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1 enzymes myeloperoxidase (MPO) and neutrophil elastase.
2 zymes, myeloperoxidase, and human neutrophil elastase.
3  histone H3 and with the specific neutrophil elastase.
4 s was upregulated by wounding and neutrophil elastase.
5 in and 82% with the azurophil granule marker elastase.
6 ssion of other virulence traits, such as the elastase.
7 e asthma were stained for OSM and neutrophil elastase.
8  protease such as trypsin, chymotrypsin, and elastase.
9 ant levels of the histone H2Ax or neutrophil elastase.
10  (AAT) Z-variant with catalytically inactive elastase.
11 f matrix metalloproteinase-12 and neutrophil elastase.
12 e stoichiometry of inhibition for neutrophil elastase.
13 mphysema by loss of inhibition of neutrophil elastase.
14 ained inhibitory activity against neutrophil elastase.
15 ury, depending on the presence of neutrophil elastase.
16 peroxidase (MPO), azurocidin, and neutrophil elastase.
17  reduced levels of membrane-bound neutrophil elastase.
18 lic and mean blood pressure was level of PMN elastase.
19 , trypsin, neutral protease, thermolysin, or elastase.
20 protect lung tissue by inhibiting neutrophil elastase.
21  EAP family member EapH1 bound to neutrophil elastase.
22 ntibodies for CD8, CD14, CD31, CD79alpha and elastase.
23 eutrophil granule serine protease neutrophil elastase.
24  the discovery of 23 hits against neutrophil elastase.
25  roles is that of an activator of neutrophil elastase.
26 ct the pool of active, functional neutrophil elastase.
27 th elevated salivary aMMP-8 but not with PMN elastase.
28 cificity against trypsin or human neutrophil elastase.
29  RCL proteolysis by endogenous and exogenous elastases.
30 electivity against pancreatic and neutrophil elastases.
31 nstrated an association of chymotrypsin-like elastase 1 (Cela1) with lung elastin remodeling, and tha
32 rkers of pancreatic function improved (fecal elastase-1 concentrations increased and serum immunoreac
33               In addition, we reveal that an elastase 2 cleavage site is present between FNIII EDA an
34 ter cleavage of the FNIII 12-13-14 domain by elastase 2.
35 Using threshold values of MMP-8 (94 ng/muL), elastase (33 ng/muL), sialidase (23 ng/muL), and levels
36 ), carbonic anhydrase II(-) (mature ductal), elastase 3a (acinar)(-) , and insulin(-) subpopulations.
37 the gene encoding pancreas-specific protease Elastase 3B (CELA3B) that cosegregates with disease.
38           We investigated whether neutrophil elastase, a biased agonist of PAR(2), causes inflammatio
39 ity, and inhibited the release of neutrophil elastase--a marker of neutrophil extracellular trap form
40        We apply PK105b to measure neutrophil elastase activation in an acute model of experimental co
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  protease inhibitory function as measured by elastase activity assay.
47 lysis showed increased fecal proteolytic and elastase activity before UC onset.
48                            This induction of elastase activity did not occur with UVB.
49 sts to monitor dynamic changes in neutrophil elastase activity during lung infection and to assess th
50 as matrix metalloproteinase 9 and neutrophil elastase activity in culture supernatant, as well as rea
51                                              Elastase activity in sputum was associated with the bron
52 , PK105b facilitates detection of neutrophil elastase activity in tissue lysates, and we have applied
53                                       Sputum elastase activity increased at exacerbations (P = 0.001)
54                                              Elastase activity inversely correlated with the relative
55                            Sputum neutrophil elastase activity is a biomarker of disease severity and
56                                   Neutrophil elastase activity is detected in inflamed, but not healt
57                                 We show that elastase activity is increased in dystrophic (mdx(4cv))
58 rement, and 381 provided sputum for baseline elastase activity measurements using an activity-based i
59  as well as by a chloroamidine sensitive and elastase activity mechanism.
60   During a 3-year follow-up, elevated sputum elastase activity was associated with a higher frequency
61                                         High elastase activity was confirmed in Bacteroides isolates
62                                       Sputum elastase activity was independently associated with FEV1
63 th both brensocatib doses, sputum neutrophil elastase activity was reduced from baseline over the 24-
64 ons (secondary end point), sputum neutrophil elastase activity, and safety were assessed.
