Cloning and expression of a cDNA coding for a human monocyte-derived plasminogen activator inhibitor.

Antalis, Toni M.; Clark, Marta A.; Barnes, Tristan S.; Lehrbach, P. R.; Devine, Peter L.; Schevzov, Galina; Goss, Neil H.; Stephens, Ross W.; Tolstoshev, Paul

doi:10.1073/pnas.85.4.985

Cited by 66 publications

(47 citation statements)

References 40 publications

(34 reference statements)

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“…Indeed, the protein sequences obtained from endopeptidase fragments which were used for primer design in isolating the original SCCA gene sequence [8], are identical in the leupin sequence. The higher levels of SCCA expression found by us in SKGIIIa Leupin GAE AAAATAVVG FG S S P AS T NEE F SCCA GT E AS AATAV K I TL L S ALV E T RT I AChT GT E AAAGT GGVM TG n T GH G G P Q-F PAI-2 G S E AAAS TAVV I [8], AChT = human ~rantichymotrypsin [25], PAI-2 = plasminogen activator inhibitor-2 [5], ATIII --antithrombin II| [26], Oval = chicken ovalbumin [27]. The putative P[-PI' cleavage site of leupin deduced from this alignment is LesSer, which is shared by human cq-antichymotrypsin.…”

Section: Discussionmentioning

confidence: 99%

“…A sub-family of serpins related to ovalbumin, the ov-serpins, has been identified based on higher sequence identity (45 55%), gene organisation, and lack of an identifiable N-terminal signal sequence [4]. Human proteins belonging to this ov-serpin family include plasminogen activitor inhibitor-2 (PAI-2) [5], leucocyte elastase inhibitor (LEI) [6], placental thrombin inhibitor (PTI) [7], and squamous cell carcinoma antigen (SCCA) [8].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Identification of a novel human serpin gene; cloning sequencing and expression of leupin

Barnes

Worrall

1995

FEBS Letters

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Identification of a novel human serpin gene; cloning sequencing and expression of leupin

Barnes

Worrall

1995

FEBS Letters

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“…Primers for HSF1 mRNA (sense, 5Ј-GACATAAAGATCCGCACGGA; and antisense, 5Ј-CTGCACCAGTGAGATCAGGA) were designed according to the sequence of HSF1 cDNA from GenBank (NM_005526). Primers for PAI-1 mRNA (sense, 5Ј-CAGACCAAGAGCCTCTCCAC; and antisense, 5ЈATCACTT GGCCCATGAAAAG) and ␤-actin gene (sense, 5Ј-CGTGGGCCGCCCTAGGCA CCA; and antisense, 5Ј-TTGGCCTTAGGGTTCAGGGGGG) were synthesized according to their reported cDNA sequences (27,28). PCR was performed at 95, 60, and 72°C for 1, 2, and 3 min for 35 cycles.…”

Section: Hsf1 In Glycated Ldl-induced Pai-1mentioning

confidence: 99%

Involvement of Heat Shock Factor-1 in Glycated LDL–Induced Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells

