HCSGD entry for SERPINE1
1. General information
| Official gene symbol | SERPINE1 |
|---|---|
| Entrez ID | 5054 |
| Gene full name | serpin peptidase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1), member 1 |
| Other gene symbols | PAI PAI-1 PAI1 PLANH1 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
This gene isn't in PPI subnetwork.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0001300 | Chronological cell aging | IEP | biological_process |
| GO:0001525 | Angiogenesis | IEP | biological_process |
| GO:0002020 | Protease binding | IPI | molecular_function |
| GO:0002576 | Platelet degranulation | TAS | biological_process |
| GO:0004867 | Serine-type endopeptidase inhibitor activity | IDA | molecular_function |
| GO:0005102 | Receptor binding | IPI | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005576 | Extracellular region | IDA TAS | cellular_component |
| GO:0005615 | Extracellular space | IDA | cellular_component |
| GO:0005886 | Plasma membrane | TAS | cellular_component |
| GO:0006351 | Transcription, DNA-templated | TAS | biological_process |
| GO:0006367 | Transcription initiation from RNA polymerase II promoter | TAS | biological_process |
| GO:0007179 | Transforming growth factor beta receptor signaling pathway | TAS | biological_process |
| GO:0007596 | Blood coagulation | TAS | biological_process |
| GO:0010467 | Gene expression | TAS | biological_process |
| GO:0010469 | Regulation of receptor activity | IDA | biological_process |
| GO:0010757 | Negative regulation of plasminogen activation | IDA IMP | biological_process |
| GO:0010951 | Negative regulation of endopeptidase activity | IDA | biological_process |
| GO:0014912 | Negative regulation of smooth muscle cell migration | IDA | biological_process |
| GO:0030168 | Platelet activation | TAS | biological_process |
| GO:0030194 | Positive regulation of blood coagulation | IMP | biological_process |
| GO:0030195 | Negative regulation of blood coagulation | IC | biological_process |
| GO:0030198 | Extracellular matrix organization | TAS | biological_process |
| GO:0030336 | Negative regulation of cell migration | IDA | biological_process |
| GO:0031012 | Extracellular matrix | IDA | cellular_component |
| GO:0031093 | Platelet alpha granule lumen | TAS | cellular_component |
| GO:0032757 | Positive regulation of interleukin-8 production | IMP | biological_process |
| GO:0033629 | Negative regulation of cell adhesion mediated by integrin | IDA | biological_process |
| GO:0035491 | Positive regulation of leukotriene production involved in inflammatory response | IMP | biological_process |
| GO:0042127 | Regulation of cell proliferation | IEA | biological_process |
| GO:0042730 | Fibrinolysis | TAS | biological_process |
| GO:0045766 | Positive regulation of angiogenesis | IMP | biological_process |
| GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | TAS | biological_process |
| GO:0048260 | Positive regulation of receptor-mediated endocytosis | IDA | biological_process |
| GO:0050729 | Positive regulation of inflammatory response | IGI | biological_process |
| GO:0050829 | Defense response to Gram-negative bacterium | IGI | biological_process |
| GO:0051918 | Negative regulation of fibrinolysis | IDA | biological_process |
| GO:0061044 | Negative regulation of vascular wound healing | IGI | biological_process |
| GO:0061045 | Negative regulation of wound healing | IC | biological_process |
| GO:0071222 | Cellular response to lipopolysaccharide | IMP | biological_process |
| GO:0090026 | Positive regulation of monocyte chemotaxis | IMP | biological_process |
| GO:1902042 | Negative regulation of extrinsic apoptotic signaling pathway via death domain receptors | IMP | biological_process |
| GO:2000098 | Negative regulation of smooth muscle cell-matrix adhesion | IDA | biological_process |
| GO:2000352 | Negative regulation of endothelial cell apoptotic process | IMP | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.0587005585 | 0.0189446981 | 0.5256476369 | 0.2699747699 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.7764047135 |
| GSE13712_SHEAR | Up | 1.3000619941 |
| GSE13712_STATIC | Up | 0.8999207715 |
| GSE19018 | Up | 0.0292852076 |
| GSE19899_A1 | Down | -0.3904727771 |
| GSE19899_A2 | Down | -0.9342218106 |
| PubMed_21979375_A1 | Down | -1.7448852300 |
| PubMed_21979375_A2 | Down | -2.3739811285 |
| GSE35957 | Up | 0.4821229805 |
| GSE36640 | Up | 1.1724085768 |
| GSE54402 | Up | 0.1944813173 |
