TY - JOUR
T1 - Heat shock-induced protection and enhancement of Na+-glucose cotransport by LLC-PK1 monolayers
AU - Sussman, Caroline R.
AU - Renfro, J. Larry
PY - 1997/10
Y1 - 1997/10
N2 - 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°C for 1 h, then 37°C for measurements) decreased transepithelial electrical resistance (TER), I(Glc), I(phz), and I(total) 50-70%. Mild heat shock (MHS; 42°C for 3 h, then 37°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 (V(max) of I(Glc)). MHS alone increased TER (50%), I(Glc) (20%), I(total) (20%), and V(max) 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.
AB - 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°C for 1 h, then 37°C for measurements) decreased transepithelial electrical resistance (TER), I(Glc), I(phz), and I(total) 50-70%. Mild heat shock (MHS; 42°C for 3 h, then 37°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 (V(max) of I(Glc)). MHS alone increased TER (50%), I(Glc) (20%), I(total) (20%), and V(max) 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.
KW - Epithelial transport
KW - Heat shock protein 70
KW - Heat shock protein 72
KW - Heat stress
KW - Sodium-dependent glucose transporter
KW - Sulfate transport
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U2 - 10.1152/ajprenal.1997.273.4.f530
DO - 10.1152/ajprenal.1997.273.4.f530
M3 - Article
C2 - 9362330
AN - SCOPUS:0030664038
SN - 1931-857X
VL - 273
SP - F530-F537
JO - American Journal of Physiology - Renal Physiology
JF - American Journal of Physiology - Renal Physiology
IS - 4 42-4
ER -