The response of renal tubular epithelial cells to physiologically and chemically induced growth arrest

Jeongmi K. Jeong, Qihong Huang, Serrine Lau, Terrence Monks

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Cells respond to a variety of stresses by activating the transcription of a battery of 'acute phase' or 'stress response' genes. The nature of this response is tailored to the nature of the stress. The extent to which physiologically and pathophysiologically induced growth arrest share common genomic responses is unclear. We therefore compared the effects of a physiologically induced (serum and nutrient depletion) and a chemically induced (2-Br-bis-(GSyl)HQ and 2-Br-6-(GSyl)HQ) stress in renal tubular epithelial cells (LLC-PK1). The response to physiological stress, induced by serum depletion, involves growth arrest characterized by an inhibition of DNA synthesis that occurs in the absence of a decrease in histone mRNA or an increase in gadd153 mRNA, one of the growth arrest and DNA damage inducible genes. In contrast, the chemical-induced stress involves growth arrest accompanied by a decrease in histone mRNA, particularly core histone H2B and H2A mRNA, and the induction of gadd153. Chemical-induced changes in histone mRNA inversely correlate to changes in the expression of a stress gene, hsp70, whose expression is dependent upon the maintenance of appropriate nucleosomal structure.

Original languageEnglish (US)
Pages (from-to)7511-7518
Number of pages8
JournalJournal of Biological Chemistry
Volume272
Issue number11
DOIs
StatePublished - Mar 14 1997
Externally publishedYes

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Epithelial Cells
Histones
Kidney
Messenger RNA
Growth
Genes
Physiological Stress
Serum
DNA
DNA Damage
Transcription
Nutrients
Maintenance
Food

ASJC Scopus subject areas

  • Biochemistry

Cite this

The response of renal tubular epithelial cells to physiologically and chemically induced growth arrest. / Jeong, Jeongmi K.; Huang, Qihong; Lau, Serrine; Monks, Terrence.

In: Journal of Biological Chemistry, Vol. 272, No. 11, 14.03.1997, p. 7511-7518.

Research output: Contribution to journalArticle

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