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1 (LPA; acting through the LPA1 receptor) and endothelin.
2 othelial cells by vasoactive signals such as endothelins.
3 orsal Jag1 expression but also by inhibiting endothelin 1 (Edn1) expression in the pharyngeal endoder
4 perturbations demonstrates complex roles for Endothelin 1 (Edn1) signaling in the intermediate joint-
5 emonstrate rs9349379 regulates expression of endothelin 1 (EDN1), a gene located 600 kb upstream of P
6 etermine the selective affinity of EDNRA for endothelin 1 (EDN1), its major physiological ligand, and
7 ular density) and the potent vasoconstrictor endothelin 1 (EDN1); we assayed the activity of angioten
9 des, of which 3 distinct isoforms exist, and endothelin 1 (ET-1) is the most abundant and the best-ch
11 mpaired vasodilator reactivity and increased endothelin 1 (ET-1)-mediated vasoconstriction, two abnor
12 th the concentration of the vasoconstrictor, endothelin 1 (P = 0.0005), and negatively with the conce
13 eased expression of vasoconstrictor molecule endothelin 1 and a concomitant decrease in vasodilatory
15 ycoprotein to proteolipid protein 1 and both endothelin 1 and vascular endothelial growth factor.
17 e C signaling, glutamate receptor signaling, endothelin 1 signaling, and cardiac hypertrophy signalin
18 ects, but not in vascular dementia, in which endothelin 1 tended to be elevated, perhaps reflecting a
19 r analysis of the Bristol cohort showed that endothelin 1 was reduced in the white matter in Alzheime
20 amma inducible protein 10 (IP10; CXCL10) and endothelin 1 were raised and strongly correlated togethe
21 e complement anaphylatoxins C3a and C5a, and endothelin 1, induced human MCs rapidly to secrete small
24 er quartile); pulmonary hypertension and low endothelin-1 <1.7 pg/mL; lower 3 quartiles); no pulmonar
25 ould be explained by an enhanced response to endothelin-1 (20% greater reduction in lumen diameter, P
28 nduced glomerulosclerosis is associated with endothelin-1 (EDN1) release by podocytes, which mediates
30 newborn arteries also expresses and releases endothelin-1 (ET-1) and initiates endothelium-dependent
31 s, correlate with increased plasma levels of endothelin-1 (ET-1) and other functional markers of PH i
38 ivation of endothelin-A receptor (ET(A)R) by endothelin-1 (ET-1) drives epithelial-to-mesenchymal tra
39 (NGAL), kidney injury molecule-1 (KIM-1) and endothelin-1 (ET-1) during EVKP in a series of discarded
40 Endothelial expression and the release of endothelin-1 (ET-1) in levels sufficient to initiate vas
45 termine whether vascular endothelial-derived endothelin-1 (ET-1) is important for skin Na(+) bufferin
46 ceptor mediating the vasodilatory effects of endothelin-1 (ET-1) is induced by OA-NO2 Inasmuch as ET-
47 tic brain injury or subarachnoid hemorrhage, endothelin-1 (ET-1) is induced resulting in cerebral vas
52 rum concentrations of the vasoactive protein endothelin-1 (ET-1) occur in the setting of systemic inf
53 The present study investigated the effect of endothelin-1 (ET-1) on cholinergic mechanisms of end-org
54 n endogenous inhibitor of NO production, and endothelin-1 (ET-1) oppose the actions of NO, suggesting
56 edominantly responsible for producing active endothelin-1 (ET-1), a mitogenic peptide implicated in t
57 ) correlated with increased plasma levels of endothelin-1 (ET-1), a potent vasoconstrictor, in sickle
59 ed an endogenous inhibitor of remyelination, Endothelin-1 (ET-1), which is highly expressed in reacti
63 ubgroup with pulmonary hypertension and high endothelin-1 (high endothelin-1: >/=1.7 pg/mL; upper qua
65 these proteins in DN, and demonstrated that endothelin-1 activates podocytes to release heparanase.