| GSE9593 | Up | 1.4607436523 |
| GSE43922 | Down | -0.1193727918 |
| GSE24585 | Up | 0.4187039714 |
| GSE37065 | Down | -0.0085910443 |
| GSE28863_A1 | Down | -0.8680794261 |
| GSE28863_A2 | Up | 0.1894907409 |
| GSE28863_A3 | Up | 0.1368461904 |
| GSE28863_A4 | Down | -0.3038593447 |
| GSE48662 | Down | -0.2307017241 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| Alteplase | DB00009 | BTD00050 | BIOD00050 |
| Urokinase | DB00013 | BTD00030 | BIOD00030 |
| Reteplase | DB00015 | BTD00013 | BIOD00013 |
| Anistreplase | DB00029 | BTD00102 | BIOD00102 |
| Tenecteplase | DB00031 | BTD00019 | BIOD00019 |
| Troglitazone | DB00197 | APRD00488 |
| Plasmin | DB05254 | - |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-143-3p | MIMAT0000435 | MIRT006316 | Immunoblot//Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22108519 |
| hsa-miR-204-5p | MIMAT0000265 | MIRT005844 | Microarray | Functional MTI (Weak) | 21282569 |
| hsa-miR-30c-5p | MIMAT0000244 | MIRT005971 | Luciferase reporter assay | Functional MTI | 21175428 |
| hsa-miR-301a-3p | MIMAT0000688 | MIRT005972 | Luciferase reporter assay | Functional MTI | 21175428 |
| hsa-miR-99a-5p | MIMAT0000097 | MIRT005973 | Luciferase reporter assay | Non-Functional MTI | 21175428 |
| hsa-miR-145-5p | MIMAT0000437 | MIRT006317 | Immunoblot//Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22108519 |
| hsa-miR-138-5p | MIMAT0000430 | MIRT021688 | qRT-PCR | Functional MTI (Weak) | 21770894 |
| hsa-miR-124-3p | MIMAT0000422 | MIRT022189 | Microarray | Functional MTI (Weak) | 18668037 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 38 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 26883561 | Truncated Plasminogen Activator Inhibitor-1 Protein Protects From Pulmonary Fibrosis Mediated by Irradiation in a Murine Model |
| 26883561 | PURPOSE: To determine whether the delivery of recombinant truncated plasminogen activator inhibitor-1 (PAI-1) protein (rPAI-1(23)) would protect from the development of radiation-induced lung injury |
| 26194321 | Importantly, our results displayed that the frequency of senescent (SA-ss-gal-positive) cells and the expression level of senescence genes (PAI-1 and p21) were significantly higher in the HG group compared with the normal glucose (NG) group, and these changes were blocked by treatment with donepezil |
| 25921542 | Microarray analysis identified differentially regulated genes in response to LPC, which included the components of senescence-associated secretory phenotype (SASP) including interleukin-8 (IL-8), IL-6, transforming growth factor-beta and plasminogen activator inhibitor-1 |
| 25173500 | Role of plasminogen activator inhibitor-1 in senescence and aging |
| 25173500 | Elevated plasminogen activator inhibitor-1 (PAI-1) levels are reported in age-associated clinical conditions including cardiovascular diseases, type 2 diabetes, obesity and inflammation |
| 25173500 | PAI-1 levels are also elevated in animal models of aging |
| 25173500 | While the association of PAI-1 with physiological aging is well documented, it is only recently that its critical role in the regulation of aging and senescence has become evident |
| 25173500 | PAI-1 is synthesized and secreted in senescent cells and contributes directly to the development of senescence by acting downstream of p53 and upstream of insulin-like growth factor binding protein-3 |
| 25173500 | Pharmacologic inhibition or genetic deficiency of PAI-1 was shown to be protective against senescence and the aging-like phenotypes in kl/kl and N(omega)-nitro-l-arginine methyl ester-treated wild-type mice |
| 24778222 | Here we show that PAI-1 deficiency retards the development of senescence and protects organ structure and function while prolonging the lifespan of kl/kl mice |
| 24709343 | The frequency of senescent (SA-ss-Gal-positive) cells and the expression level of senescence genes (PAI-1 and p21) were significantly higher in the HG group compared with the NG group, and these changes were blocked by DNJ |
| 24000115 | Real-time PCR analyses showed that berberine, NAX012 and NAX014 compounds increased the expression of some cell-cycle checkpoint molecules involved in cell senescence such as p53, p21(WAF1) , p16(INK4a) , and PAI-1, already after 24 h of 50 microM treatments |
| 22778398 | The senescence-inducing activity of IGFBP3 is inhibited by tissue-type plasminogen activator-mediated proteolysis, which is counteracted by plasminogen activator inhibitor 1 (PAI-1), another secreted mediator of senescence |
