ライフサイエンスコーパス: PAI-1

1 PAI-1 (4G/4G) homozygotes were not significantly differe

2 PAI-1 deficiency (PAI-1(-/-)) increased APAP-induced liv

3 PAI-1 expression is significantly increased in the epith

4 PAI-1 expression was significantly increased in epitheli

5 PAI-1 expression was significantly less in RAAA tissue (

6 PAI-1 gain-of-function variants promote airway fibrosis

7 PAI-1 inhibition had no effect on dermal collagen levels

8 PAI-1 inhibition significantly decreased baseline and TG

9 PAI-1 is an essential repressor of cardiac fibrosis in m

10 PAI-1 levels varied considerably, but a statistically si

11 PAI-1 levels varied from 0.1 to 4.5 ng/mL (mean, 2.4 ng/

12 PAI-1 was found to comparably relocate with a subset of

13 PAI-1 was no longer associated with OLD status after VFA

14 PAI-1 was prominently expressed in PC12 pheochromocytoma

15 complex (520 vs 409 mug/L, overall P = .04), PAI-1 (10 vs 7 ng/mL, overall P = .02), and vWF (142% vs

16 Plasminogen activator inhibitor 1 (PAI-1) is a serpin inhibitor of the plasminogen activato

17 line, and plasminogen activator inhibitor 1 (PAI-1) levels were significantly elevated at the end of

18 ession of plasminogen activator inhibitor 1 (PAI-1), a key enzyme in the fibrinolytic cascade, was as

19 racted by plasminogen activator inhibitor 1 (PAI-1), another secreted mediator of senescence.

20 nhibitor, plasminogen activator inhibitor 1 (PAI-1), in Puumala hantavirus (PUUV)-infected patients a

21 levels of plasminogen activator inhibitor 1 (PAI-1), regardless of their glycemic control.

22 ate serum plasminogen activator inhibitor 1 (PAI-1), tumor necrosis factor-alpha (TNF-alpha), and hig

23 encoding plasminogen activator inhibitor 1 (PAI-1).

24 ctin, and plasminogen activator inhibitor 1 (PAI-1).

25 pair for plasminogen activator inhibitor 1 (PAI-1).

26 Plasminogen activator inhibitor 1 (PAI-1/serpinE1) can be induced by TGF-beta1, but its rol

27 increased plasminogen activator inhibitor-1 (PAI-1) activity in the lungs, thus favoring elevated coa

28 d produce plasminogen activator inhibitor-1 (PAI-1) and stimulate the expression and secretion of the

29 TAFI) and plasminogen activator inhibitor-1 (PAI-1) are causal factors for thrombolytic failure.

30 rculating plasminogen activator inhibitor-1 (PAI-1) concentration, and examined functional implicatio

31 y in 4, a plasminogen-activator inhibitor-1 (PAI-1) deficiency in 2, and 1 patient each with protein

32 er of the plasminogen activator inhibitor-1 (PAI-1) gene that recruits a novel protein-DNA complex re

33 plasminogen activator (PA), PA inhibitor-1 (PAI-1) has a paradoxical protumorigenic role in cancer,

34 ession of plasminogen activator inhibitor-1 (PAI-1) in human and murine FL-fibroblasts was reduced, w

35 Levels of plasminogen activator inhibitor-1 (PAI-1) increased significantly with increasing severity

36 PAR), and plasminogen activator inhibitor-1 (PAI-1) into the early and late endosomes by 4- to 5-fold

37 Plasminogen activator inhibitor-1 (PAI-1) is increased in the lungs of patients with pulmon

38 Plasminogen activator inhibitor-1 (PAI-1) is known to protect mice against cardiac fibrosis

39 Plasminogen activator inhibitor-1 (PAI-1) is the main inhibitor of the tissue type and urok

40 (uPA) and plasminogen activator inhibitor-1 (PAI-1) levels in the regulation of alveolar epithelial i

41 ic factor plasminogen activator inhibitor-1 (PAI-1) observed in humans is driven by an endogenous mec

42 d using a plasminogen activator inhibitor-1 (PAI-1) reporter transfected in HGFs.