67 of ARHGAP18 resulted in a failure to secrete endothelin-1 and a reduction in neutrophil transmigratio
68 r basal conditions and after the addition of endothelin-1 and abnormal spontaneous Ca(2+) release eve
70 y PGP levels associate with both circulating endothelin-1 and acute rejection in cardiac transplant p
71 eraction with GRK2 is inversely regulated by endothelin-1 and CAV1 scaffolding domain after liver inj
72 lacylcarnitines correlated with increases in endothelin-1 and creatinine/cystatin C, respectively.
74 -beta1 signaling and increased expression of endothelin-1 and genes involved in VSMC contraction, hig
78 Despite pathophysiological links between endothelin-1 and pulmonary vascular remodeling, to our k
79 e previously showed that both heparanase and endothelin-1 are essential for the development of DN.
80 es of evidence have demonstrated the role of endothelin-1 as both a constrictor of uterine myometrial
88 Stimulation of primary mouse podocytes with endothelin-1 elicited rapid calcium transients mediated
92 fibroblasts were treated with 20 and 100 nM endothelin-1 for 6 and 24 hours and then collected to as
93 en a modest ( approximately 35%) decrease in endothelin-1 gene (Edn1) expression is sufficient to cau
96 generated low-expressing and high-expressing endothelin-1 genes (L and H) and have bred mice with fou
97 phy signaling triggered by angiotensin II or endothelin-1 in HEK293T cells as well as in neonatal and
100 s not known whether elevated serum levels of endothelin-1 indicate future risk of kidney disease in t
102 0.05), but not in vascular endothelial cell endothelin-1 knockout (VEET KO) mice (76.4 +/- 5.7 pg/mg
103 ular risk in black adults, we measured serum endothelin-1 level at baseline (2000-2004; n=3538).
104 Phenotyping by pulmonary hypertension and endothelin-1 level showed mortality decreasing in order
106 ur knowledge, the association between plasma endothelin-1 levels and pulmonary hypertension has not b
107 ied African American individuals with plasma endothelin-1 levels and tricuspid regurgitation on echoc
109 en-binding activity, soluble E-selectin, and endothelin-1 levels by using ELISA and BRAHMS Kryptor te
112 g for potential confounders, log-transformed endothelin-1 levels were associated with increased odds
115 terminal telopeptide of collagen type I, and endothelin-1 levels were higher in diabetic patients (p
118 tion of the endothelin-A receptor (EDNRA) by endothelin-1 may play a role in the disease because the
119 However, no direct pathogenic effect of endothelin-1 on podocytes has been shown in vivo and end
120 hese results indicate that activation of the endothelin-1 pathways selectively in podocytes mediates
124 Our data do not support the use of the dual endothelin-1 receptor antagonist, bosentan, in patients
126 , whereas pretreatment of rats with the dual endothelin-1 receptor blocker, bosentan, improved cell e
127 ion was associated with increased glomerular endothelin-1 receptor type A (Ednra) expression and incr
130 in-1 on podocytes has been shown in vivo and endothelin-1 signaling in podocytes has not been investi
134 anti-angiotensin II type-1 receptor and anti-endothelin-1 type A receptor autoantibodies are associat
135 tatus for angiotensin II type-1 receptor and endothelin-1 type A receptor autoantibodies pre-LT, and
138 the effect of IRL-1620 [Suc-[Glu9,Ala11,15]-Endothelin-1(8-12)] on astrocytes, neurons, and vascular
139 ious pruritogens (histamine, chloroquine, or endothelin-1) and recorded spontaneous scratching before
140 ddressing 1 abnormality (eg, upregulation of endothelin-1) and were not developed specifically for PA
141 en-binding activity, soluble E-selectin, and endothelin-1) were significantly increased during HAE at
142 to histaminergic (histamine, compound 48/80, endothelin-1), not non-histaminergic (chloroquine) pruri
145 (adjusted hazard ratio per log increment in endothelin-1, 1.57, 95% CI, 1.05-2.37; median follow-up,
147 (adjusted hazard ratio per log increment in endothelin-1, 1.69; 95% CI, 1.27-2.25; median follow-up,
150 is determined by venous endothelium-derived endothelin-1, acting through its specific receptor Ednra
151 activation, such as smooth muscle actin and Endothelin-1, and all of these genes play a key role in
153 transforming growth factor beta1 (TGFbeta1), endothelin-1, and NAD(P)H oxidase 4 also occur in parall
154 k involving transforming growth factor-beta, endothelin-1, angiotensin II, CCN2 (connective tissue gr
155 procalcitonin, MR-pro-adrenomedullin, CT-pro-endothelin-1, CT-pro-arginine vasopressin, and MR-pro-at
156 such as transforming growth factor beta1 and endothelin-1, enhance RBC NADPH oxidase activity and inc
158 l as in human disease, including the role of endothelin-1, pulmonary monocytes, and angiogenesis.