| 22744176 | Forty weeks of hyperglycemia induced significant vascular cell senescence in aortas of mice, as indicated by upregulation of expression of senescence-associated markers including p53, p21 and plasminogen activator inhibitor-1 (PAI-1) |
| 22744176 | However, SIRT1-Tg diabetic mice displayed dramatically decreased expression of p53, p21 and PAI-1 compared with diabetic WT mice |
| 21636552 | BRAF(V600E)-expressing cells subsequently stopped proliferating and induced markers of oncogene-induced senescence including acidic beta-galactosidase, PAI-1, and p16(INK4a) whereas controls did not |
| 21515304 | Increase in senescent associated markers such as p21, HMGA2 and PAI-1 was more prominent in DPV treated cells compared to similar dose of H(2)O(2) |
| 21110788 | Bach1-deficient MEFs bypassed the senescence state when the expression of a subset of p53 target genes, including p21, Pai1, Noxa, and Perp, was simultaneously reduced by using RNAi |
| 20053980 | Protein levels of IRAK1 and PAI-1 were analyzed by Western blot and those of IL6 and IL8 by ELISA |
| 20053980 | Overexpression of either IRAK1 or PAI-1 inhibited the effects of miR-146a on cell proliferation and iROS production in senescent cells |
| 20053980 | Among the different proteins repressed by miR-146a, the inhibition of PAI-1 may act to minimize the effects of senescence on the generation of iROS and growth arrest and prevent alterations of the extracellular proteolytic activity of the TM |
| 20006787 | Chronic inflammation, characterized by increased serum levels of tumor necrosis factor-alpha, interleukin-6, C-reactive protein, and plasminogen activator inhibitor-1, and the presence of inflammatory-related diseases, are seen commonly in aging |
| 19523975 | The Pro/Pro genotype of the p53 codon 72 polymorphism modulates PAI-1 plasma levels in ageing |
| 19523975 | Plasminogen activator inhibitor 1 (PAI-1) is over-expressed during ageing and it has been linked to cellular senescence |
| 19523975 | Recently, PAI-1 has been also identified in vitro as a critical downstream target of p53 |
| 19523975 | In the attempt to demonstrate an in vivo role of p53 in the relationship between PAI-1 and age, we studied PAI-1 on 570 healthy subjects (aged from 18 to 92yrs |
| 19523975 | PAI-1 showed significant relationship with age (r=0 |
| 19523975 | Stratifying by genotype, it became evident that the association between PAI-1 and age was mainly due to Pro/Pro subjects (partial r=0 |
| 19523975 | This is the first demonstration of an in vivo role of TP53 polymorphism in PAI-1 regulation, supporting the hypothesis that the effects of this polymorphism are age-dependent |
| 19520256 | METHODS: Senescent human umbilical vein endothelial cells (HUVEC) were judged by senescence-associated beta-galactosidase assay (SA-betagal), morphological appearance, and plasminogen activator inhibitor (PAI)-1 |
| 19520256 | RESULTS: Treatment with paclitaxel, sirolimus, and everolimus significantly caused a senescent phenotype and PAI-1 up-regulation, associated with a decrease in endothelial nitric oxide synthase (eNOS) and Sirt1 expression |
| 19520256 | 6% with cilostazol [100 micromol/l]) and PAI-1 up-regulation, but had no influence on the effects of paclitaxel |
| 19407340 | Herein, we show that lithium induces a rapid and pronounced up-regulation of the matrix metalloproteinase (MMP)-1, an inflammation and senescent cell marker, at the mRNA and protein levels, whereas the induction of two other senescent cell markers is either weak (interleukin-8) or delayed (plasminogen activator inhibitor-1) |
| 18838863 | Importantly, our data adds to that presented by several groups suggesting that also other factors secreted during senescence (such as PAI-1, IGFBP-7 or IL-6) contribute to the senescent response |
| 17916362 | Sirt1 inhibition by sirtinol or Sirt1 siRNA increased PAI-1 expression and decreased both protein expression and activity of eNOS |
| 17916362 | Conversely, overexpression of Sirt1 prevented hydrogen peroxide-induced SA-beta-gal activity, morphological changes and deranged expression of PAI-1 and eNOS |
| 17916362 | These results showed that Sirt1 inhibition increased p53 acetylation and induced premature senescence-like phenotype in parallel with increased PAI-1 and decreased eNOS expression |
| 17916362 | Our data suggest that Sirt1 may exert protective effects against endothelial dysfunction by preventing stress-induced premature senescence and deranged expression of PAI-1 and eNOS |