43 rphism in plasminogen activator inhibitor-1 (PAI-1) with airway obstruction is modified by asthma sta

44 ciency in plasminogen activator inhibitor-1 (PAI-1), an endogenous inhibitor of fibrinolysis, increas

45 e protein plasminogen activator inhibitor-1 (PAI-1), an established regulator of these properties in

46 markers, plasminogen activator inhibitor-1 (PAI-1), and fibronectin, when compared to contralateral

47 VEGF, plasminogen activator inhibitor-1 (PAI-1), and pigment epithelium-derived factor (PEDF) wer

48 or-alpha, plasminogen activator inhibitor-1 (PAI-1), and urinary oxidative stress marker 15-F2t-isopr

49 ession of plasminogen activator inhibitor-1 (PAI-1), PDGF-B (PDGF-B), the transdifferentiation marker

50 , leptin, plasminogen activator inhibitor-1 (PAI-1), resistin, hepatocyte growth factor, interleukin-

51 erexpress plasminogen activator inhibitor-1 (PAI-1), S. aureusclfA expression and fibrin-encapsulated

52 Plasminogen activator inhibitor-1 (PAI-1), which inhibits fibrinolysis, is a key circulatin

53 n p53- or plasminogen activator inhibitor-1 (PAI-1)-deficient mice.

54 he serpin plasminogen activator inhibitor-1 (PAI-1).

55 apidly by plasminogen activator inhibitor-1 (PAI-1).

56 levels of plasminogen activator inhibitor-1 (PAI-1).

57 lpha) and plasminogen activator inhibitor-1 (PAI-1).

58 phisms in plasminogen activator inhibitor-1 (PAI-1, SERPINE1) and tissue plasminogen activator (tPA,

59 dose plasminogen activator inhibitor type 1 (PAI-1) to bile did not attenuate the lytic activity towa

60 /80, plasminogen activator inhibitor type 1 (PAI-1), and type III and IV collagen significantly decre

61 for plasminogen activator inhibitor type 1 (PAI-1), represented by AZ3976, was identified in a high

62 Plasminogen activator inhibitor type-1 (PAI-1) is a member of the serine protease inhibitor (ser

63 inolysis (plasminogen activator inhibitor-1 [PAI-1]) contribute to any identified relationship.

64 lex, plasminogen activator inhibitor type 1 [PAI-1], D-dimer, and von Willebrand factor [vWF]) were m

65 felong anticoagulation therapy if they had a PAI-1, protein C, or protein S deficiency.

66 HIF2alpha-dependent genes, including VEGF-A, PAI-1, and cyclin D1 in ccRCC cell lines and tumor xenog

67 f miR-30c and synthesize considerable active PAI-1.

68 ced accelerated latency transition of active PAI-1 may, together with supporting x-ray data, provide

69 y enhancing the latency transition of active PAI-1.

70 nt with cleaved PAI-1, suggested that active PAI-1 was present.

71 Surprisingly, AZ3976 did not bind to active PAI-1 but bound to latent PAI-1 with a K(D) of 0.29 mum

72 a small fraction in equilibrium with active PAI-1, a latent-like prelatent form, from which latent P

73 on of an adenovirus PAI-1 cDNA construct (Ad-PAI-1) suppressed expression of uPA and collagen-I and a

74 which were reversed by transduction with Ad-PAI-1.

75 Transduction of an adenovirus PAI-1 cDNA construct (Ad-PAI-1) suppressed expression of

76 ibutions incompatible with the high affinity PAI-1/LRP1 interaction.

77 sting blood glucose (FBG), hsCRP, TNF-alpha, PAI-1, and periodontal parameters (including plaque inde

78 9), whereas PAI-1 expression (P = 0.022) and PAI-1/tPA complexes in plasma (P = 0.015) were lower aft

79 pathway mediates the expressions of ET-1 and PAI-1 and migration and proliferation of contractile cel

80 inhibitors of metalloproteinases, TIMP-1 and PAI-1 protein levels, increased at MOI 25.

81 of multiple genes, including HIF-1alpha and PAI-1, in AECs.

82 n molecule-1, fibrinogen-like protein 2, and PAI-1, the secretion of TNFalpha, IL-8, and monocyte che

83 showed increased activation of caspase-3 and PAI-1 with a parallel reduction in uPA expression.

