ライフサイエンスコーパス: elastase

1 f matrix metalloproteinase-12 and neutrophil elastase.

2 e stoichiometry of inhibition for neutrophil elastase.

3 mphysema by loss of inhibition of neutrophil elastase.

4 ained inhibitory activity against neutrophil elastase.

5 ury, depending on the presence of neutrophil elastase.

6 peroxidase (MPO), azurocidin, and neutrophil elastase.

7 zymes, myeloperoxidase, and human neutrophil elastase.

8 reduced levels of membrane-bound neutrophil elastase.

9 lic and mean blood pressure was level of PMN elastase.

10 , trypsin, neutral protease, thermolysin, or elastase.

11 histone H3 and with the specific neutrophil elastase.

12 s was upregulated by wounding and neutrophil elastase.

13 xplore the S1-S4 pockets of human neutrophil elastase.

14 in and 82% with the azurophil granule marker elastase.

15 of MMP12 protein, which is functional as an elastase.

16 vessel wall, PMNs are activated and release elastase.

17 ssion of other virulence traits, such as the elastase.

18 efficiency than commonly used substrates of elastase.

19 m that of other isoforms of chymotrypsin and elastase.

20 e asthma were stained for OSM and neutrophil elastase.

21 protease such as trypsin, chymotrypsin, and elastase.

22 ant levels of the histone H2Ax or neutrophil elastase.

23 enzymes myeloperoxidase (MPO) and neutrophil elastase.

24 (AAT) Z-variant with catalytically inactive elastase.

25 electivity against pancreatic and neutrophil elastases.

26 atrix metalloproteinases-2 and 9 (MMP2,9) or elastases.

27 RCL proteolysis by endogenous and exogenous elastases.

28 nstrated an association of chymotrypsin-like elastase 1 (Cela1) with lung elastin remodeling, and tha

29 Fecal elastase-1 levels from these CF animals were similar to

30 aluated were pancreatic insufficient (<2 mug elastase-1 per gram of feces).

31 In addition, we reveal that an elastase 2 cleavage site is present between FNIII EDA an

32 ter cleavage of the FNIII 12-13-14 domain by elastase 2.

33 likrein-related peptidase (KLK) 5, KLK7, and elastase-2 (ELA2), which are suggested to be part of a p

34 Using threshold values of MMP-8 (94 ng/muL), elastase (33 ng/muL), sialidase (23 ng/muL), and levels

35 ), carbonic anhydrase II(-) (mature ductal), elastase 3a (acinar)(-) , and insulin(-) subpopulations.

36 We investigated whether neutrophil elastase, a biased agonist of PAR(2), causes inflammatio

37 eptidase I, resulting in neutrophils lacking elastase, a serine protease required for NET production.

38 ity, and inhibited the release of neutrophil elastase--a marker of neutrophil extracellular trap form

39 (MYHCre+ flx/flx, flx/wt, and wt/wt) in the elastase AAA model compared with control.

40 ection using ERTCre+ KLF4 flx/wt mice in the elastase AAA model.

41 Areas of stretch-induced elastase activity and Cela1 binding colocalized.

42 study aimed to determine the association of elastase activity and desmosine with exacerbations and l

43 unistic pathogen from CD patients, exhibited elastase activity and produced peptides that better tran

44 In Sugen/hypoxia rats, elafin reduced elastase activity and reversed pulmonary hypertension, j

45 d 1 displayed low nanomolar IC50 in blocking elastase activity and strong ability in protecting bronc

46 This induction of elastase activity did not occur with UVB.

47 Free neutrophil elastase activity in BAL fluid at 3 months of age was as

48 Neutrophil elastase activity in BAL fluid in early life was associa

49 as matrix metalloproteinase 9 and neutrophil elastase activity in culture supernatant, as well as rea

50 Elastase activity in sputum was associated with the bron

51 Sputum elastase activity increased at exacerbations (P = 0.001)

52 Sputum neutrophil elastase activity is a biomarker of disease severity and

53 We show that elastase activity is increased in dystrophic (mdx(4cv))

54 rement, and 381 provided sputum for baseline elastase activity measurements using an activity-based i

55 as well as by a chloroamidine sensitive and elastase activity mechanism.