65 coinfections had higher levels of neutrophil elastase activity, as well as myeloperoxidase levels com
66 t this early/rapid mechanism is dependent on elastase activity, but independent of ROS generation and
67  probes have been used to measure neutrophil elastase activity, though these tools lack specificity a
68  receptor 2 (BMPR2) signaling, and increased elastase activity.
69 lA) and increased neutrophil recruitment and elastase activity.
70 deoxyguanosine (8-OHdG) and human neutrophil elastase/alpha1-proteinase inhibitor (HNE/alpha1-PI) com
71 plied to detect the presence and activity of elastase, an enzyme released by the cercarial larvae sta
72 latile reporters upon cleavage by neutrophil elastase, an inflammation-associated protease with eleva
73 roduced through cleavage by human neutrophil elastase and aggregate lipopolysaccharide (LPS) and the
74  9 activity in resolvin-treated mice in both elastase and angiotensin II models.
75                              An imbalance of elastase and antielastase, along with innate inflammatio
76 y, reduced serine protease activity in BALF (elastase and cathepsin G), plasma elastase footprint (Aa
77 hilic granules to release the Ser proteases, elastase and cathepsin G, resulting in the proteolytic d
78 tly improved inhibition of human neuthrophil elastase and chymotrypsin.
79 er of the serpin superfamily and a leukocyte elastase and crosstalk between neurons and T cells in th
80                   NET protein complexes (DNA-elastase and histone-elastase complexes), cell-free DNA,
81  airway obstruction, reduction in neutrophil elastase and inflammation.
82 f A1A1 and A1A2 variants of beta-casein with elastase and leucine aminopeptidase revealed the release
83 ein, sensitivity against the human leukocyte elastase and microcolony formation.
84              Proteases, including neutrophil elastase and MMPs (matrix metalloproteases), modulate ce
85 loperoxidase and higher levels of neutrophil elastase and myeloperoxidase activity in apical surface
86 ptor 9 (TLR9)-mediated release of neutrophil elastase and proteinase 3 and subsequent down-regulation
87        A leukocyte origin of human leukocyte elastase and proteinase-3 in diabetic ketoacidosis was c
88                                  Circulating elastase and proteinase-3 were associated with infection
89 nal region by neutrophil proteases including elastase and proteinase-3, generating the 33-kDa isoform
90 racellular trap (NET) release independent of elastase and reduced NAD phosphate-oxidase activation.
91                 RATIONALE: Sputum neutrophil elastase and serum desmosine, which is a linked marker o
92  which dose-dependently inhibited neutrophil elastase and shortened resolution intervals.
93  variant was more sensitive to cleavage with elastase and the "C5a" generated was biologically active
94 jor by macrophages in response to neutrophil elastase and TLR4 via TNFalpha and IFNbeta.
95 ed Q0(bolton)-AAT protein to bind neutrophil elastase and to inhibit protease activity.
96 ing neutrophil markers (CD66b and neutrophil elastase) and NET markers (citrullinated histone H3 [H3C
97 hilic (CD63, myeloperoxidase, and neutrophil elastase) and specific (CD66b and lactoferrin) granule m
98 oteases, such as myeloperoxidase, neutrophil elastase, and matrix metalloproteinase 9, activates macr
99 phils in the pleural exudates, inhibition of elastase, and modulation of the survival-controlling pro
100 in Results: Mice exposed to chronic CS or to elastase, and patients with chronic obstructive pulmonar
101 e enzymes (matrix metalloproteinase [MMP]-8, elastase, and sialidase) in GCF and subgingival plaque l
102 ollowing markers (CD4, CD5, CD8, CD14, CD19, Elastase, and Syndecan).