84 The changes in miR-30c and PAI-1 levels were identified in platelets from healthy a

85 ansforming growth factor-beta (TGF-beta) and PAI-1 regulated TGF-beta synthesis by cardiomyocytes in

86 fibrosis genes (CCN2, Col1a2, TGF-beta1, and PAI-1) seen in placebo-treated diabetic mice.

87 d a prediction model of serum creatinine and PAI-1 mRNA is as accurate as the model that includes the

88 eta-induced collagen accumulation, CTGF, and PAI-1 expression, but enhances Smad7 protein expression

89 agen I, alpha-smooth muscle actin, CTGF, and PAI-1, but decreased Smad7 expression.

90 odels for prognosticating graft failure, and PAI-1 mRNA level was the only independent predictor (odd

91 ase expression and increased fibronectin and PAI-1 expression.

92 sangial cell hypertrophy and fibronectin and PAI-1 expression.

93 pertrophy, and expression of fibronectin and PAI-1.

94 ture and elevated levels of plasma FXIII and PAI-1.

95 ted with reduced circulating VEGF, PEDF, and PAI-1, and could provide incentive for reducing weight a

96 tPA Alu (I/D) (rs4646972) and PAI-1 (4G/5G) (rs1799889) polymorphisms were studied by

97 TGFbeta signaling through p-SMAD2 and PAI-1 was highly active in all chondrosarcoma subtypes,

98 neered bispecific inhibitor against TAFI and PAI-1 (heterodimer diabody, Db-TCK26D6x33H1F7) in severa

99 n of a bispecific inhibitor against TAFI and PAI-1 results in a prominent profibrinolytic effect in m

100 e and endothelial cells, cLDL induced TF and PAI-1 expression.

101 and tPA), and protease modulators (TIMP1 and PAI-1).

102 To investigate whether changes in uPA and PAI-1 by ATII cells contribute to EMT, ATII cells from p

103 ding of p53 to uPA, uPA receptor (uPAR), and PAI-1 mRNA.

104 of p53-binding sequences from uPA, uPAR, and PAI-1 mRNA 3' untranslated regions in ATII cells suppres

105 p53-binding sequences from uPA, uPAR, and PAI-1 mRNA 3' untranslated regions neither interfered wi

106 l markers such as fibronectin, vimentin, and PAI-1, together with the repression of epithelial marker

107 -1 levels by incubating PC12 cells with anti-PAI-1 IgG caused a marked decrease in nicotine-mediated

108 e plasminogen activator (tPA, PLAT), such as PAI-1 (-675 4G/5G deletion/insertion) and tPA (Alu inser

109 expression of inflammatory mediators such as PAI-1 (plasminogen activator inhibitor 1), suggesting th

110 -1 levels did not mitigate this association, PAI-1 may contribute to airway obstruction in the contex

111 On the contrary, inhibition of basal PAI-1 in NL-fibroblasts increased collagen-I and alpha-s

112 atistically significant correlations between PAI-1 and clinical periodontal parameters (PI, PD, and C

113 PAI-1 by TGF-beta1, the relationship between PAI-1 and esophageal fibrosis, and the role of PAI-1 in

114 ulatory mechanism for TGF-beta production by PAI-1, which explains the paradoxical effect of PAI-1 de

115 ory SASP components (i.e., IL-6, IL-8, CCL2, PAI-1) was also highest in PSC cholangiocytes.

116 ted a robust circadian rhythm in circulating PAI-1 with a peak corresponding to approximately 6:30 am

117 PA, as well as bands consistent with cleaved PAI-1, suggested that active PAI-1 was present.

118 in 2 otherwise healthy humans with complete PAI-1 deficiency because of a homozygous frameshift muta

119 (23)- and saline-treated mice, but complexed PAI-1 was 1.6-fold greater in rPAI-1(23)-treated mice.

120 PAI-1 deficiency (PAI-1(-/-)) increased APAP-induced liver injury and hepa

121 s after AngII-Ald infusion, PAI-1-deficient (PAI-1(-/-)) mice developed severe cardiac fibrosis.

122 ate a major contribution by platelet-derived PAI-1 in the treatment of lenti-miR-30c to thrombus form

123 the transcriptional regulation of endogenous PAI-1 expression.