| 17172853 | Senescence, wound healing and cancer: the PAI-1 connection |
| 17172853 | Recently, we described that the p53 target gene plasminogen activator inhibitor-1 (PAI-1) is an essential mediator of replicative senescence |
| 17172853 | PAI-1 antagonizes the protease urokinase-type plasminogen activator (uPA) |
| 17172853 | Both uPA and PAI-1 are expressed in senescent cells and their relative abundance controls proliferation downstream of p53 |
| 17172853 | Here, we present data that the effects of PAI-1 and uPA in the senescence response are not strictly cell autonomous |
| 17172853 | We discuss these findings in the context of the emerging roles of PAI-1 and uPA in heterotypic cellular signaling in senescence, wound healing and metastasis |
| 16862142 | Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence |
| 16862142 | Here, we report that suppression of the p53 target gene encoding plasminogen activator inhibitor-1 (PAI-1) by RNA interference (RNAi) leads to escape from replicative senescence both in primary mouse embryo fibroblasts and primary human BJ fibroblasts |
| 16862142 | PAI-1 knockdown results in sustained activation of the PI(3)K-PKB-GSK3beta pathway and nuclear retention of cyclin D1, consistent with a role for PAI-1 in regulating growth factor signalling |
| 16862142 | Conversely, ectopic expression of PAI-1 in proliferating p53-deficient murine or human fibroblasts induces a phenotype displaying all the hallmarks of replicative senescence |
| 16862142 | Our data indicate that PAI-1 is not merely a marker of senescence, but is both necessary and sufficient for the induction of replicative senescence downstream of p53 |
| 16786104 | Premature senescence of HUVECs was evidenced by detecting the SA-beta-Gal activity and PAI-1 expression |
| 16786104 | The results indicated that the HUVECs became enlarged and flattened, both SA-beta-Gal activity and PAI-1 expression increased obviously, while cell proliferation was inhibited and G(1) phase cell cycle arresting occurred when HUVECs were treated with continued hypoxia for 96 h |
| 16786104 | The results obtained indicated that after continued hypoxia for 48 h, HUVECs infected by V12Rac1 showed obvious senescence accompanied with SA-beta-Gal activation, PAI-1 expression increase, G(1) phase arrest and cell proliferation inhibition which were similar to HUVECs after continued 96-hour hypoxia treatment, while the senescence of HUVECs infected by N17Rac1 was significantly inhibited even if the cells were exposed to hypoxia for more than 96 h |
| 16731828 | Activation of the ASK1 signal also enhanced plasminogen activator inhibitor-1 (PAI-1) expression in HUVECs |
| 16731828 | Induction of senescent endothelial cells in aortas and elevation of plasma PAI-1 levels were observed in streptozotocin (STZ) diabetic mice, whereas these changes induced by STZ were attenuated in ASK1-knockout mice |
| 16731828 | Our results suggest that hyperglycemia accelerates endothelial cell senescence and upregulation of PAI-1 expression through activation of the ASK1 signal |
| 16288006 | In MRT cell lines, reexpression of hSNF5 induces G1 cell cycle arrest, elevated p16INK4a, and activated replicative senescence markers, such as beta-galactosidase (beta-Gal) and plasminogen activator inhibitor-1 |
| 15711127 | Although some of these differences between Taxol and discodermolide were dose dependent, only discodermolide produced a doxorubicin-like induction of a senescence phenotype, including a senescence-associated beta-galactosidase activity, up-regulation of PAI-1 and p66Shc, and a strong, sustained, Erk1/2 activation |
| 15659039 | Cultured pressure ulcer fibroblasts show replicative senescence with elevated production of plasmin, plasminogen activator inhibitor-1, and transforming growth factor-beta1 |
| 15659039 | Senescent pressure ulcer fibroblasts generated significantly more plasminogen activator inhibitor-1 (1179 |
| 15659039 | Although senescent ulcer fibroblasts produce elevated levels of plasminogen activator inhibitor-1 and transforming growth factor-beta1, the ratio of these factors to plasmin levels suggests that this may have little influence on extracellular matrix synthesis or maintenance in the chronic wound |
| 15555582 | They had increased senescence-associated beta-Gal activity, lipofuscin pigment, and plasminogen activator inhibitor-1 expression |