Zhao

Shen²

2007

Diabetes

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Coronary artery disease is the predominant cause of death in diabetic patients. Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor of plasminogen activators. Heat shock protein (Hsp) was upregulated in uncontrolled diabetic patients. Our previous studies demonstrated that glycated LDL stimulated the generation of PAI-1 from vascular endothelial cells. The present study examined the effect of glycated LDL on the expression of heat shock factor-1 (HSF1), a physiological transcription factor of Hsp, and the involvement of HSF-1 in glycated LDL-induced production of PAI-1 in cultured human umbilical vein endothelial cells ( T he incidence of diabetes in North America has rapidly increased during the last three decades, and the trend is expected to continue (1). The most common cause of death in diabetic patients is coronary artery disease (CAD). Acute coronary syndrome is often associated with thrombosis at the lesions of atherosclerotic plaques (2,3). Thrombogenesis depends on an imbalance between coagulation and fibrinolysis in local blood circulation. Attenuated fibrinolytic activity has been detected in peripheral circulation of type 1 or type 2 diabetic patients (4,5). Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor for fibrinolysis, which modulates the activity of tissue and urokinase plasminogen activators on the formation of plasmin. PAI-1 is also implicated in inflammation, endothelial dysfunction, and extracellular matrix remodeling (6). An elevated level of PAI-1 in plasma has been considered as a nontraditional risk factor for CAD and a marker of endothelial dysfunction (7).Hyperglycemia and dyslipoproteinemia are two major biochemical markers of diabetes. Elevated LDL is a classical risk factor for atherosclerotic cardiovascular disease. LDL clearance via the LDL receptor is attenuated by glycation (8). Elevated levels of small, dense LDL and glycated LDL were frequently detected in diabetic patients (9 -11). Previous studies in our laboratory demonstrated that glycated LDL increased the production of PAI-1 in cultured venous or arterial endothelial cells. LDL isolated from diabetic patients or glycated LDL modified in vitro enhanced the activity of PAI-1 promoter in endothelial cells (12)(13)(14)(15). Glycated LDL stimulated the generation of reactive oxygen species (ROS) and decreased the abundance of reduced glutathione in endothelial cells (16). The findings imply that glycated LDL may induce oxidative stress in vasculature. Heat shock, mechanical shear, or oxidative stress induces stress responses in cells, which are mediated by heat shock proteins (Hsps). The transcription of Hsp is mediated by heat shock factor (HSF) (17). HSF1 is the most widely distributed form of HSF in human body (18 -20). The activation of HSF1 is detected during embryo growth (21) or in diet-induced atherosclerotic animal models (22). The levels of Hsp-70 were increased in the peripheral circulation of diabetic patients with ketoacidosis (23). Neither the impact of ...

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“…The resulting plasmid, pACskCMVu-PA, was cotransfected with ClaI digested Ad5dl309 into 293 cells using standard methods. 35 The cDNA of human PAI-2 38 provided by Toni Antalis (Queensland Institute of Medical Research, Brisbane, Australia) was used for the construction of AdCMVPAI-2. An EcoRI-HindIII fragment was subcloned into the shuttle plasmid pACCMVpLpA(−) 35 to yield pACCMVPAI-2.…”

Section: Constructionmentioning

confidence: 99%

Reduction of tumor cell migration and metastasis by adenoviral gene transfer of plasminogen activator inhibitors

et al. 1999

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Recombinant adenoviral vectors expressing u-PA, t-PA, virus expressing either PAI-1 or PAI-2 before implantation PAI-1 and PAI-2 were employed to correlate the significantly reduced the incidence of lung metastasis by expression of components of the fibrinolytic system with 60% compared with control virus. However, only PAI-2 the invasiveness of HT 1080 tumor cells. Migration through reduced the incidence of lung and brain metastasis followTranswell inserts in vitro in the presence of plasminogen ing liver gene transfer. Although PAI gene transfer by either was increased up to 22% by overexpression of u-PA, route reduced primary tumor size, it had little effect on whereas t-PA had no effect. Gene transfer of PAI-1 or PAItumor vascularization or host survival. The migratory and 2 both reduced migration in a dose-dependent manner by metastatic phenotype of HT 1080 tumor cells is thus up to 43% with PAI-1 and 29% with PAI-2. Two routes of directly dependent on u-PA expression levels and can be gene transfer were used to alter metastasis of subcutanealtered by gene transfer of u-PA or plasminogen activator ously implanted HT 1080 cells expressing firefly luciferase inhibitors. in nude mice. Infection of cultured tumor cells with adeno-

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Cloning and expression of a cDNA coding for a human monocyte-derived plasminogen activator inhibitor.

Cited by 66 publications

References 40 publications

Identification of a novel human serpin gene; cloning sequencing and expression of leupin

Identification of a novel human serpin gene; cloning sequencing and expression of leupin

Involvement of Heat Shock Factor-1 in Glycated LDL–Induced Upregulation of Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells

Reduction of tumor cell migration and metastasis by adenoviral gene transfer of plasminogen activator inhibitors

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