124 CRR, FR, and FEV1 and increased FENO , EOS, PAI-1, FXIII, and CD in patients with asthma compared wi

125 Epithelial PAI-1 might serve as a marker of EoE severity and form p

126 Esophageal PAI-1 expression correlated with basal zone hyperplasia,

127 ETP, PAI-1, and vWF levels increased with increasing asthma s

128 Excessive PAI-1 activity is associated with human disease, making

129 This study identifies the extracellular PAI-1/urokinase-type plasminogen activator (uPA) balance

130 cR2) and secretory phenotype (SASP) factors (PAI-1 and IL6).

131 Binding sites for PAI-1 within LRP1 have been localized to CR clusters II

132 Fibroblasts isolated from PAI-1-deficient mice without lung injury also showed inc

133 ma, FR negatively correlated with CD, FXIII, PAI-1, FENO , and EOS and positively with FEV1 .

134 the promoter of the TGFbeta-responsive gene PAI-1.

135 promoter, using the TGFbeta-responsive gene PAI-1.

136 lic steatohepatitis had significantly higher PAI-1 values than those with normal liver (P < 0.001).

137 The underlying mechanism of how PAI-1 expression is upregulated in DM2 is poorly underst

138 ad higher median values for FBG, TRG, hsCRP, PAI-1, PI, and CAL than did the groups with a BMI < 25 (

139 s of plasminogen activator inhibitor type I (PAI-1) have been shown to promote fibrosis in multiple o

140 ith a 7.7% decrease (95% CI: -12.6, -2.5) in PAI-1.

141 As in PAI-1(-/-) mice, administration of recombinant tissue pl

142 ensin II-induced hypertension was blunted in PAI-1(-/-) mice, cardiac hypertrophy was accelerated.

143 e able to promote large and rapid changes in PAI-1 expression.

144 in PAI-1 was 8-times larger than changes in PAI-1 induced by standardized behavioral stressors, incl

145 There was a 51.8% net decrease in PAI-1 (plasminogen activator inhibitor-1), a 12.1% net d

146 ge at sampling, there were no differences in PAI-1 to PAI-2 or MMA ratios between trial arms, but the

147 = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.

148 were associated with a parallel increase in PAI-1 and reduced uPA expression.

149 independently contributes to the increase in PAI-1 levels, whereas other coagulation factors are unal

150 tPA(-/-) and uPA(-/-) mice but increased in PAI-1(-/-) mice compared with wild-type (WT) mice.

151 ablation of cardiac fibrosis was observed in PAI-1(-/-) mice that express inactive plasmin (Pm) but n

152 eduction in cardiac fibrosis was observed in PAI-1(-/-)/uPA(-/-) double knockout mice that was associ

153 We tested whether this morning peak in PAI-1 is caused by the internal circadian system or by b

154 If this large endogenous morning peak in PAI-1 persists in vulnerable individuals, it could help

155 stically significantly greater reductions in PAI-1 at 12 months compared with controls (-19.3% vs. +3

156 hat pharmacologically mediated reductions in PAI-1 using PAI-039 would normalize cutaneous wound heal

157 with linear trends of greater reductions in PAI-1, PEDF, and VEGF.

158 This rhythm in PAI-1 was 8-times larger than changes in PAI-1 induced b

159 waist circumference, 21% of the variance in PAI-1.

160 nd markers of vascular remodeling, including PAI-1 and RhoB.

161 ted after exclusion of factors that increase PAI-1 including tobacco exposure and obesity.

162 ccounting for common exposures that increase PAI-1 level.

163 As exposures known to increase PAI-1 levels did not mitigate this association, PAI-1 ma

164 r (EGF) interact synergistically to increase PAI-1 mRNA and protein levels in human HepG2 and mink Mv

165 l cells with recombinant TGF-beta1 increased PAI-1 transcription, intracellular protein expression, a

166 d the 4G allele is associated with increased PAI-1 levels.

167 emia-induced repression of miR-30c increases PAI-1 expression and thrombus formation in DM2.

