ライフサイエンスコーパス: PAI-1

1 PAI-1 expression is significantly increased in the epith

2 PAI-1 expression was significantly increased in epitheli

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

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

5 PAI-1 has been shown to play a role in a number of diver

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

7 PAI-1 inhibition restores tPA activity, rescues neurovas

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 mRNA was time-dependently upregulated, with a 305-

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

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

15 or (tPA), plasminogen activator inhibitor 1 (PAI-1) and platelets.

16 inhibitor plasminogen activator inhibitor 1 (PAI-1) controlled both the extent of lysis propagation a

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

18 (TF) and plasminogen activator inhibitor 1 (PAI-1) levels in venous endothelial cells in an AHR-depe

19 plexes of plasminogen-activator inhibitor 1 (PAI-1) with its target enzymes bind tightly to low-densi

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

21 or (tPA), plasminogen activator inhibitor 1 (PAI-1), and platelets.

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

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

24 bition of plasminogen activator inhibitor 1 (PAI-1), which was the most abundant ASC adipokine, led t

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

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

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

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

29 ase (uPA):plasminogen activator inhibitor-1 (PAI-1) and uPA:plasminogen complexes.

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

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

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

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

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

35 Plasminogen activator inhibitor-1 (PAI-1) is a serine protease inhibitor (serpin) that regu

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

37 Plasminogen activator inhibitor-1 (PAI-1) is the key endogenous inhibitor of fibrinolysis,

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

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

40 d the tPA inhibitor plasminogen inhibitor-1 (PAI-1) was increased in male mice expressing the Swedish

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

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

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

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

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

46 ubsequent plasminogen activator inhibitor-1 (PAI-1), connective tissue growth factor, fibronectin, an

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

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

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

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

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

52 ndogenous inhibitor plasminogen inhibitor-1 (PAI-1).

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

54 e protein plasminogen activator inhibitor-1 (PAI-1).

55 lation of plasminogen activator inhibitor-1 (PAI-1).

56 dation by plasminogen activator inhibitor-1 (PAI-1).

57 ng [e.g., plasminogen activator inhibitor-1 (PAI-1; serine protease inhibitor, clade E, member 1), co

58 Plasminogen activator inhibitor type-1 (PAI-1) is a serine protease inhibitor (serpin) implicate

59 Plasminogen activator inhibitor type-1 (PAI-1; encoded by the SERPINE1 gene), a u-PA inhibitor a

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

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

62 t explained by elevated PAI-1 because active PAI-1 concentrations required to inhibit the PG assay we

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

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

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

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

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

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

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

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

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

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

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

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

75 y biomarkers MMP-3, VE-cadherin, 6Ckine, and PAI-1 were correlated to each other in TMJOA patients an

76 xes to achieve combined CXCR4 antagonism and PAI-1 inhibition is a promising strategy for treatment o

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

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

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

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

81 atment with combined inhibition of CXCR4 and PAI-1 in ALI and various disease stages of IPF.

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

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

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

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

86 p21 and PAI-1, which are two p53 downstream targets critical for

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

88 bypassed by Rac1, p22(phox), p47(phox), and PAI-1 silencing.

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

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

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

92 inhibition of AHR activity suppressed TF and PAI-1 expression in endothelial cells of the IVC and red

93 revealed nuclear AHR and upregulated TF and PAI-1 expression, telltale signs of an activated AHR-TF/

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

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

96 significantly associated with plasma tPA and PAI-1, suggesting endothelial cells as a potential sourc

97 significantly associated with plasma tPA and PAI-1, suggesting that endothelial cells could be a pote

98 Wild-type and PAI-1 knockout (KO) mice on a high-fat diet both became

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

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

101 tivator inhibitor 1 (Serpine1, also known as PAI-1), due in part to uncoupled TGF-beta-mediated suppr

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

103 -1 levels did not mitigate this association, PAI-1 may contribute to airway obstruction in the contex

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

105 The interaction between PAI-1 and eNOS is a direct interaction as supported in e

106 strate a protein-protein interaction between PAI-1 and eNOS.