159 iewed, including nitric oxide, prostacyclin, endothelin-1, reactive oxygen species, and endothelial a
160 with elevated vasoconstrictor signalling via endothelin-1, reduces the local vasodilatory response to
161 activated gene networks involved in calcium, endothelin-1, renin-angiotensin, and cardiac beta-adrene
162 pro-B-type natriuretic peptide, aldosterone, endothelin-1, troponin I, and C-telopeptide for type I c
163 s elicited by phenylephrine, angiotensin II, endothelin-1, U46619, and K(+)-induced membrane depolari
164 n enhances epidermal expression of TRPV4 and endothelin-1, underscoring the potential of keratinocyte
165 ce has been associated with raised levels of endothelin-1, which are common both before and after Fon
170 ary hypertension and high endothelin-1 (high endothelin-1: >/=1.7 pg/mL; upper quartile); pulmonary h
171 artiles); no pulmonary hypertension and high endothelin-1; and no pulmonary hypertension and low endo
172 a and recruitment of vasoconstrictors (e.g., endothelin-1; Edn1) leads to clearance of transplanted c
173 ased pressor responses to angiotensin II and endothelin-1; these effects are prevented by treatment w
175 e mice, infusion of vasoconstrictors (either endothelin 2 or angiotensin 2) into the bursa restored t
176 responsible for this regenerative effect of endothelin 2, analysis of both remyelination following e
177 etinae identified several cytokines (CXCL13, endothelin 2, CCL20 and CXCL2) to be significantly upreg
178 Although increasing evidence indicates that endothelin-2 (Edn2) has distinct roles in tissue patholo
180 in white mutants a transcriptional defect in endothelin 3 (edn3), encoding a peptide factor that prom
181 d by molecules such as the signaling protein endothelin 3 (EDN3), its receptor (the endothelin recept
187 dothelin signaling via the activation of the endothelin-A receptor (EDNRA) by endothelin-1 may play a
189 o three groups: placebo (RVD+PTRAS), chronic endothelin-A receptor (ET-A) blockade (RVD+PTRAS+ET-A),
190 g-term treatment strategy with the selective endothelin-A receptor (ETA) antagonist, ambrisentan, des
195 ion of natriuretic peptides, adrenomedullin, endothelin, and galectin-3 with new-onset HF was stronge
197 oncentration of catecholamines, vasopressin, endothelin, and renin activity in 14 patients with CIPA,
198 consisting of prostacyclin and its analogs, endothelin antagonists, phosphodiesterase-5 inhibitors,
204 nd release of endothelin-1 (ET-1) binding to endothelin B (ETB) receptors, overexpressed in the lung
206 to a cysteine sulfenic acid modification in endothelin B receptor and consequently decreased endothe
207 BR-4628 against IR was lost when a selective endothelin B receptor antagonist was coadministered.
208 a nicotinic receptor (CHRNG, 6 subjects) and endothelin converting enzyme-like 1 (ECEL1, 4 subjects).