168 Four weeks after AngII-Ald infusion, PAI-1-deficient (PAI-1(-/-)) mice developed severe cardi

169 e experiments revealed that AZ3976 inhibited PAI-1 by enhancing the latency transition of active PAI-

170 eficient in plasminogen activator inhibitor (PAI-1) are resistant to lung injury and pulmonary fibros

171 hism in the plasminogen activator inhibitor (PAI-1) gene impacts transcription and the 4G allele is a

172 Plasminogen activator inhibitor (PAI-1) levels were quantified by ELISA.

173 a levels of plasminogen activator inhibitor (PAI-1), and factor XIII (FXIII), NO in exhaled breath (F

174 -1), tissue plasminogen activator inhibitor (PAI-1), and regulated on activation, normal T cell expre

175 tor, type I plasminogen activator inhibitor (PAI-1), controls blood clotting and tissue remodeling ev

176 (CTGF), and plasminogen activator inhibitor (PAI-1).

177 hrough an allosteric mechanism that inhibits PAI-1 binding to proteases and to its cofactor vitronect

178 2)-isoprostane (P=0.003), and intraoperative PAI-1 (P=0.04) concentrations also independently predict

179 3976 only had measurable affinity for latent PAI-1, we propose that its mechanism of inhibition is ba

180 not bind to active PAI-1 but bound to latent PAI-1 with a K(D) of 0.29 mum at 35 degrees C and a bind

181 atent-like prelatent form, from which latent PAI-1 is then generated more rapidly.

182 y structure of AZ3976 in complex with latent PAI-1 was determined at 2.4 A resolution.

183 n and high levels of proinflammatory leptin, PAI-1, and IL-6 were associated with increased colorecta

184 ype carrier osteomyelitis patients had lower PAI-1/tPA complex levels compared to those with the D al

185 hat has led to the testing of small-molecule PAI-1 inhibitors, initially developed as antithrombotic

186 e genetically modified to express the mutant PAI-1 proteins.

187 A dominant negative PAI-1 mutant (PAI-1R) that binds to VN but does not inhi

188 d illustrate the potential of developing new PAI-1- and CCL5-targeting therapy for patients with TNBC

189 the development of efficacious and nontoxic PAI-1 inhibitors as anticancer agents.

190 oncordance, hantaviruses induced tPA but not PAI-1 in microvascular endothelial cells, and the induct

191 In this study, we evaluated a novel PAI-1 inhibitor, annonacinone, a natural product from th

192 We have identified a novel PAI-1-dependent mechanism that regulates cardiomyocyte-d

193 unoprecipitation assays demonstrated a novel PAI-1-plasminogen complex in protein from the descending

194 s generating mice with selective ablation of PAI-1 demonstrate a major contribution by platelet-deriv

195 by logistic regression) and a combination of PAI-1 mRNA and creatinine levels (P = 0.001) were the be

196 0.80-1.0; P < 0.001) for the combination of PAI-1 mRNA and creatinine.

197 A combination of PAI-1 mRNA level, BKVN biopsy stage, and creatinine leve

198 area under the curve for the combination of PAI-1 mRNA, biopsy, and creatinine was 0.92 (95% CI, 0.8

199 togogue stimulation resulted in corelease of PAI-1 with catecholamines.

200 adoxically, homozygous genetic deficiency of PAI-1 is associated with spontaneous age-dependent, card

201 rast, no change was observed on depletion of PAI-1 or thrombin activatable fibrinolysis inhibitor (TA

202 -1, which explains the paradoxical effect of PAI-1 deficiency in promoting cardiac-selective fibrosis

203 determine if the cardioprotective effect of PAI-1 is mediated through its ability to directly regula

204 tent state; correctly predict the effects of PAI-1 mutations on the kinetics; and provide a potential

205 We propose that the greater efficiency of PAI-1.uPA complex binding and clearance by LRP1, compare

206 ies (LCB) on the secretion and expression of PAI-1, IL-6, MCP-1 and leptin in mature 3T3-L1 adipocyte

207 e chemotactic protein-1 and the formation of PAI-1/tissue plasminogen activator complexes.

208 yte chemotactic protein-1), and formation of PAI-1/tissue plasminogen activator complexes.

209 wed that annonacinone inhibited formation of PAI-1/tPA complex via enhancement of the substrate pathw

210 role of the vitronectin-binding function of PAI-1 in fibrosis was confirmed in the bleomycin model u

211 ude that the vitronectin-binding function of PAI-1 is necessary and sufficient in its ability to exac

212 in support of the protumorigenic function of PAI-1 that has led to the testing of small-molecule PAI-

213 terization of a high affinity inactivator of PAI-1.