103 rsely, overexpression of CCN3 mitigated both elastase- and angiotensin II-induced AAA formation in mi
104 ], polymorphonuclear leukocyte elastase [PMN elastase], and total protein, albumin, immunoglobulin A,
105 hanism of AATD-induced emphysema from a pure elastase-antielastase imbalance to a much more complex o
106 tory proteins, including myeloperoxidase and elastase, are associated with tissue damage and are hall
107 ophil serine proteases, including neutrophil elastase, are increased in the sputum of patients with b
108       Using Pseudomonas aeruginosa producing elastase as a model, we show gluten-independent, PAR-2 m
109 g 3 d before abdominal aortic perfusion with elastase as prevention.
110  serine proteases, and especially neutrophil elastase, as candidates.
111  and alveolar epithelial cell markers in the elastase, as well as in CS-induced models of COPD.
112 flammatory cortisol to inflamed tissues upon elastase-based proteolysis of the exposed reactive cente
113 ntial digestion, as had been shown by us for elastase before.
114                                    Thus, the elastase-biased agonism of PAR(2) causes Galphas-depende
115 motaxis), a reduction in systemic neutrophil elastase burden, and improved Sequential Organ Failure A
116 ed significantly by inhibition of neutrophil elastase but not caspase-1.
117 proteins, we have identified that neutrophil elastase, but not other neutrophil derived proteases, cl
118            We also measured fecal pancreatic elastase by enzyme-linked immunosorbent assay and perfor
119  decline (n = 60) and plasma anti-neutrophil elastase capacity (n = 20).Measurements and Main Results
120                     Finally, anti-neutrophil elastase capacity did not differ between former smokers
121 s we also excluded ADAM10, ADAM8, neutrophil elastase, cathepsin G, and proteinase 3 from contributin
122 ine proteases polymorphonuclear (neutrophil) elastase, cathepsin G, and proteinase 3, but not neutrop
123 eutrophil serine proteases (NSPs) neutrophil elastase, cathepsin-G, and proteinase-3.
124 ange of proteases (neutrophil and pancreatic elastases, cathepsin G, subtilisin, and trypsin) with a
125                                              Elastase caused PAR(2)-dependent sensitization of TRPV4
126                            Chymotrypsin-like elastases (CELAs) are pancreatic serine proteinases that
127 utations in the gene encoding the pancreatic elastase chymotrypsin-like elastase family member 2A (CE
128                                              Elastase cleaved human PAR(2) at Ala(66) downward arrowS
129          Here, we show that human neutrophil elastase cleaves thrombin, generating 11-kDa thrombin-de
130 A comparison of the interaction network with elastase complexes of canonical inhibitors from the chel
131  protein complexes (DNA-elastase and histone-elastase complexes), cell-free DNA, and neutrophil bioma
132  contribute to the development of novel anti-elastase compounds that resist rapid oxidation and prote
133 c expression of CXCL1, CXCL5, and neutrophil elastase correlated with measures of MS lesion burden an
134  for Pdx1 in pancreas organogenesis, we used Elastase-Cre-mediated recombination to inactivate Pdx1 i
135                    In contrast to neutrophil elastase, CTSS activity was detectable in 100% of CF BAL
136 owth factor beta1), downstream of neutrophil elastase, decreased mucociliary parameters in vitro.
137                                     Although elastase did not promote recruitment of G protein-couple
138 s inability to promote receptor endocytosis, elastase did stimulate GRK6 recruitment.
139 is initiated at the codon ATG) of neutrophil elastase (ELANE) result in the production of N-terminall
140 dem mass spectrometry in BAL fluid of CS- or elastase-exposed mice, and GCS was detected by Western b
141 ated closely with the peak of neutrophil and elastase expression and activity.
142 ated matrix-metalloprotease-9 and neutrophil elastase expression, two proteases involved in blister f
143 ng the pancreatic elastase chymotrypsin-like elastase family member 2A (CELA2A).
144 estionnaire was completed, and weight, fecal elastase (FE), albumin, vitamins, and micronutrients mea
145 y in BALF (elastase and cathepsin G), plasma elastase footprint (Aalpha-Val(360)), and markers of ela
146 el, ewes inhaled CFTR(inh)172 and neutrophil elastase for 3 days, which resulted in prolonged trachea
147 tease inhibitor therapy targeting neutrophil elastase for the treatment of alpha-1 antitrypsin defici
148 ranslocation of VLA-3, VLA-6, and neutrophil elastase from intracellular vesicles to the surface of M
149 that this SNP in C5 alters the rate at which elastase generates active C5a in rheumatoid joints, henc
150                              NET components (elastase, histones, neutrophil gelatinase-associated lip
151 matory salivary biomarkers, Human Neutrophil Elastase (HNE) and Cathepsin-G, was constructed as proof
152 athelicidin, and the enzyme human neutrophil elastase (HNE) were measured in over 1,000 cervicovagina
153  inhibit bovine trypsin and human neutrophil elastase (HNE) with low nanomolar affinities.
