na+, MHS increased I(Glc) 50% and had no effect on transepithelial
Na+-dependent sulfate reabsorptive flux measured concurrently or in
Na+-replete tissues. These effects of MHS were not reflected in effects on
cell survival or luminal membrane surface area as indicated by lactate
dehydrogenase or alkaline phosphatase release. In conclusion,
HSP-72-inducing heat treatment both protected and enhanced Na+-glucose
cotransport independently of the luminal membrane Na+ gradient and
selectively with respect to effects on TER, reabsorptive sulfate transport,
cell survival, and luminal membrane surface area.
