7 Cyclic nucleotide regulation of plasminogen activator-inhibitor mRNA stability in rat hepatoma cells: Identification of CIS-acting sequences

Heaton, Joanne H.; Tillmann-Bogush, Maribeth; Leff, N.S.; Gelehrter, Thomas D.

doi:10.1016/s0268-9499(97)80122-1

Cited by 11 publications

(14 citation statements)

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“…Similar findings were previously reported in cells exposed to phorbol 12-myristate 13-acetate, insulin, insulin-like growth factor, and cyclic nucleotide analogs (40)(41)(42)(43). Cytokines expressed in the setting of ALI or in the tumor microenviron- Figure 8.…”

Section: Discussionsupporting

confidence: 89%

Induction of Tissue Factor by Urokinase in Lung Epithelial Cells and in the Lungs

Shetty¹,

Bhandary²,

Shetty³

et al. 2010

Am J Respir Crit Care Med

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Rationale: Urokinase-type plasminogen activator (uPA) regulates extracellular proteolysis in lung injury and repair. Although alveolar expression of uPA increases, procoagulant activity predominates. Objectives: This study was designed to investigate whether uPA alters the expression of tissue factor (TF), the major initiator of the coagulation cascade, in lung epithelial cells (ECs). Methods: Bronchial, primary airway ECs and C57B6 wild-type, uPAdeficient (uPA 2/2 ) mice were exposed to phosphate-buffered saline, uPA, or LPS. Immunohistochemistry, protein, cellular, and molecular techniques were used to assess TF expression and activity. Measurements and Main Results: uPA enhanced TF mRNA and protein expression, and TF-dependent coagulation in lung ECs. uPA-induced expression of TF involves both increased synthesis and enhanced stabilization of TF mRNA. uPA catalytic activity had little effect on induction of TF. By contrast, deletion of the uPA receptor binding growth factor domain from uPA markedly attenuated the induction of TF, suggesting that uPA receptor binding is sufficient for TF induction. Lung tissues of uPA-deficient mice expressed less TF protein and mRNA compared with wild-type mice. In addition, intratracheal instillation of mouse uPA increased TF mRNA and protein expression and accelerated coagulation in lung tissues. uPA 2/2 mice exposed to LPS failed to induce TF. Conclusions: uPA increased TF expression and TF-dependent coagulation in the lungs of mice. We hypothesize that uPA-mediated induction of TF occurs in lung ECs to promote increased fibrin deposition in the airways during acute lung injury.

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Section: Discussionsupporting

confidence: 89%

Induction of Tissue Factor by Urokinase in Lung Epithelial Cells and in the Lungs

Shetty¹,

Bhandary²,

Shetty³

et al. 2010

Am J Respir Crit Care Med

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“…Alternatively, ER␤ may indirectly influence PAI-1 promoter activity by signaling through a membrane linked-receptor system as recently reported. 13,23,43 To further explore the role of the ERs in modulating the PAI-1 promoter activity in BAECs, we investigated the roles of 2 AP1-like promoter elements, the P-box and D-box, in mediating the ER responses at the PAI-1 promoter. 42 Mutation of the P-box element severely impaired the serum-responsiveness of the PAI-1 promoter but did not appreciably modulate the ER␣ or ER␤ actions.…”

Section: Smith Et Almentioning

confidence: 99%

Differential and Opposing Regulation of PAI-1 Promoter Activity by Estrogen Receptor α and Estrogen Receptor β in Endothelial Cells

