Navglucose cotransport by LLC-PK, cells is selectively enhanced by heat shock

Cells respond to heat shock by altering multiple aspects of their physiology including activating kinase cascades and changing gene expression. We have investigated the effects of heat shock (42°C 3h, 37°C 10-15h) on transport of glucose and sulfate by monolayers of the porcine kidney cell line, LLC-PK₁. Tissues were mounted in Ussing chambers for determination of transepithelial currents (glucose dependent (5 mM, I_glc) and kinetics), and ³⁵SO₄ fluxes. Transepithelial fluxes of sulfate (0.4 mM) were measured under short-circuited conditions. LLC-PK₁ cells performed net reabsorption of sulfate. Neither apical to basolateral (A->B) nor basolateral to apical (B->A) sulfate flux was affected by heat shock (A->B= 3.9±0.2 (control.C) vs. 3.7±0.2 (heat shock,HS); B->A=2.7±0.2 (C) vs. 2.2±0.1 (HS) nmol/cm²/h). In contrast glucose dependent current measured in the same tissues was increased by heat shock (I_glc and V_max increased ∼20%). Na⁺ dependent sulfate flux was measured by subtracting sulfate flux observed in the absence of Na⁺ from that observed upon subsequent replacement of Na⁺. Unidirectional Na⁺ dependent sulfate flux (A->B) was unaffected by heat shock (4.8 (C) vs. 4.6 (HS) nmol/cm²/h). In the same tissues glucose dependent currents were increased ∼50% by heat shock. These data illustrate that heat shock increases Na⁺/glucose cotransport and that this is a specific effect: not all Na⁺ dependent transport processes are affected.