154 , myeloperoxidase (MPO) and human neutrophil elastase (HNE), are inflammatory markers in CF airways,
155 F purine aptamers that bind human neutrophil elastase (HNE).
156 n of covalent inhibitors of human neutrophil elastase (hNE).
157 fered considerably from that with neutrophil elastase, however, with far greater contributions from t
158                                              Elastase(+) human neutrophils were maximal during menstr
159                                Additionally, elastase impairs differentiation of both primary and C2C
160 ivity-based probe, which binds to neutrophil elastase in an activity-dependent manner.
161  for lysosomal destabilization or neutrophil elastase in pneumolysin-mediated IL-1beta processing in
162 n cohort, a high concentration of neutrophil elastase in the wound was associated with infection and
163 roteolysis by co-existing host and bacterial elastases in inflamed/infected tissues remain unknown.
164                                              Elastase induced PAR(2) coupling to Galphas but not Galp
165                  Using an established murine elastase-induced AAA model, we demonstrate that segmenta
166    Our results identify a novel mechanism of elastase-induced activation of TRPV4 and expand the role
167            Adenylyl cyclase and PKA-mediated elastase-induced activation of TRPV4 and hyperexcitabili
168 rotecting bronchial epithelial cells against elastase-induced antiproliferation and abrogating the el
169 res from patients with COPD and in mice with elastase-induced COPD-like changes.
170                 Blockade of RAGE ameliorates elastase-induced emphysema development and progression v
171 pression exacerbated airspace enlargement in elastase-induced emphysema in vivo.
172                      Using a murine model of elastase-induced emphysema we demonstrated that the most
173      Fam13a(-/-) mice were also resistant to elastase-induced emphysema, and this resistance was reve
174 literative changes in pulmonary arteries via elastase inhibition and caveolin-1-dependent amplificati
175        Collectively, these results show that elastase inhibition not only inhibits inflammation but a
176 ed whether co-administration of a neutrophil elastase inhibitor (NEI) could rescue the ability of EdT
177                               The endogenous elastase inhibitor elafin attenuates hypoxic pulmonary h
178 cus sabdariffa, as a knottin-type neutrophil elastase inhibitor.
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 philic granules causes leakage of neutrophil elastase into the cytosol, resulting in secondary cleava
183                Mice were challenged with LPS/elastase intranasally over 4 weeks, resulting in a chron
184                                  We injected elastase intratracheally and the RAGE antagonist FPS-ZM1
185 In vitro studies demonstrate that neutrophil elastase is a key player in the LTB4 inflammatory cycle
186                                   Neutrophil elastase is a serine protease that has been implicated i
187 als suggesting that affinity between AAT and elastase is strongly modulated by so-far overlooked addi
188 t has been shown that Pseudomonas aeruginosa elastase (LasB) and Clostridium histolyticum (Hathewaya
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                    Differences in pancreatic elastase levels associated with significantly (P < .0001
192                                              Elastase-like enzymes are involved in important diseases
193 nhibitory activities to trypsin/chymotrypsin/elastase-like enzymes based on the amino acids in cleave
194 dical and biotechnological potential, toward elastase-like enzymes by substitution of the P1 residue
195 structural aspects of their interaction with elastase-like enzymes have not been elucidated.
196 action between a BPTI-Kunitz-type domain and elastase-like enzymes.
197 tivity of BPTI-Kunitz-type inhibitors toward elastase-like enzymes.
198 neutrophilic CatC without affecting those of elastase-like serine proteases.