56 recombinant form of AAT (rAAT) without anti-elastase activity reduces lung inflammatory responses to

57 utilize more specific markers of neutrophil elastase activity to inform on the efficacy of inhibitio

58 ed by specific markers of neutrophil-derived elastase activity to target inhibition to the sites of i

59 During a 3-year follow-up, elevated sputum elastase activity was associated with a higher frequency

60 Sputum elastase activity was independently associated with FEV1

61 otoxicity in vitro, inhibit human neutrophil elastase activity, and inhibit the migration of neutroph

62 t this early/rapid mechanism is dependent on elastase activity, but independent of ROS generation and

63 This process is regulated by elastase activity, previously shown to regulate formatio

64 receptor 2 (BMPR2) signaling, and increased elastase activity.

65 lA) and increased neutrophil recruitment and elastase activity.

66 deoxyguanosine (8-OHdG) and human neutrophil elastase/alpha1-proteinase inhibitor (HNE/alpha1-PI) com

67 plied to detect the presence and activity of elastase, an enzyme released by the cercarial larvae sta

68 9 activity in resolvin-treated mice in both elastase and angiotensin II models.

69 An imbalance of elastase and antielastase, along with innate inflammatio

70 urface, and allows the control of neutrophil elastase and cathepsin G by their natural inhibitors.

71 n C and its downstream proteases (neutrophil elastase and cathepsin G) and serum levels of IL-1beta,

72 hilic granules to release the Ser proteases, elastase and cathepsin G, resulting in the proteolytic d

73 tly improved inhibition of human neuthrophil elastase and chymotrypsin.

74 er of the serpin superfamily and a leukocyte elastase and crosstalk between neurons and T cells in th

75 Cathepsin V is a highly effective elastase and has been implicated in physiological and pa

76 NET protein complexes (DNA-elastase and histone-elastase complexes), cell-free DNA,

77 f A1A1 and A1A2 variants of beta-casein with elastase and leucine aminopeptidase revealed the release

78 We report here that both neutrophil elastase and proteinase-3 cleave the human PAR1 N termin

79 A leukocyte origin of human leukocyte elastase and proteinase-3 in diabetic ketoacidosis was c

80 Circulating elastase and proteinase-3 were associated with infection

81 nal region by neutrophil proteases including elastase and proteinase-3, generating the 33-kDa isoform

82 racellular trap (NET) release independent of elastase and reduced NAD phosphate-oxidase activation.

83 RATIONALE: Sputum neutrophil elastase and serum desmosine, which is a linked marker o

84 which dose-dependently inhibited neutrophil elastase and shortened resolution intervals.

85 variant was more sensitive to cleavage with elastase and the "C5a" generated was biologically active

86 jor by macrophages in response to neutrophil elastase and TLR4 via TNFalpha and IFNbeta.

87 ing neutrophil markers (CD66b and neutrophil elastase) and NET markers (citrullinated histone H3 [H3C

88 s (CD68, CD3, CD8, CD4, CD20, and neutrophil elastase) and selected inflammatory markers (matrix meta

89 hilic (CD63, myeloperoxidase, and neutrophil elastase) and specific (CD66b and lactoferrin) granule m

90 alloproteinases, cathepsin K, and neutrophil elastase, and a variety of invertebrates and pathogens p

91 oteases, such as myeloperoxidase, neutrophil elastase, and matrix metalloproteinase 9, activates macr

92 phils in the pleural exudates, inhibition of elastase, and modulation of the survival-controlling pro

93 ncreatic enzymes (trypsin, carboxypeptidase, elastase, and others) not previously reported in DC.

94 e enzymes (matrix metalloproteinase [MMP]-8, elastase, and sialidase) in GCF and subgingival plaque l

95 rsely, overexpression of CCN3 mitigated both elastase- and angiotensin II-induced AAA formation in mi

96 hanism of AATD-induced emphysema from a pure elastase-antielastase imbalance to a much more complex o

97 Inhibitors of neutrophil elastase are now entering clinical trials with promising

98 tory proteins, including myeloperoxidase and elastase, are associated with tissue damage and are hall

99 g 3 d before abdominal aortic perfusion with elastase as prevention.

100 PAO1 transposon library identified the LasB elastase as the secreted effector involved in biofilm di

101 serine proteases, and especially neutrophil elastase, as candidates.

102 and alveolar epithelial cell markers in the elastase, as well as in CS-induced models of COPD.

103 flammatory cortisol to inflamed tissues upon elastase-based proteolysis of the exposed reactive cente

104 Thus, the elastase-biased agonism of PAR(2) causes Galphas-depende

105 ed significantly by inhibition of neutrophil elastase but not caspase-1.