| 12414954 | Primary human embryo lung fibroblasts and adult diploid fibroblasts infected by the human cytomegalovirus (HCMV) display beta-galactosidase (beta-Gal) activity at neutral pH (senescence-associated beta-Gal [SA-beta-Gal] activity) and overexpression of the plasminogen activator inhibitor type 1 (PAI-1) gene, two widely recognized markers of the process designated premature cell senescence |
| 10722838 | Chronic exposure of endothelial cells to homocysteine also increases the expression of two surface molecules linked to vascular disease, intracellular adhesion molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1) |
| 10722838 | Interestingly, the level of expression of both ICAM-1 and PAI-1 correlates with the degree of endothelial senescence |
| 10567948 | In RT-PCR experiments, tissue type PA (tPA) mRNA levels in both aged hGF and rGF were higher than in young cells, whereas plasminogen activator inhibitor 1 (PAI-1) mRNA remained unchanged and urotype PA (uPA) mRNA was not detected |
| 10222156 | Differential regulation of PAI-1 gene expression in human fibroblasts predisposed to a fibrotic phenotype |
| 10222156 | Synthesis of the major negative physiologic regulator of plasmin activation [plasminogen activator inhibitor type-1 (PAI-1)] is elevated during progressive cellular senescence, in premature aging disorders (e |
| 10222156 | Dermal fibroblasts derived from Werner's patients as well as from keloid lesions markedly overexpress PAI-1 mRNA transcripts compared to normal skin fibroblasts |
| 10222156 | Such cell type-related differences in steady-state PAI-1 mRNA content, and variances in the relative abundance of the 3 |
| 10222156 | 2-kb PAI-1 mRNA species, served to discriminate normal from Werner's and keloid fibroblasts |
| 10222156 | This disparity in PAI-1 mRNA levels paralleled transcriptional activities of the PAI-1 gene; de novo synthesis of PAI-1 protein among the three cell types, moreover, closely approximated the respective differences in total PAI-1 mRNA content |
| 10222156 | Despite the markedly elevated levels of PAI-1 mRNA and protein evident in newly confluent keloid fibroblasts, these cells effectively suppressed PAI-1 synthesis (as did normal dermal fibroblasts) upon culture in serum-free medium |
| 10222156 | Werner's syndrome skin fibroblasts, in contrast, continued to maintain high-level PAI-1 expression even after 3 days of growth arrest |
| 10222156 | Adhesion-mediated attenuation of serum-stimulated PAI-1 expression, a characteristic of normal cells involving sequences which mapped to the distal 5' flanking region of the PAI-1 gene, was retained in keloid but not Werner's fibroblasts |
| 10222156 | Collectively, these data suggest that (1) specific controls on PAI-1 gene expression are fundamentally different between these two clinically significant high PAI-1-synthesizing cell types and (2) the localized keloid may define the emergence of a distinct profibrotic dermal fibroblastoid phenotype in genetically predisposed individuals |
| 9512419 | These include a reduced proliferative capacity, an altered size and shape, the presence of underphosphorylated retinoblastoma protein (pRb), increased expression of plasminogen activator inhibitor (PAI-1) and the appearance of senescence-associated beta-galactosidase (SA-beta-gal) activity [2,3,13-15] |
| 9397159 | The type-1 inhibitor of plasminogen activator (PAI-1) is a major physiologic regulator of pericellular proteolytic activity and, as such, influences matrix integrity, cell-to-substrate adhesion, and cellular proliferation |
| 9397159 | Excessive accumulation of both PAI-1 mRNA and protein correlates with the progressive acquisition of morphological and growth traits characteristic of the senescent phenotype (Mu and Higgins, 1995, J |
| 9397159 | Compared to early-passage IMR-90 human diploid fibroblasts, a late-passage senescence-associated 11-fold elevation in steady-state PAI-1 mRNA content reflected a 15-fold increase in constitutive PAI-1 gene transcription |
| 9397159 | Differential mRNA stability was not a factor in age-associated PAI-1 overexpression in IMR-90 cells |
| 9397159 | Upon removal of serum, early-passage human fibroblasts enter into a state of growth arrest with marked down-regulation of PAI-1 synthesis |
| 9397159 | 2-kb PAI-1 mRNA species was evident upon serum-induced "activation" of quiescent early-passage fibroblasts; induced PAI-1 transcripts were maximal at 2 hr post-serum stimulation and declined in late G1 prior to entry into S phase |
