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Department of Medical Specialties, The University of Texas Health Center at Tyler, Tyler, Texas 75710
The urokinase receptor (uPAR) influences several
biological functions relevant to lung injury and repair, including
proteolysis, cell migration, and adhesion. In malignant mesothelioma
cells, we recently found that a posttranscriptional mechanism involving a
cis-trans
interaction between a uPAR mRNA sequence and a cytoplasmic uPAR mRNA
binding protein (mRNABP) regulates uPAR gene expression (S. Shetty, A. Kumar, and S. Idell. Mol. Cell
Biol. 17: 1075-1083, 1997). In this study, we
sought to determine if uPAR expression in lung and pleural cells
involves a similar posttranscriptional pathway. We first identified and
characterized the uPAR mRNABP in rabbit tissues using gel mobility
shift, ultraviolet (UV) cross-linking, and RNase protection assays and
detected it in liver, heart, brain, spleen, colon, and lung. Phorbol
12-myristate 13-acetate, lipopolysaccharide, transforming growth
factor-
, tumor necrosis factor-
, or cycloheximide induced uPAR
and uPAR mRNA expression in cultured rabbit pleural mesothelial cells
and lung fibroblasts and concurrently reduced the uPAR mRNA-uPAR mRNABP
interaction. Using conventional and affinity chromatography, we
purified a 50-kDa uPAR mRNABP that selectively binds to a
51-nucleotide fragment of the uPAR coding region. This protein migrates
as a monomer when analyzed by SDS-PAGE and UV cross-linking and does
not possess intrinsic RNase activity in vitro. A uPAR mRNABP
physicochemically and functionally similar to that of human malignant
mesothelioma is constitutively expressed in the rabbit lung and other
nonneoplastic tissues. In rabbit lung fibroblasts and mesothelial
cells, expression of uPAR involves posttranscriptional regulation
whereby the uPAR mRNABP appears to interact with a specific coding
region cis-element to decrease the
stability of uPAR mRNA.
messenger ribonucleic acid binding protein
This article has been cited by other articles:
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  S. Shetty, J. Padijnayayveetil, T. Tucker, D. Stankowska, and S. Idell The fibrinolytic system and the regulation of lung epithelial cell proteolysis, signaling, and cellular viability Am J Physiol Lung Cell Mol Physiol, December 1, 2008; 295(6): L967 - L975. [Abstract] [Full Text] [PDF]
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S. Idell, T. Allen, S. Chen, K. Koenig, A. Mazar, and A. Azghani Intrapleural activation, processing, efficacy, and duration of protection of single-chain urokinase in evolving tetracycline-induced pleural injury in rabbits Am J Physiol Lung Cell Mol Physiol, January 1, 2007; 292(1): L25 - L32. [Abstract] [Full Text] [PDF]
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 V. B. Antony Fibrinolysis in the Pleural Space: Breaking the Bonds That Bind Am. J. Respir. Crit. Care Med., October 1, 2002; 166(7): 909 - 910. [Full Text]
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S. Idell, A. Mazar, D. Cines, A. Kuo, G. Parry, S. Gawlak, J. Juarez, K. Koenig, A. Azghani, W. Hadden, et al. Single-Chain Urokinase Alone or Complexed to Its Receptor in Tetracycline-induced Pleuritis in Rabbits Am. J. Respir. Crit. Care Med., October 1, 2002; 166(7): 920 - 926. [Abstract] [Full Text]
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S. Shetty and S. Idell Posttranscriptional regulation of plasminogen activator inhibitor-1 in human lung carcinoma cells in vitro Am J Physiol Lung Cell Mol Physiol, January 1, 2000; 278(1): L148 - L156. [Abstract] [Full Text] [PDF]
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 S. Shetty and S. Idell Urokinase Induces Expression of Its Own Receptor in Beas2B Lung Epithelial Cells J. Biol. Chem., June 29, 2001; 276(27): 24549 - 24556. [Abstract] [Full Text] [PDF]
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