Smith

Coats

Qin

et al. 2004

Circulation Research

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Abstract-To investigate the molecular mechanisms involved in the estrogen-dependent control of plasminogen activator inhibitor-1 (PAI-1) gene expression in vascular cells, we compared the transactivation properties of estrogen receptors (ER␣ and ER␤) in regulating the activity of a human PAI-1 promoter reporter construct in transfected bovine aortic endothelial cells (BAECs). ER␣ increased PAI-1 promoter activity in BAECs by an estrogen-dependent mechanism, whereas ER␤ suppressed PAI-1 promoter activity by an estrogen-independent mechanism. The suppressive activity of ER␤ was dominant over the inductive activity of ER␣. Mutation of a putative estrogen response element (ERE) located at position Ϫ427 in the proximal promoter abolished the ER␣ action without influencing the suppressive effects of ER␤. Mutation of either AP1-like site did not eliminate the ER␣ or ER␤ actions at the PAI-1 promoter, suggesting that other promoter elements are involved in these responses. These mutations significantly reduced the Ϫ3.4kbp PAI-1 promoter response to serum. We concluded that ER␣ and ER␤ exert differential effects on the PAI-1 promoter activity in transfected BAECs. ER␣ activated the PAI-1 promoter through a proximal ERE (Ϫ427) and possibly additional EREs located within the PAI-1 promoter, whereas ER␤ suppressed the promoter construct via an unidentified mechanism. This is the first demonstration of the differential regulation of a vascular gene promoter by ER␣ and ER␤. Key Words: estrogen receptors Ⅲ plasminogen activator inhibitor-1 promoter Ⅲ estrogen response element Ⅲ bovine aortic endothelial cell

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“…While the 2.4-kb form is stabilized only by IGF-1, the 3.2-kb form is stabilized by both insulin and IGF-1 and also by cycloheximide [405]. In rat hepatoma cells, 8-bromo-cAMP reduces the levels of PAI-1 mRNA, mainly through post-transcriptional regulation [406]. Analysis using chimeric i-globin constructs showed that the 3%UTR sequence is sufficient to confer cyclic nucleotide responsiveness to the otherwise stable globin mRNA.…”

Section: Pai-1 Mrnamentioning

confidence: 99%

“…Analysis using chimeric i-globin constructs showed that the 3%UTR sequence is sufficient to confer cyclic nucleotide responsiveness to the otherwise stable globin mRNA. At least two regions in the 3%UTR of PAI-1 mRNA are involved in the modulation of mRNA decay; one of these is located in the most 3% 134 nucleotides and contains both U-rich and A-rich elements [406]. A 38-kDa cytoplasmic protein interacts with the U-rich element in the cyclic nucleotide responsive region, while cytoplasmic 50-, 61-, and 76-kDa proteins and a multi-protein complex interact with the A-rich element.…”

Section: Pai-1 Mrnamentioning

confidence: 99%

The plasminogen activator system: biology and regulation

Irigoyen

Muñoz‐Cánoves²,

Montero

et al. 1999

CMLS, Cell. Mol. Life Sci.

348

271

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The regulation of plasminogen activation involves genes for two plasminogen activators (tissue type and urokinase type), two specific inhibitors (type 1 and type 2), and a membrane-anchored urokinase-type plasminogen-activator-specific receptor. This system plays an important role in various biological processes involving extracellular proteolysis. Recent studies have revealed that the system, through interplay with integrins and the extracellular matrix protein vitronectin, is also involved in the regulation of cell migration and proliferation in a manner independent of proteolytic activity. The genes are expressed in many different cell types and their expression is under the control of diverse extracellular signals. Gene expression reflects the levels of the corresponding mRNA, which should be the net result of synthesis and degradation. Thus, modulation of mRNA stability is an important factor in overall regulation. This review summarizes current understanding of the biology and regulation of genes involved in plasminogen activation at different levels.

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7 Cyclic nucleotide regulation of plasminogen activator-inhibitor mRNA stability in rat hepatoma cells: Identification of CIS-acting sequences

Cited by 11 publications

References 0 publications

Induction of Tissue Factor by Urokinase in Lung Epithelial Cells and in the Lungs

Induction of Tissue Factor by Urokinase in Lung Epithelial Cells and in the Lungs

Differential and Opposing Regulation of PAI-1 Promoter Activity by Estrogen Receptor α and Estrogen Receptor β in Endothelial Cells

The plasminogen activator system: biology and regulation

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