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                                   Macrophage elastase [matrix metalloproteinase (MMP)-12] is the most
202 ell survival correlates with the kinetics of elastase-mediated degradation of the substrate to which
203 inin), affords protection against neutrophil elastase-mediated ENaC activation and Pseudomonas aerugi
204  developing as a pharmacotherapeutic against elastase-mediated pathologies.
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    Measurements and Main Results: Neutrophil elastase, MMP-2, and MMP-9 activities and protein levels
208 nzymes proteinase 3, cathepsin G, neutrophil elastase, MMP7 or MMP9/12 were prognostic biomarkers for
209                                     Using an elastase model, we demonstrated that absence of IgG resu
210 ression of NET-bound antimicrobial proteins, elastase, myeloperoxidase, and cathepsin G, in response
211 Nucleosomes, double-stranded DNA, neutrophil elastase, myeloperoxidase, and myeloid-related protein 8
212 n NPs, showed colocalization with neutrophil elastase (n = 10), and did not colocalize with markers f
213 (controls), mice with deletion of neutrophil elastase (NE(-/-)) or peptidyl arginine deiminase type I
214 terized by the presence of excess neutrophil elastase (NE) activity in tissues, including cystic fibr
215                 Neutrophil proteases such as elastase (NE) and cathepsin G (CG) attach to NETs and co
216 o neutrophil proteases, including neutrophil elastase (NE) and cathepsin G.
217 ependent upon the enzymes (PAD4), neutrophil elastase (NE) and myeloperoxidase (MPO).
218 es the RCL cleavage rate by human neutrophil elastase (NE) and Pseudomonas aeruginosa elastase (PAE)
219                         Levels of neutrophil elastase (NE) and the nuclear factors CCAAT/enhancer-bin
220                                   Neutrophil elastase (NE) can be rapidly taken up by tumor cells tha
221 a-arrestins, cathepsin-S (CS) and neutrophil elastase (NE) cleave PAR(2) at distinct sites and activa
222 oteolytic cleavage of EC JAM-C by neutrophil elastase (NE) drove this cascade of events as supported
223 anovesicles acquire surface-bound neutrophil elastase (NE) during PMN degranulation, NE being oriente
224  expression and downregulation of neutrophil elastase (NE) expression induced by obstructive injury.
225                      The protease neutrophil elastase (NE) has been implicated in the formation of NE
226       Mutations in ELANE encoding neutrophil elastase (NE) have been identified in the majority of pa
227  permeability, elevated levels of neutrophil elastase (NE) have been reported in inflamed colonic muc
228 ant with its primary target human neutrophil elastase (NE) in lipoprotein-containing plasma, but not
229                                   Neutrophil elastase (NE) is a serine protease of relevance in infla
230 e peptidases (ISP) 2, inactivates neutrophil elastase (NE) present at the macrophage surface, resulti
231 and factor and reveal significant neutrophil elastase (NE) proteolytic activity.
232 t C-sep isolated PMNs show higher neutrophil elastase (NE) release following activation by phorbol 12
233 gulated hepatocyte clock-genes by neutrophil elastase (NE) secretion.
234                   We investigated neutrophil elastase (NE), a potent serine protease detected in vuln
235 e (MMP)-9, myeloperoxidase (MPO), neutrophil elastase (NE), and MMP-9/tissue inhibitor of MMP-1 (TIMP
236 ses, such as cathepsin G (CG) and neutrophil elastase (NE), have been implicated in the protective re
237      To investigate the levels of neutrophil elastase (NE), matrix metalloproteinases (MMPs), and mye
238 utrophil serine proteases (NSPs): neutrophil elastase (NE), proteinase 3, and cathepsin G.
239 ively exocytose the primary granule protease elastase (NE), whose extracellular activity correlates w
240 mutations in ELANE, which encodes neutrophil elastase (NE).
241 of the epithelial barrier against neutrophil elastase (NE).
242 se because of germline mutations in the gene elastase, neutrophil-expressed (ELANE) encoding the neut
243                          While the effect of elastase on C2C12 cell survival correlates with the kine
244 C12 cells, suggesting a detrimental role for elastase on myogenesis in vivo.
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      ADAMTS13 treated with either neutrophil elastase or plasmin was inhibited to a lesser extent, es
248 c 2' substituents that bind human neutrophil elastase or the blood coagulation protein factor IXa.
