Literature DB >> 10959483

During ischemia-reperfusion in rat kidneys, heat shock response is not regulated by expressional changes of heat shock factor 1.

Z Akçetin1, R Pregla, D Darmer, H J Brömme, J Holtz.   

Abstract

Ischemia-reperfusion injury is known to induce the inducible form of the 70 kDa heat shock protein HSP70i (or HSP72) mainly via rapid activation of heat shock transcription factor 1 (HSF1). However, little is known about the regulation of the HSF1 gene. We therefore studied the time course of HSF1 mRNA transcription and its relation to the expression pattern of the HSP70i mRNA in the renal cortex, this being the most vulnerable and functionally most important part of the kidney, after different periods of unilateral renal ischemia (10-180 min) and reperfusion (up to 60 min) in male Wistar rats (10 weeks old). Immediately after ischemia there was a significant induction of HSP70i genes. While HSP70i expression constantly increased (up to 4-fold) during reperfusion, even to a higher extent with prolongation of ischemia, HSF1 mRNA remained constitutively expressed under all conditions. Thus, we conclude that during ischemia-reperfusion in rat kidneys, the heat shock response is regulated by other means than expressional changes of HSF1.

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Year:  2000        PMID: 10959483     DOI: 10.1007/s001470050705

Source DB:  PubMed          Journal:  Transpl Int        ISSN: 0934-0874            Impact factor:   3.782


  2 in total

1.  Heat shock factor 1 induces crystallin-αB to protect against cisplatin nephrotoxicity.

Authors:  Qiang Lou; Yanzhong Hu; Yuanfang Ma; Zheng Dong
Journal:  Am J Physiol Renal Physiol       Date:  2016-05-18

Review 2.  Heat shock proteins in the genitourinary system.

Authors:  R William G Watson; Thierry Lebret; John M Fitzpatrick
Journal:  Curr Urol Rep       Date:  2003-02       Impact factor: 2.862

  2 in total

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