ArticleProceedings of the National Academy of Sciences of the United States of America1992
Thermoprotection of a functional epithelium: heat stress effects on transepithelial transport by flounder renal tubule in primary monolayer culture.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 46 citations in OpenAlex.
- GSH and Zinc Supplementation Attenuate Cadmium-Induced Cellular Stress and Stimulation of Choline Uptake in Cultured Neonatal Rat Choroid Plexus Epithelia.International journal of molecular sciences · 2021Article
- Estrogen modulates ClC-2 chloride channel gene expression in rat kidney.Pflugers Archiv : European journal of physiology · 2003Article
- Tissue-level cytoprotection.Cell stress & chaperones · 2000Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary monolayer cultures of winter flounder renal proximal-tubule cells were used to determine whether transepithelial transport could be protected from the damaging effects of extreme temperature by previous mild heat shock. Renal tubule epithelial cells were enzymatically dispersed and reorganized as confluent monolayer sheets on native rat tail collagen. Transepithelial electrical properties (potential difference, resistance, short-circuit current, and Na(+)-dependent glucose current) and unidirectional [35S]sulfate fluxes were measured in Ussing chambers at 22 degrees C. Examination of transepithelial electrical properties following acute 1-hr elevation of temperature over a range of 22-37 degrees C provided the basis for the "mild" versus "severe" thermal stress protocols. Severe elevation from 22 degrees C to 32 degrees C for 1.5 hr followed by 1.5 hr at 22 degrees C significantly decreased glucose current (7 +/- 0.7 to 3 +/- 0.8 microA/cm2) as well as net sulfate secretion [131 +/- 11 to 33 +/- 11 nmol/(cm2.hr)]. Mild heat shock of 27 degrees C for 6 hr prior to this severe heat shock completely protected both glucose transport (6 +/- 0.7 microA/cm2) and sulfate flux (149 +/- 13 nmol/(cm2.hr)]. Scanning electron microscopy showed that the number of microvilli on the apical (luminal) surface of the epithelium was decreased after a 32 degrees C heat shock. Monolayers exposed to 27 degrees C for 6 hr prior to incubation at 32 degrees C showed no loss of microvilli. SDS/PAGE analysis of protein patterns from the cultures showed that three classes of heat shock proteins were maximally induced at 27 degrees C. Inhibition of protein synthesis by cycloheximide prevented the thermoprotective effect of mild heat shock. This suggests that certain renal transport functions can be protected from sublethal but debilitating thermal stress by prior mild heat shock and that heat shock proteins may play a role in this protection.
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