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

108 g residues of uPA and the P3 residue of both PAI-1 and plasminogen.

109 sidues in PAI-1 for the interactions of both PAI-1 and uPA:PAI-1 complexes with LRP1.

110 s, potent activity against vitronectin-bound PAI-1 in vivo, and efficacy in a murine model of venous

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

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

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

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

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

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

117 ysis, in part by decreasing platelet-derived PAI-1.

118 ably, a key marker of cardiovascular disease PAI-1 showed a difference in concentration between the o

119 es in PG were also not explained by elevated PAI-1 because active PAI-1 concentrations required to in

120 ts role in preventing fibrinolysis, elevated PAI-1 inhibits HGF's activation by u-PA and the resultan

121 the transcriptional regulation of endogenous PAI-1 expression.

122 ve regulator of eNOS and disruptions in eNOS-PAI-1 binding promote increases in NO production and enh

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

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

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

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

127 We evaluated PAI-1 as a possible new target in a mouse controlled cor

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

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

130 this study, we examined the binding of free PAI-1 and complexes of PAI-1 with low-molecular-weight u

131 arding the nature of the interaction of free PAI-1 with LRP1.

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 esenchymal transition (EndoMT)-related genes PAI-1, collagen, and periostin expression in endothelial

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

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

139 n a way not previously described for a human PAI-1 inhibitor.

140 hits and identified leads that inhibit human PAI-1 in the high-protein environments present in vivo U

141 and specificity to the active form of human PAI-1.

142 n umbilical vein endothelial cells (HUVECs), PAI-1 and eNOS colocalize and proximity ligation assays

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

144 antly accelerates the process of identifying PAI-1 inhibitors that can be rapidly deployed in vivo, a

145 In PAI-1-deficient mice, the therapeutic effect of PAI-039

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

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

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

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

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

151 = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.

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

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

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

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

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

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

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

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

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

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

162 essential requirement of lysine residues in PAI-1 for the interactions of both PAI-1 and uPA:PAI-1 c

163 examic acid, and we confirmed our results in PAI-1-deficient animals.

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

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

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

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

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

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

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

171 ted collagen degradation regulators (induced PAI-1 and reduced Mmp3), collagen crosslinker (induced P

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

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

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

175 min, active plasminogen activator inhibitor (PAI-1), and fibrin formation, but not fibrin crosslinkin

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

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

178 Interestingly, PAI-1 remained important even when its concentration was

179 Furthermore, the source of intracellular PAI-1 interacting with eNOS was shown to be endocytosis

180 These associations have made PAI-1 an attractive pharmaceutical target.

181 h increased the PAI-1/TPA ratio, thus making PAI-1-induced inhibition relevant for the regulation of

182 over, the majority of current small-molecule PAI-1 inhibitors are poor pharmaceutical candidates.

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

184 Moreover, PAI-1 directly inhibits eNOS activity, reducing NO synth

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

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

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

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

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

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

191 ynthesis, and the knockdown or antagonism of PAI-1 increases NO bioavailability.

192 erpins, and the high-affinity association of PAI-1 with vitronectin in vivo have made it difficult to

193 d the binding of free PAI-1 and complexes of PAI-1 with low-molecular-weight urokinase-type plasminog

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

195 acological inhibition or genetic deletion of PAI-1 completely reversed the attenuation of the CBF inc

196 ion, with inhibition or genetic depletion of PAI-1 attenuating clot formation and lesion expansion af

197 -1, which explains the paradoxical effect of PAI-1 deficiency in promoting cardiac-selective fibrosis

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

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

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

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

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

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

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

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

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

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

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

209 ctivity also increased with the induction of PAI-1.