106 proteins, we have identified that neutrophil elastase, but not other neutrophil derived proteases, cl

107 s we also excluded ADAM10, ADAM8, neutrophil elastase, cathepsin G, and proteinase 3 from contributin

108 Whereas neutrophil elastase, cathepsin G, and proteinase 3 have been known

109 nules, including the major serine proteases, elastase, cathepsin G, and proteinase 3, were absent.

110 ange of proteases (neutrophil and pancreatic elastases, cathepsin G, subtilisin, and trypsin) with a

111 Elastase caused PAR(2)-dependent sensitization of TRPV4

112 Chymotrypsin-like elastases (CELAs) are pancreatic serine proteinases that

113 Elastase cleaved human PAR(2) at Ala(66) downward arrowS

114 We showed previously that elastase cleaves CXCR1 and thereby impairs antibacterial

115 Here, we show that human neutrophil elastase cleaves thrombin, generating 11-kDa thrombin-de

116 A comparison of the interaction network with elastase complexes of canonical inhibitors from the chel

117 protein complexes (DNA-elastase and histone-elastase complexes), cell-free DNA, and neutrophil bioma

118 contribute to the development of novel anti-elastase compounds that resist rapid oxidation and prote

119 c expression of CXCL1, CXCL5, and neutrophil elastase correlated with measures of MS lesion burden an

120 for Pdx1 in pancreas organogenesis, we used Elastase-Cre-mediated recombination to inactivate Pdx1 i

121 In contrast to neutrophil elastase, CTSS activity was detectable in 100% of CF BAL

122 mponents by DNAse1 application or neutrophil elastase-deficient mice protected mice from ALI, whereas

123 educes lung inflammatory responses to LPS in elastase-deficient mice.

124 In vitro, LPS-induced cytokines from WT and elastase-deficient mouse neutrophils, as well as neutrop

125 zymes such as myeloperoxidase and neutrophil elastase did not contribute in mounting CNS inflammation

126 Although elastase did not promote recruitment of G protein-couple

127 s inability to promote receptor endocytosis, elastase did stimulate GRK6 recruitment.

128 and revealed the specific presence of active elastase during the process of neutrophil extracellular

129 is initiated at the codon ATG) of neutrophil elastase (ELANE) result in the production of N-terminall

130 Mutations in the gene for neutrophil elastase, ELANE, cause cyclic neutropenia (CyN) and seve

131 emphysema in a low AAT, and high neutrophil elastase environment in the lungs of affected individual

132 ated closely with the peak of neutrophil and elastase expression and activity.

133 ated matrix-metalloprotease-9 and neutrophil elastase expression, two proteases involved in blister f

134 estionnaire was completed, and weight, fecal elastase (FE), albumin, vitamins, and micronutrients mea

135 rat aortic smooth muscle cells treated with elastase for 1, 6, or 24 hours demonstrated that the p30

136 ranslocation of VLA-3, VLA-6, and neutrophil elastase from intracellular vesicles to the surface of M

137 ed construct under control of the insulin or elastase gene promoter, which targeted beta-cells and no

138 that this SNP in C5 alters the rate at which elastase generates active C5a in rheumatoid joints, henc

139 Elastase has also been shown to induce a pro-inflammator

140 NET components (elastase, histones, neutrophil gelatinase-associated lip

141 matory salivary biomarkers, Human Neutrophil Elastase (HNE) and Cathepsin-G, was constructed as proof

142 Human neutrophil elastase (HNE) is an attractive target for treating chro

143 Human neutrophil elastase (HNE) is an important therapeutic target for tr

144 inhibit bovine trypsin and human neutrophil elastase (HNE) with low nanomolar affinities.

145 ses, proteinase 3 (PR3) and human neutrophil elastase (HNE), are considered as targets for chronic in

146 , myeloperoxidase (MPO) and human neutrophil elastase (HNE), are inflammatory markers in CF airways,

147 ent from its structural homologue neutrophil elastase (HNE).

148 F purine aptamers that bind human neutrophil elastase (HNE).

149 Therapeutic inhibition of neutrophil-derived elastases holds promise with powerful treatment effects

150 atients is based on inhibition of neutrophil elastase; however, the benefit of this treatment remains

151 Elastase(+) human neutrophils were maximal during menstr

152 Additionally, elastase impairs differentiation of both primary and C2C

153 ttenuated the downstream cellular effects of elastase in an epithelial lung airway model system, alle

154 for lysosomal destabilization or neutrophil elastase in pneumolysin-mediated IL-1beta processing in

155 n cohort, a high concentration of neutrophil elastase in the wound was associated with infection and

156 roteolysis by co-existing host and bacterial elastases in inflamed/infected tissues remain unknown.