| 9397159 | Although the PAI-1 gene was further responsive to serum in senescent cells, transcript abundance remained elevated and actually increased over the 12 to 16 hr post-serum addition period (a time when early-passage fibroblasts down-regulate PAI-1 mRNA content) |
| 9397159 | Development of the senescent phenotype in human fibroblasts is associated, therefore, with significant changes in PAI-1 gene regulation |
| 9397159 | Such reprogramming involves predominantly transcriptional events and results in a marked increase in steady-state PAI-1 transcript abundance involving both the 3 |
| 9080393 | Characterization of IGFBP-3, PAI-1 and SPARC mRNA expression in senescent fibroblasts |
| 9080393 | The RNA species encoded by IGFBP-3 (insulin-like growth factor binding protein-3), PAI-1 (plasminogen activator inhibitor-1) and SPARC (secreted protein-acidic and rich in cysteine; a |
| 9080393 | Characterization of the rates of transcription and the levels of message stability of these genes in early passage (young) versus late passage (old) HDF revealed that IGFBP-3, PAI-1 and SPARC are coordinately overexpressed but not regulated by a unique or simple mechanism encompassing all three transcripts |
| 9080393 | Only PAI-1 shows an increase in the rate of transcription, while all three show evidence that their overexpression is due to an increase in the stability of RNA |
| 8972724 | With the exception of the plasminogen activator inhibitor (PAI)-1 transcript, other IL-1 alpha-response gene mRNAs were not induced in senescent IMR-90, although the mRNA for each gene was induced by exogenous IL-1 alpha |
| 8706787 | Young and senescent cells were compared in quiescent and activated growth conditions for the secretion of tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) |
| 8706787 | Whereas young cells showed decreased levels of PAI-1 in the secreted and extracellular matrix pools upon serum deprivation, senescent cells showed a more constitutive pattern of gene expression, with no noticeable decrease of the levels in a low concentration of serum |
| 8706787 | RNA analysis revealed that senescent lung and skin cells, independent of the growth state, constitutively express levels of u-PA and PAI-1 comparable to the expression levels in young mitotically growing cells |
| 8706787 | Increases in PAI-1 was also observed in senescent human umbilical vein endothelial cells |
| 7593245 | Subconfluent late-passage IMR-90 human fibroblasts and normal rat kidney (NRK) cells, both at the stage of replicative senescence accumulated 15- to 30-fold more undersurface PAI-1 protein compared to early-passage, actively-proliferating, cultures |
| 7593245 | Senescence-associated elevations in PAI-1 expression by IMR-90 cells reflected corresponding 11-fold increases in the 3 |
| 7593245 | 2-kb PAI-1 mRNA species |
| 7593245 | Since PAI-1 expression is coupled to growth activation in serum-deprived cultures (Ryan and Higgins, 1993, J |
| 7593245 | In contrast to early-passage cultures, senescent IMR-90 fibroblasts did not down-regulate either PAI-1 protein expression or steady-state levels of PAI-1 mRNA transcripts upon serum-deprivation |
| 7593245 | Late-passage human fibroblasts at their proliferative end-stage, thus, appear to regulate PAI-1 mRNA levels through different mechanisms than do young, actively-proliferating, cells |
| 7593245 | PAI-1 overexpression during in vitro cellular aging, therefore, may contribute to the acquisition of specific senescence-associated phenotypic traits (e |
| 7628547 | Type 1 plasminogen activator inhibitor (PAI-1) is the primary inhibitor plasminogen activator and has been found to be increased in a number of clinical conditions generally defined as prothrombotic |
| 7628547 | Interestingly the increase of PAI-1 levels correlates with the upregulation of interleukin 1 alpha, which characterizes endothelial cell senescence |
| 7628547 | Since PAI-1 expression is not increased in young cells made nondividing by contact inhibition, we anticipate that PAI-1 expression can be used as an appropriate marker of endothelial senescence |
| 7628547 | Moreover, PAI-1 was not upregulated in senescent or in progeric human fibroblasts, which do not overexpress interleukin 1 alpha, thus suggesting that multiple pathways may exist to regulate aging of human fibroblasts and endothelial cells |
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