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       Seven days after aneurysm induction by elastase perfusion, mice were randomly administered DMSO
253 ls, including angiotensin II-induced AAA and elastase perfusion-stimulated AAA.
254             Aortas were collected 14 d after elastase perfusion.
255 nase-8 [aMMP-8], polymorphonuclear leukocyte elastase [PMN elastase], and total protein, albumin, imm
256 wley rats to intra-aortic porcine pancreatic elastase (PPE) (12 U/mL), AAA rupture was induced by dai
257 3L) exhibits a novel anti-porcine pancreatic elastase (PPE) activity together with a significantly im
258 -3 were associated with infection, and serum elastase predicted delayed healing.
259 01) with PRAGMA-CF was related to neutrophil elastase presence at age 3, whereas only the change in b
260 ad NSGM so identified neutralized neutrophil elastase present in the sputum of CF patients in the pre
261 inar cells by using a full-length pancreatic elastase promoter-driven Cre.
262                                   Neutrophil elastase promotes Leishmania donovani infection via inte
263 ctions of C. violaceum CVO26 (violacein) and elastase, protease, pyocyanin and alginate production in
264         Desmosine was correlated with sputum elastase (r = 0.42; P < 0.0001) and was associated with
265                               Elimination of elastase-related neutrophil proteases may reduce the pro
266               A depletion of proinflammatory elastase-related proteases in neutrophils is observed in
267 dress and counterbalance unwanted effects of elastase-related proteases, chemical inhibitors of CatC
268 dase that activates most of tissue-degrading elastase-related serine proteases.
269  as significantly lower levels of neutrophil-elastase release, O(2)(-) production and phagolysosome f
270 cated both trypsin-responsive and neutrophil elastase-responsive polymeric Nano-in-Microgel to show t
271 le to reduce QS-regulated virulence factors (elastase, rhamnolipid, and pyocyanin) and successfully i
272                                              Elastase showed good discrimination for severe exacerbat
273 ophilin, programmed cell death-ligand 1, and elastase staining and other patient, tumor and treatment
274                                              Elastase stimulated PAR(2)-dependent cAMP accumulation a
275                                              Elastase stimulated PAR(2)-dependent cAMP formation and
276 n the previously determined EapH1-neutrophil elastase structure.
277 ice expressing CeD risk genes, P. aeruginosa elastase synergizes with gluten to induce more severe in
278                                              Elastase that is produced by neutrophils both coats the
279  the K(i) for EapH1 inhibition of neutrophil elastase, the time dependence of inhibition was maintain
280  These findings strongly indicate neutrophil elastase to be a key enzyme in the biological function o
281                    Intraplantar injection of elastase to mice caused edema and mechanical hyperalgesi
282 quential-digestion strategy with trypsin and elastase to penetrate regions with a low density of tryp
283 ntrinsic substrate-recognition properties of elastase to specifically target larger tryptic peptides.
284 ellular trap (NET) formation, and neutrophil elastase translocation.
285 richness and diversity were decreased in LPS/elastase-treated mice, with an increased representation
286                                   Similarly, elastase-treated TRPV4(-/-) mice had a significant decre
287  a specific TRPV4 antagonist, GSK2193874, in elastase-treated WT mice and in AngII-treated ApoE(-/-)
288 mmation, and vascular remodeling compared to elastase-treated WT mice on Day 14.
289 s provided to mice with small AAAs 3 d after elastase treatment (n = 8 per group).
290 er day) or vehicle alone (control) underwent elastase treatment.
291                                          The elastase-treatment model of AAA in C57BL6 (WT) mice and
292 induced antiproliferation and abrogating the elastase-triggered induction of pro-inflammatory cytokin
293 ntraluminal aorta to PPE (porcine pancreatic elastase) under pressure to induce aneurysmal degenerati
294  mediated via their production of neutrophil elastase, was rendered less effective.
295 defective neutrophil infiltration or lacking elastase were protected against steatosis correlating wi
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 eting the heparin-binding site of neutrophil elastase would offer a therapeutic paradigm.
300 racotomy with application of periadventitial elastase (WT TAA) or saline (WT control; n=30 per group)

 
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