The effect of lead on the metabolism of a nuclear matrix protein which becomes prominent in lead-induced intranuclear inclusion bodies

Eric Klann, K. R. Shelton

Research output: Contribution to journalArticle

Abstract

The influence of lead and calcium on the metabolism of a nuclear matrix protein has been studied in mouse neuroblastoma 2a (Nb2a) cells. This protein, p32/6.3, has an unusual distribution in that it is relatively abundant only in normal neural tissues and in intranuclear inclusion bodies induced in kidney tubule-lining cells of chronically lead-intoxicated animals (Egle, P.M., and Shelton, K.R. (1986) J. Biol. Chem. 261, 2294-2298). The mechanism(s) whereby lead increases p32/6.3 content are of interest, but its slow accumulation in intact animals over a period of weeks to months precludes studies with metabolic inhibitors. However, the enriched levels of p32/6.3 in mouse neuroblastoma 2a (Nb2a) cells permit these studies. The relative abundance of this protein was found to increase in mouse Nb2a cells after 1- and 3-day exposures to lead. This increase could be attributed to a decreased rate of degradation rather than either increased transcription or increased translation. A role for calcium in p32/6.3 regulation was also explored. Although neither increased extracellular calcium nor calcium ionophores had an effect, treatment of the cells with the calcium chelator [ethylenebis(oxyethylenenitrilo)]tetraacetic acid decreased p32/6.3 levels in a concentration-dependent manner, suggesting a role for calcium in the normal metabolism of the protein.

Original languageEnglish (US)
Pages (from-to)16969-16972
Number of pages4
JournalJournal of Biological Chemistry
Volume264
Issue number29
StatePublished - 1989

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Nuclear Matrix-Associated Proteins
Intranuclear Inclusion Bodies
Metabolism
Calcium
Neuroblastoma
Animals
Proteins
Calcium Ionophores
Kidney Tubules
Transcription
Linings
Cells
Tissue
Degradation
Acids
Lead

ASJC Scopus subject areas

  • Biochemistry

Cite this

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abstract = "The influence of lead and calcium on the metabolism of a nuclear matrix protein has been studied in mouse neuroblastoma 2a (Nb2a) cells. This protein, p32/6.3, has an unusual distribution in that it is relatively abundant only in normal neural tissues and in intranuclear inclusion bodies induced in kidney tubule-lining cells of chronically lead-intoxicated animals (Egle, P.M., and Shelton, K.R. (1986) J. Biol. Chem. 261, 2294-2298). The mechanism(s) whereby lead increases p32/6.3 content are of interest, but its slow accumulation in intact animals over a period of weeks to months precludes studies with metabolic inhibitors. However, the enriched levels of p32/6.3 in mouse neuroblastoma 2a (Nb2a) cells permit these studies. The relative abundance of this protein was found to increase in mouse Nb2a cells after 1- and 3-day exposures to lead. This increase could be attributed to a decreased rate of degradation rather than either increased transcription or increased translation. A role for calcium in p32/6.3 regulation was also explored. Although neither increased extracellular calcium nor calcium ionophores had an effect, treatment of the cells with the calcium chelator [ethylenebis(oxyethylenenitrilo)]tetraacetic acid decreased p32/6.3 levels in a concentration-dependent manner, suggesting a role for calcium in the normal metabolism of the protein.",
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AB - The influence of lead and calcium on the metabolism of a nuclear matrix protein has been studied in mouse neuroblastoma 2a (Nb2a) cells. This protein, p32/6.3, has an unusual distribution in that it is relatively abundant only in normal neural tissues and in intranuclear inclusion bodies induced in kidney tubule-lining cells of chronically lead-intoxicated animals (Egle, P.M., and Shelton, K.R. (1986) J. Biol. Chem. 261, 2294-2298). The mechanism(s) whereby lead increases p32/6.3 content are of interest, but its slow accumulation in intact animals over a period of weeks to months precludes studies with metabolic inhibitors. However, the enriched levels of p32/6.3 in mouse neuroblastoma 2a (Nb2a) cells permit these studies. The relative abundance of this protein was found to increase in mouse Nb2a cells after 1- and 3-day exposures to lead. This increase could be attributed to a decreased rate of degradation rather than either increased transcription or increased translation. A role for calcium in p32/6.3 regulation was also explored. Although neither increased extracellular calcium nor calcium ionophores had an effect, treatment of the cells with the calcium chelator [ethylenebis(oxyethylenenitrilo)]tetraacetic acid decreased p32/6.3 levels in a concentration-dependent manner, suggesting a role for calcium in the normal metabolism of the protein.

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