157 blocking experiments provided evidence that elastase increased intracellular presenilin-1 expression

158 Elastase induced PAR(2) coupling to Galphas but not Galp

159 Using an established murine elastase-induced AAA model, we demonstrate that segmenta

160 Using an elastase-induced AAA mouse model that recapitulates key

161 ment protein mannan-binding lectin abrogates elastase-induced AAA.

162 Our results identify a novel mechanism of elastase-induced activation of TRPV4 and expand the role

163 Adenylyl cyclase and PKA-mediated elastase-induced activation of TRPV4 and hyperexcitabili

164 rotecting bronchial epithelial cells against elastase-induced antiproliferation and abrogating the el

165 Blockade of RAGE ameliorates elastase-induced emphysema development and progression v

166 pression exacerbated airspace enlargement in elastase-induced emphysema in vivo.

167 Fam13a(-/-) mice were also resistant to elastase-induced emphysema, and this resistance was reve

168 LY294002 also inhibited elastase-induced p308 formation more in female smooth mu

169 literative changes in pulmonary arteries via elastase inhibition and caveolin-1-dependent amplificati

170 Collectively, these results show that elastase inhibition not only inhibits inflammation but a

171 ase profiling to reveal potent and selective elastase inhibition.

172 tory properties of AAT can be independent of elastase inhibition.

173 The endogenous elastase inhibitor elafin attenuates hypoxic pulmonary h

174 tivity comparable to the clinically approved elastase inhibitor sivelestat in short-term assays and d

175 Sivelestat, a neutrophil elastase inhibitor, and aquaporumab, a nonpathogenic IgG

176 by NET inhibition with DNAse or a neutrophil elastase inhibitor.

177 Clinical trials with neutrophil elastase inhibitors in lung and cardiovascular disease a

178 sults of preclinical studies with neutrophil elastase inhibitors remains challenging.

179 Synthetic elastase inhibitors reverse experimental pulmonary hyper

180 characterization of potent human neutrophil elastase inhibitors, which offer reversible covalent bin

181 reviously reported structural assignment and elastase inhibitory activity of the isolated natural pro

182 Here we show that clinical grade AAT (with elastase inhibitory activity) and a recombinant form of

183 Native and oxidized (lacking elastase inhibitory activity) forms of AAT were equally

184 using either a combination of mechanical and elastase injury at one site of mouse aorta (elastase mod

185 Mice were challenged with LPS/elastase intranasally over 4 weeks, resulting in a chron

186 We injected elastase intratracheally and the RAGE antagonist FPS-ZM1

187 In vitro studies demonstrate that neutrophil elastase is a key player in the LTB4 inflammatory cycle

188 als suggesting that affinity between AAT and elastase is strongly modulated by so-far overlooked addi

189 DRG after nerve injury and release leukocyte elastase (LE), which was inhibited by SerpinA3N derived

190 caspase-3, caspase-7, caspase-8, neutrophil elastase, legumain, and two matrix metalloproteinases (M

191 Elastase-like enzymes are involved in important diseases

192 nhibitory activities to trypsin/chymotrypsin/elastase-like enzymes based on the amino acids in cleave

193 dical and biotechnological potential, toward elastase-like enzymes by substitution of the P1 residue

194 structural aspects of their interaction with elastase-like enzymes have not been elucidated.

195 action between a BPTI-Kunitz-type domain and elastase-like enzymes.

196 tivity of BPTI-Kunitz-type inhibitors toward elastase-like enzymes.

197 neutrophilic CatC without affecting those of elastase-like serine proteases.

198 carried the characteristic histone proteins, elastase, lysozyme, myeloperoxidase, and metabolic enzym

199 RATIONALE: Macrophage elastase (matrix metalloproteinase [MMP]-12) is a potent

200 the tissue-destructive proteases macrophage elastase (matrix metalloproteinase-12) and gelatinase B

201 ell survival correlates with the kinetics of elastase-mediated degradation of the substrate to which

202 inin), affords protection against neutrophil elastase-mediated ENaC activation and Pseudomonas aerugi

203 developing as a pharmacotherapeutic against elastase-mediated pathologies.