214 These studies show that induction of PAI-1 and inhibition of uPA during fibrosing lung injury

215 y experiments to understand the induction of PAI-1 by TGF-beta1, the relationship between PAI-1 and e

216 Urinary cell level of PAI-1 mRNA, measured at the time of BKVN diagnosis, is a

217 -order of magnitude increase in the level of PAI-1.

218 High levels of PAI-1 are correlated with an increased risk of thromboti

219 The median levels of PAI-1 during the acute stage did not differ from those d

220 brain cancer suggest that elevated levels of PAI-1 may contribute to VTE.

221 bustly associated with circulating levels of PAI-1.

222 Genetic loss of PAI-1 in mdx dystrophic mice anticipated muscle fibrosis

223 ave shown that experimental manipulations of PAI-1 levels directly influence the extent of scarring t

224 Modulation of PAI-1 levels by incubating PC12 cells with anti-PAI-1 Ig

225 as well as suppressed the overexpression of PAI-1 induced by H2O2.

226 eatosis remained an independent predictor of PAI-1 levels, explaining, together with fasting C-peptid

227 erentiation with subsequent up-regulation of PAI-1 and down-regulation of tPA, resulting in inhibitio

228 The contribution of EGF to the regulation of PAI-1 involves the MAPK pathway, and the synergistic int

229 I-1 and esophageal fibrosis, and the role of PAI-1 in fibrotic gene expression.

230 However, the in vivo role of PAI-1 in inactivating uPA and limiting the generation of

231 ght to understand the expression and role of PAI-1 in patients with EoE.

232 This study defines a new role of PAI-1 in the control of fibroblast activation and expans

233 in turn, accelerates TNBC cell secretion of PAI-1 and promotes TNBC cell metastasis, thus forming a

234 at IGFBP3 is a critical downstream target of PAI-1-induced senescence.

235 with that of tPA and inversely with that of PAI-1 in rTx-TMA.

236 of KLF2, KLF4, and tPA was lower and that of PAI-1 was higher in rTx-TMA than in the controls.

237 that miR-30c directly targeted the 3' UTR of PAI-1 and negatively regulated its expression.

238 of CR456 to arginine and lysine variants of PAI-1 and definitively identified the binding site as co

239 esis studies to identify the binding site on PAI-1 for LRP1 have given conflicting results or implied

240 The rPAI-1(23) protein opposed PAI-1 antiproteolytic function by stimulating a 1.6-fold

241 In contrast, adjustment for IL-6 or PAI-1 did not substantially alter the association betwee

242 ated that F(2)-isoprostanes, but not IL-6 or PAI-1, partially mediate the relationship between obesit

243 tions account quantitatively for the overall PAI-1/LRP1 affinity.

244 pression of precursor-miR-34a increased p53, PAI-1, and apoptosis in AECs of mice unexposed to bleomy

245 of miR-34a inhibited bleomycin-induced p53, PAI-1, and apoptosis and prevented PF, whereas overexpre

246 Further, partial PAI-1 deficiency, attributable to a polymorphism in huma

247 lasmin (Pm) but normal levels of zymogen Pg (PAI-1(-/-)/Pg(S743A/S743A)).

248 Plasma PAI-1/tPA complex was assessed by enzyme-linked immuosor

249 tin, and matrix metalloproteases, and plasma PAI-1 levels correlated with plasma TGF-beta1 levels.

250 By targeting extracellular airway proteases, PAI-1 inhibits IAV glycoprotein cleavage, thereby reduci

251 n ratio) (73%), and much lower prothrombotic PAI-1 levels (19%).

252 EGF and TGFbeta regulate PAI-1 by synergistically activating transcription, which

253 TGFbeta1-treated HCFs secreted PAI-1 (0.5 uM) that bound to VN, competing with alphavbe

254 e-associated targets Cdkn1a (p21), Serpine1 (PAI-1), Tagln (Sm22), Fn1 and Clu (ApoJ).

255 However, like other serpins, PAI-1 has a labile structure, making it a difficult targ

256 Serum PAI-1 levels may play an important role in the associati

257 Interestingly, although all of the simulated PAI-1 variants readily access the prelatent intermediate

258 tic proteins including TGF-beta1, alpha-SMA, PAI-1, CTGF, FN and collagen-1.