210 Pharmacological inhibition of PAI-1 increased tPA activity, prevented neurovascular un

211 performed the pharmacological inhibition of PAI-1 with PAI-039 and stimulation by tranexamic acid, a

212 and binding of a small-molecule inhibitor of PAI-1, CDE-096, confirming an important role for Lys-207

213 rtant role for Lys-207 in the interaction of PAI-1 with LRP1 and of the orientations of Lys-207, -88,

214 two charged residues for the interaction of PAI-1 with LRP1 and three charged residues for the inter

215 such is able to modulate the interaction of PAI-1 with tPA and uPA in a way not previously described

216 Knockdown of PAI-1 or eNOS eliminates the proximity ligation assay (P

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

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

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

220 Chemical modification of PAI-1 confirmed an essential requirement of lysine resid

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

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

223 to 76% of rt-PA activity in the presence of PAI-1, whereas only 24% activity was preserved for unenc

224 579 Fab to the reactive centre loop (RCL) of PAI-1 and at the same exosite used by both tissue and ur

225 al controlling process; although the role of PAI-1 concentration was much less in the presence of flo

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

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

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

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

230 er the multiple patho-physiological roles of PAI-1, and understanding the relative contributions of t

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

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

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

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

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

236 ent binding model in which multiple sites on PAI-1 and uPA:PAI-1 complexes interact with complementar

237 LRP1 with ~100-fold increased affinity over PAI-1 alone.

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

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

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

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

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

243 Taken together, these findings place PAI-1 as a negative regulator of eNOS and disruptions in

244 Plasma PAI-1 increased from the MHL to the MHO to the MUO group

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

246 s to insulin resistance by increasing plasma PAI-1 concentrations and decreasing AT BCAA catabolism a

247 les that deliver miR-30c antagomiRs promoted PAI-1-dependent tumor growth and increased fibrin abunda

248 an emphasis on the potent fibrosis-promoting PAI-1 gene.

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

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

251 increase TSP-1 and decrease VEGF by reducing PAI-1 (plasminogen activator inhibitor-1/SERPINE1) level

252 ectin-3), tissue injury and repair (Serpine1/PAI-1) and growth factors (brain-derived neurotrophic fa

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

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

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

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

257 nd restored uPA expression while suppressing PAI-1.

258 Overexpression of eNOS and HA-tagged PAI-1 in COS7 cells confirmed the colocalization observa

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

260 se metabolites and the control of the AHR-TF/PAI-1 axis and VTE in cancer.

261 ssion, telltale signs of an activated AHR-TF/PAI-1 axis.

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

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

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

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

266 In the present study, we hypothesized that PAI-1 mediates post-traumatic malfunction of coagulation

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

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

269 the GJA1 repression profile, suggesting that PAI-1 may mediate actions of ASC on transcriptional regu

270 tic secondary brain damage and suggests that PAI-1 may be a central endogenous inhibitor of the fibri

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

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

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

274 x in the clotted vessel, which increased the PAI-1/TPA ratio, thus making PAI-1-induced inhibition re

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

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

277 pport the possibility that modulation of the PAI-1-tPA pathway may be beneficial in diseases associat

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

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

280 otein-protein interactions, we produced uPA, PAI-1, and plasminogen from human and zebrafish to repre

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

282 del in which multiple sites on PAI-1 and uPA:PAI-1 complexes interact with complementary sites on LRP

283 1 for the interactions of both PAI-1 and uPA:PAI-1 complexes with LRP1.

284 inding interfaces of uPA:plasminogen and uPA:PAI-1 may have coevolved to maintain tight interactions.

285 numerous polar interactions in the human uPA:PAI-1 Michaelis complex.

286 xplanation for the increased affinity of uPA:PAI-1 complexes for LRP1.

287 207, -88, and -80 for the interaction of uPA:PAI-1 complexes with LRP1.

288 charged residues for the interaction of uPA:PAI-1 complexes with LRP1.

289 Our results confirmed that uPA:PAI-1 complexes bind LRP1 with ~100-fold increased affin

290 the interaction of three regions of the uPA:PAI-1 complex with LDLa repeats on LRP1 provided an expl

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

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

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

294 elial dysfunction orchestrated, in part, via PAI-1 up-regulation.

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

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

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

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

299 y inhibits serine protease interactions with PAI-1 while conserving vitronectin binding.

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