204 tase activities are functionally involved in elastase-mediated regulation of CXCR1 surface expression

205 lammation in muscular dystrophy and indicate elastase-mediated regulation of myoblast behaviour as a

206 rier, and roles have also been described for elastase, MMP-13, gelatinases, mast cell proteases and p

207 ther functions of human neutrophils, such as elastase, MMP-9 and IL-8 production.

208 entration of 100 muM inhibited NEP activity, elastase, MMP-9 and IL-8 release from neutrophils by 77.

209 elastase injury at one site of mouse aorta (elastase model) or continuous infusion of angiotensin II

210 , findings were consistent with those in the elastase model, with a lower severity grade in PLTP-defi

211 ression of NET-bound antimicrobial proteins, elastase, myeloperoxidase, and cathepsin G, in response

212 Nucleosomes, double-stranded DNA, neutrophil elastase, myeloperoxidase, and myeloid-related protein 8

213 n NPs, showed colocalization with neutrophil elastase (n = 10), and did not colocalize with markers f

214 or of neutrophil serine proteases neutrophil elastase (NE) and cathepsin G (CG).

215 o neutrophil proteases, including neutrophil elastase (NE) and cathepsin G.

216 ependent upon the enzymes (PAD4), neutrophil elastase (NE) and myeloperoxidase (MPO).

217 es the RCL cleavage rate by human neutrophil elastase (NE) and Pseudomonas aeruginosa elastase (PAE)

218 Levels of neutrophil elastase (NE) and the nuclear factors CCAAT/enhancer-bin

219 Neutrophil elastase (NE) can be rapidly taken up by tumor cells tha

220 oteolytic cleavage of EC JAM-C by neutrophil elastase (NE) drove this cascade of events as supported

221 expression and downregulation of neutrophil elastase (NE) expression induced by obstructive injury.

222 Mutations in ELANE encoding neutrophil elastase (NE) have been identified in the majority of pa

223 ant with its primary target human neutrophil elastase (NE) in lipoprotein-containing plasma, but not

224 MP)-1, myeloperoxidase (MPO), and neutrophil elastase (NE) in patients with hypertension and chronic

225 Neutrophil elastase (NE) is a serine protease of relevance in infla

226 and factor and reveal significant neutrophil elastase (NE) proteolytic activity.

227 t C-sep isolated PMNs show higher neutrophil elastase (NE) release following activation by phorbol 12

228 om clinical studies suggests that neutrophil elastase (NE) released in neutrophilic airway inflammati

229 wnregulating the translocation of neutrophil elastase (NE) to the nucleus.

230 We investigated neutrophil elastase (NE), a potent serine protease detected in vuln

231 e (MMP)-9, myeloperoxidase (MPO), neutrophil elastase (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP

232 Purified NSPs cathepsin G (CG), neutrophil elastase (NE), and proteinase 3 cleaved C5aR to a 26- to

233 Deltaisp2/isp3), an inhibitor of neutrophil elastase (NE), died in RAW cells or macrophages from 129

234 ses, such as cathepsin G (CG) and neutrophil elastase (NE), have been implicated in the protective re

235 To investigate the levels of neutrophil elastase (NE), matrix metalloproteinases (MMPs), and mye

236 utrophil serine proteases (NSPs): neutrophil elastase (NE), proteinase 3, and cathepsin G.

237 evels of the natural inhibitor of neutrophil elastase (NE), secretory leukocyte protease inhibitor (S

238 mutations in ELANE, which encodes neutrophil elastase (NE).

239 of the epithelial barrier against neutrophil elastase (NE).

240 ema, much interest has focused on neutrophil elastase (NE).

241 ations in the ELANE gene encoding neutrophil elastase (NE).

242 While the effect of elastase on C2C12 cell survival correlates with the kine

243 C12 cells, suggesting a detrimental role for elastase on myogenesis in vivo.

244 This compound attenuated the effects of elastase on receptor activation, proteolytic processing

245 ate to which the cells adhere, the effect of elastase on satellite cell-derived primary myoblast grow

246 at inhibiting NETosis by blocking neutrophil elastase or by degrading NETs with DNase protects mice f

247 s the deletion of either caspase alone or of elastase or neutrophil proteinase 3 failed to prevent in

248 ADAMTS13 treated with either neutrophil elastase or plasmin was inhibited to a lesser extent, es

249 onchiectasis score was related to neutrophil elastase (P < 0.001) with CF-CT.