210 nists (BQ123 plus BQ788) or by inhibition of endothelin-converting enzyme (phosphoramidon or SM19712)
212 ned whether agonist degradation by endosomal endothelin-converting enzyme 1 (ECE-1) controls SSTR2A t
213 -1 expression, indicating the presence of an endothelin-converting enzyme 1/endothelin 1-SphK positiv
216 t inhibition of SphK leads to suppression of endothelin-converting enzyme-1 expression, indicating th
217 ltiplex consanguineous family to identify in endothelin-converting enzyme-like 1 (ECEL1) mutations th
221 strictive and vascular remodeling actions of endothelin (ET) 1 and angiotensin (Ang) II via endotheli
222 nd tumor necrosis factor-alpha, to stimulate endothelin (ET) and ET receptor (ETR) expression in brea
223 receptors (GPCRs), including adrenergic and endothelin (ET) receptors, after elevated neurohormonal
224 n the renin-angiotensin system (RAS) and the endothelin (ET) system as dual vasopeptidase inhibitors
226 osis factor-alpha, IL-1b, troponin, vascular endothelin growth factor, IL-17a, matrix metallopeptidas
228 C-dependent, positive-feedback mechanism for Endothelin induction and establish MEF2C as an immediate
230 alyzed the expression of the complete set of endothelin ligands and receptors in the jawless vertebra
231 S/MS to identify NT-proET-1 (ppET-1[18-50]), Endothelin-Like Domain Peptide (ELDP, ppET-1[93-166]) an
232 ELDP contains the evolutionary conserved endothelin-like domain sequence, which potentially confe
238 angiogenesis by Edn2 requires expression of Endothelin receptor A but not Endothelin receptor B in t
241 us epoprostenol were weaned off post-LT, and endothelin receptor antagonist or phosphodiesterase type
242 mendation for either prostacyclin agonist or endothelin receptor antagonist therapy and a strong reco
244 s of disease-targeted therapy (predominantly endothelin receptor antagonists [47.3%] or phosphodieste
247 were receiving riociguat in combination with endothelin receptor antagonists or prostanoids, or both.
248 erent classes of drugs are now available-ie, endothelin receptor antagonists, phosphodiesterase-5 inh
253 In mice, podocyte-specific knockout of the endothelin receptor prevented the diabetes-induced incre
255 dothelin (ET) 1 and angiotensin (Ang) II via endothelin receptor type A (ETAR) and Ang receptor type-
257 otein endothelin 3 (EDN3), its receptor (the endothelin receptor type B [EDNRB]), and the transcripti
259 n post-mortem tissue revealed high levels of endothelin receptor type B in oligodendrocyte lineage ce
260 genome sequencing, we discovered that EDNRB (Endothelin receptor type B) is a candidate gene involved
261 development and suggest that modification of endothelin receptor-ligand specificity was a key step in
262 essed the efficacy of macitentan, a new dual endothelin-receptor antagonist, using a primary end poin
264 hypertension and patients who were receiving endothelin-receptor antagonists or (nonintravenous) pros
266 c receptors, alpha-adrenergic receptors, and endothelin receptors (among others) have been associated
267 d podocyte loss through direct activation of endothelin receptors and NF-kappaB and beta-catenin path
269 ednra and ednrb, the genes encoding the two Endothelin receptors in mice, were born at predicted Men
270 he endothelin axis and in particular the two endothelin receptors, ETA and ETB, are targets for thera
273 These data suggest that OA-NO2 modulates endothelin signaling by increasing Nrf2-dependent expres
274 duplication and specialization of vertebrate Endothelin signaling coincided with the appearance of hi
275 ednr expression, we also analyzed all known Endothelin signaling components in the African clawed fr
277 nscriptional effectors directly activated by Endothelin signaling during neural crest development rem
278 he cardiac conduction system in mice lacking Endothelin signaling has not been previously addressed.
284 r neural crest development, and dysregulated Endothelin signaling is associated with several neural c
285 thin the developing mammalian heart and that Endothelin signaling is dispensable for specification an
288 primarily on gain-of-function studies, that Endothelin signaling is responsible for myocyte-to-Purki
289 enzyme-1 (Ece-1), a crucial component of the Endothelin signaling pathway, is required for embryonic
296 FRET-based biosensors, we show that LPA and endothelin transiently activate Cdc42 through Gi, concur
297 es to angiotensin type 1 receptor (AT1R) and endothelin type A receptor (ETAR) is associated with all
298 s significantly increased by blockade of the endothelin type A receptor with ABT-627 (0.116 +/- 0.006
299 licited rapid calcium transients mediated by endothelin type A receptors (ETARs) and endothelin type
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