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A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes.

A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes. Research Abstract Details 

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  • A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes. Abstract Text:

    yongchang qianYongchang Qian,ying zhengYing Zheng,deanna weberDeanna Weber,evelyn tiffany-castiglioniEvelyn Tiffany-Castiglioni,

    Interleukin (IL)-6 is a cytokine produced mainly by microglia and astrocytes and plays a pleiotropic role in the central nervous system. In this study, we cloned rat IL-6 cDNA into an enhanced green fluorescent protein (EGFP) or a red fluorescent protein (DsRed2) vector and rat 78-kDa glucose-regulated protein (GRP78) cDNA into an EGFP vector to construct IL-6-EGFP, IL-6-DsRed2, and GRP78-EGFP chimeras for the investigation of the mechanism of IL-6 secretion from astrocytes. The data showed that constructed IL-6-EGFP and IL-6-DsRed2 chimeras retained the secretory property, and the secretion of IL-6-EGFP from astrocytes could be attenuated by GRP78 depletion with double-stranded RNA interference. Coexpression of IL-6-DsRed2 and dysfunctional GRP78-EGFP abolished IL-6-DsRed2 secretion, and two chimeric proteins colocalized inside living astrocytes. Coimmunoprecipitation analysis indicated that IL-6 and GRP78 resided in the same complex. The data further revealed that IL-6-EGFP secretion from astrocytes was blocked by the heavy metal lead (Pb) in a concentration-dependent manner. Analysis of the Pb interaction with protein on a Pb-affinity column demonstrated that Pb bound to GRP78 but failed to bind to IL-6. Therefore, these data suggest that IL-6-EGFP or IL-6-DsRed2 chimeras can be used as imaging probes to study IL-6 secretion from living cells, that GRP78 is involved in IL-6 secretion from astrocytes, and that Pb can block IL-6 secretion from astrocytes via targeting GRP78.

    A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes. Publishing Authors By Initials

    y qianY Qian,y zhengY Zheng,d weberD Weber,e tiffany-castiglioniE Tiffany-Castiglioni,

    For similar investigative techniques: genetic techniques: gene transfer techniques: transfection research abstracts see: investigative techniques: genetic techniques: gene transfer techniques: transfection research

    PUBMED ID PMID:

    MEDLINE DATE:

    A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: American journal of physiology. Cell physiology

    VOLUME: 293

    Page Numbers: C897-905

    Journal Abbreviation: Am. J. Physiol., Cell Physiol.

    ISSN: 0363-6143

    DAY: 13

    MONTH: 06

    YEAR: 2007

    A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901225

    A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes. Keywords Mesh Terms:

    KEYWORDS: Transfection

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes. Information

    Substance Name: Lead

    Registry Number: 7439-92-1

    Grant and Affiliation Information for A 78-kDa glucose-regulated protein is involved in the decrease of interleukin-6 secretion by lead treatment from astrocytes.

    AFFILIATION: Dept. of Veterinary Integrative Biosciences, Texas A&M Univ., College Station, TX 77843-4458, USA. yqian@cvm.tamu.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIEHS

    GRANT: ES04917

    ACRONYM: ES

    MEDLINETA: Am J Physiol Cell Physiol

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