250 acidosis patients, including human leukocyte elastase (p < 0.001), proteinase-3 (p < 0.01), and myelo

251 hil elastase (NE) and Pseudomonas aeruginosa elastase (PAE) by different mechanisms.

252 ls (B2: 93% of total B cells) and T cells in elastase-perfused aortas compared with saline-perfused o

253 al IgG that binds to fibrinogen deposited in elastase-perfused aortic tissues, activates the compleme

254 Separately, exogenous A2AR antagonism in elastase-perfused WT mice also resulted in larger aneury

255 a of wild-type (C57BL/6) mice at day 7 after elastase perfusion and persisted through day 21.

256 increased at days 3, 7, and 14 after aortic elastase perfusion in C57BL/6 mice.

257 Elastase perfusion to induce AAA formation in A2AR-knock

258 Seven days after aneurysm induction by elastase perfusion, mice were randomly administered DMSO

259 ls, including angiotensin II-induced AAA and elastase perfusion-stimulated AAA.

260 Aortas were collected 14 d after elastase perfusion.

261 Elastase-positive neutrophils in the bronchial wall were

262 wley rats to intra-aortic porcine pancreatic elastase (PPE) (12 U/mL), AAA rupture was induced by dai

263 3L) exhibits a novel anti-porcine pancreatic elastase (PPE) activity together with a significantly im

264 -3 were associated with infection, and serum elastase predicted delayed healing.

265 01) with PRAGMA-CF was related to neutrophil elastase presence at age 3, whereas only the change in b

266 inar cells by using a full-length pancreatic elastase promoter-driven Cre.

267 ctions of C. violaceum CVO26 (violacein) and elastase, protease, pyocyanin and alginate production in

268 Desmosine was correlated with sputum elastase (r = 0.42; P < 0.0001) and was associated with

269 IgG-mediated elastase release and intracellular Ca(2+) mobilization w

270 with its native form, as shown by increased elastase release and intracellular calcium mobilization.

271 pofol did not alter superoxide generation or elastase release in a cell-free system.

272 activity, adhesion molecules expression and elastase release might play a role in the protective eff

273 erobic exercise on neutrophil degranulation (elastase release), activation of T lymphocytes (CD69 exp

274 significantly reduced superoxide generation, elastase release, and chemotaxis in human neutrophils ac

275 le to reduce QS-regulated virulence factors (elastase, rhamnolipid, and pyocyanin) and successfully i

276 dies establish a novel functional network of elastase, secretases, and PAR-2 that regulate CXCR1 expr

277 Elastase showed good discrimination for severe exacerbat

278 Elastase stimulated PAR(2)-dependent cAMP accumulation a

279 Elastase stimulated PAR(2)-dependent cAMP formation and

280 trypsin substrate, but not chymotrypsin and elastase substrates.

281 tation study identified adipsin as the major elastase that is induced in the Mgp(-/-) vascular smooth

282 These findings strongly indicate neutrophil elastase to be a key enzyme in the biological function o

283 Intraplantar injection of elastase to mice caused edema and mechanical hyperalgesi

284 Periadventitial application of elastase to murine thoracic aortas reproducibly produced

285 ellular trap (NET) formation, and neutrophil elastase translocation.

286 6 hours and were significantly higher in the elastase-treated cells compared with controls.

287 , as well as pro-MMP-2 and active MMP-2 from elastase-treated male rat aortic smooth muscle cells.

288 richness and diversity were decreased in LPS/elastase-treated mice, with an increased representation

289 Elastase-treated Raw cells produced increased p308 and s

290 s provided to mice with small AAAs 3 d after elastase treatment (n = 8 per group).

291 Male C57BL/6 mice undergoing elastase treatment showed a typical AAA phenotype (80% o

292 Elastase treatment to thoracic aortas resulted in progre

293 er day) or vehicle alone (control) underwent elastase treatment.

294 induced antiproliferation and abrogating the elastase-triggered induction of pro-inflammatory cytokin

295 KRK(178)), plasmin (Lys-189), and neutrophil elastase (Val-182 and Val-193) sites.

296 only approved small molecule drug targeting elastase, which indicated its potential in developing as

297 in the production of N-terminally truncated elastase, which mislocates to the nucleus and results in

298 helial-bound MPO than for circulating MPO or elastase with respect to blood pressure regulation.

299 racotomy with application of periadventitial elastase (WT TAA) or saline (WT control; n=30 per group)

300 shared by human proteinase 3 and neutrophil elastase, yielded an agonist that was resistant to neutr