259 ern blotting, Western blotting, and specific PAI-1 ELISA.

260 induced p53 activation (>95%) and subsequent PAI-1, fibronectin, connective tissue growth factor, and

261 In summary, PAI-1 is expressed in chromaffin cells, sorted into the

262 tion of p53 transcription failed to suppress PAI-1 or induce uPA mRNA in BLM-treated ATII cells.

263 ntranslated regions in ATII cells suppressed PAI-1 and induced uPA after BLM treatment, leading to in

264 nd restored uPA expression while suppressing PAI-1.

265 aled that cLDL induced the expression of TF, PAI-1, and LOX-1 mRNA in vascular cells.

266 t improved cutaneous wound healing, and that PAI-1 inhibition improves skeletal muscle repair in mice

267 fter Angiotensin II treatment confirmed that PAI-1 deficiency significantly enhanced multiple TGF-bet

268 It has been demonstrated that PAI-1-deficient mice exhibit improved cutaneous wound he

269 is in multiple species, we hypothesized that PAI-1 also regulates fibrosis during cardiac injury.

270 Our findings indicate that PAI-1 protects mice from hypertension-induced cardiac fi

271 It has been speculated that PAI-1 may regulate cardiac fibrosis by inactivating urok

272 The PAI-1-miR-21 fibrogenic axis also appeared dysregulated

273 The PAI-1/tPA complexes, D-dimers, and prothrombin fragment

274 an interaction between asthma status and the PAI-1 polymorphism on FEV1 /FVC (P=.03).

275 by lenti-miR-30c significantly decreased the PAI-1 expression and prolonged the time to occlusion in

276 01 to 2008 for the 4G/5G polymorphism in the PAI-1 gene.

277 its receptor, thereby making binding of the PAI-1 moiety to LRP1 a two-dimensional surface-localized

278 the Smad2/3 pathway and the activity of the PAI-1 reporter.

279 We estimated the relationship of the PAI-1 risk allele with FEV1/FVC by multivariate linear r

280 Thus, PAI-1 is a molecular switch that controls the cardiac TG

281 This molecule binds to PAI-1 reversibly and acts through an allosteric mechanis

282 biliary environment may be unsusceptible to PAI-1 inhibition.

283 e-induced lung injury were analyzed for uPA, PAI-1, and EMT markers.

284 Two-chain uPA (1-20 nM) and uPA-PAI-1 induced phosphorylation of endothelial NOS-Ser(117

285 and inhibition of PKA prevented uPA- and uPA-PAI-1-induced permeability of PMVEC monolayers in vitro

286 reased the total cellular content of the uPA-PAI-1 protein complex.

287 r fibrin(ogen) had significantly upregulated PAI-1 expression in all cortical layers assessed (p < 0.

288 esign in the hunt for therapeutically useful PAI-1 inhibitors.

289 enhance EMT-induced TNBC cell metastasis via PAI-1 and CCL5 signaling and illustrate the potential of

290 e-negative breast cancer cell metastasis via PAI-1 and CCL5 signaling.

291 Aortic wall PAI-1, uPA, and tPA concentrations were determined by we

292 as significantly higher (P = 0.009), whereas PAI-1 expression (P = 0.022) and PAI-1/tPA complexes in

293 f pro-MMP-1, -3, and -9 also decreased while PAI-1 and TIMP-1 and -3 increased.

294 malemma, remained abnormally associated with PAI-1 in early and late endosomes.

295 binding and clearance by LRP1, compared with PAI-1 alone, is due solely to simultaneous binding of th

296 mplexes by Western blotting, consistent with PAI-1 complexed with t-PA, as well as bands consistent w

297 e shown to prevent tPA from interacting with PAI-1, although preformed complexes were not destabilize

298 ation of biglycan, collagen V, collagen XII, PAI-1, Scleraxis, and Mohawk by TGF-beta1.

299 e, as well as exacerbated dystrophy in young PAI-1(-/-) mdx mice, could be reversed by miR-21 or uPA-

300 Treatment of young PAI-1(-/-) mice with Angiotensin II induced extensive hy