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Impairment of NF-kB activation and modulation of gene expression by calpastatin.

Authors
Chen-F; Demers-LM; Vallyathan-V; Lu-Y; Castranova-V; Shi-X
Source
Am J Physiol, Cell Physiol 2000 Sep; 279(3):C709-C716
NIOSHTIC No.
20020638
Abstract
To address the involvement of the calpain system in both basal and silica-induced nuclear factor (NF)-kappaB activation, several human bronchial epithelial cell lines were established in which an intracellular inhibitor of calpain, calpastatin, was stably expressed. Reduced basal and silica-induced inhibitor (IkappaBalpha) degradation and NF-kappaB activation were observed in cells stably overexpressing calpastatin. In addition, the cells in which calpain was constitutively inhibited by the overexpression of calpastatin exhibited a notable morphological change. Whereas empty vector-transfected cells displayed a morphology indistinguishable from that of parental cells, cells overexpressing calpastatin exhibited a mosaic morphological change with reduced formation of lamella 30 min after the cells were seeded. Genefilter microarray experiments, in which 3,965 human genes can be evaluated for their expression at the same time, showed that calpastatin downregulated genes encoding several membrane-associated proteins or nuclear proteins and upregulated genes of collagen alpha2, DAZ, and mitochondrial capsule selenoprotein. These results suggest that, in addition to their proteolytic activities on cytoskeletal proteins and other cellular regulatory proteins, calpain-calpastatin systems can also affect the expression levels of genes encoding structural or regulatory proteins.
Keywords
Genes; Silica-dusts; Silicates; Morphology; Cell-morphology; Proteins
Contact
X. Shi, Pathology and Physiology Research Branch, National Institute for Occupational Safety and Health, 1095 Willowdale Rd., Morgantown, WV 26505
CAS No.
14808-60-7; 7631-86-9
Publication Date
20000901
Document Type
Journal Article
Email Address
xas0@cdc.gov
Fiscal Year
2000
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
0363-6143
NIOSH Division
HELD
Source Name
American Journal of Physiology: Cell Physiology
State
WV; PA
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