ライフサイエンスコーパス: ET-1

1 (ISO), phenylephrine (PE), and endothelin-1 (ET-1).

2 positive inotropic response to endothelin-1 (ET-1).

3 effects on MAP are mediated through central ET-1.

4 blocking peptides prevented these actions of ET-1.

5 ble for reduced expression of HIF-1alpha and ET-1.

6 No treatment affected plasma ET-1.

7 dilatation in arterioles pre-contracted with ET-1.

8 HE fluorescence) and contraction elicited by ET-1.

9 s lost basal tone and failed to constrict to ET-1.

10 d that endothelial cells are a key source of ET-1.

11 f human peripheral arterioles in response to ET-1.

12 hacholine-induced sweating is not altered by ET-1.

13 d levels of ATF3 and increased expression of ET-1.

14 cmH(2)O luminal pressure and constricted to ET-1 (0.1 nM) with a 40 +/- 6% reduction in resting diam

15 h lactated Ringer solution (Control), 400 nm ET-1, 10 mm N(G) -nitro-l-arginine (l-NNA; a NOS inhibit

16 e reporter assays using wild-type and mutant ET-1 3' untranslated region (UTR) constructs, and transf

17 ) both with and without pre-contraction with ET-1 (3 x 10(-9) M).

18 DI activity was increased in the presence of ET-1 (3.1+/-0.2 to 5.6+/-0.4%, P<0.0001) through a mecha

19 A high dose of ET-1 (400 nm) co-infused with l-NNA further attenuated C

20 sponsible for producing active endothelin-1 (ET-1), a mitogenic peptide implicated in the aetiology o

21 ith increased plasma levels of endothelin-1 (ET-1), a potent vasoconstrictor, in sickle cell disease

22 timulates the transcription of endothelin-1 (ET-1), a secreted proinvasive polypeptide that acts thro

23 ur results suggest that increases in central ET-1 activity could possibly play a role in chronic E2-i

24 We also discovered that ET-1 acts mechanistically by promoting Notch activation

25 ET-1 administration also increased endothelial tube form

26 ET-1 also stimulated p-phospholipase C (PLC)gamma1 level

27 a NOS inhibitor) or a combination of 400 nm ET-1 and 10 mm l-NNA; in Protocol 3 (n = 8), only two si

28 Gene expression of ET-1 and ETA but not ETB receptors were upregulated in t

29 to endothelial stimulation, rapidly release ET-1 and initiate powerful ET-1-mediated constriction.

30 IHC confirmed the presence of both ET-1 and its receptors in the syncytiotrophoblast.

31 ET-1 and its receptors were expressed in the peritoneal

32 for gene expression and protein analysis of ET-1 and its receptors.

33 Shc/MAPK pathway mediates the expressions of ET-1 and PAI-1 and migration and proliferation of contra

34 bolished basal tone and vasoconstrictions to ET-1 and PDBu.

35 o BK-SS mice significantly attenuated plasma ET-1 and PlGF levels.

36 Protein levels and immunoreactivity of ET-1 and the endothelin B receptor (ETBR) were increased

37 Serum levels of ET-1 and the expression of the ETAR in fibrocytes were s

38 es also expresses and releases endothelin-1 (ET-1) and initiates endothelium-dependent constriction.

39 Expression of preproendothelin-1 (ET-1) and its ET(A) receptor in the kidney was higher in

40 ith increased plasma levels of endothelin-1 (ET-1) and other functional markers of PH in SCD.

41 of the potent vasoconstrictor endothelin-1 (ET-1) and PHT.

42 ed increases in the content of endothelin-1 (ET-1) and transforming growth factor-beta (TGF-beta).

43 We show here that ETAR, ET-1, and ECE-1 are expressed and colocalize in murine d

44 sed vasoconstrictive responses to Ang II and ET-1, and implicated cross-talk between both pathways de

45 )-9, reported to be potentially regulated by ET-1, and MMP-8, considered as neutrophil collagenase, a

46 Synthesis of these peptides correlated with ET-1, and plasma ELDP and CT-proET-1 were elevated in pa

47 sess the effect of the administration of the ET-1 antagonist bosentan.

48 Endothelin-1 (ET-1) antagonists are a possibility because elevated ET-

49 the ET-1 receptors ETa or ETb or by an anti-ET-1 antibody but not by an isotype control.

50 dothelial migration, which were repressed by ET-1 antibody or ETR inhibitors.

51 on of HIF-1alpha and its downstream effector ET-1 are post-transcriptionally regulated.

52 neal damage and fibrosis, and they highlight ET-1 as a potential therapeutic target in the treatment

53 rofiling identified inter alia endothelin-1 (ET-1) as one of the target genes of P2Y4 in ischemic hea

54 ET-1 at 400 nm (P < 0.05) compared to lower doses (40 pm

55 We investigated whether ET-1 attenuates cholinergic cutaneous vasodilatation and

56 We evaluated the hypothesis that ET-1 attenuates cholinergic cutaneous vasodilatation and

57 We also demonstrate that ET-1 attenuates cutaneous vasodilatation in response to

58 We show that ET-1 attenuates cutaneous vasodilatation through a NOS-i

59 Our findings show that ET-1 attenuates methacholine-induced cutaneous vasodilat

60 gic significance of this newly discovered Lf-ET-1 axis in the manifestation of TNBC phenotypes is rev

61 pportunity to treat TNBC by targeting the Lf-ET-1 axis using an approved developmental drug.

62 atic production and release of endothelin-1 (ET-1) binding to endothelin B (ETB) receptors, overexpre

63 T cells and endothelin (ET-1) both contribute to angiotensin II (AngII)-dependen

64 ET-1 (+/-BQ788) was given to cultured rat pulmonary micr

65 ay alleviate the vasoconstrictive effects of ET-1 by removing it from the circulation.

66 Our observations demonstrate that ET-1 can lead to increases in gene expression, including

67 In cultured mouse podocytes, ET-1 caused loss of the podocyte differentiation marker

68 Exogenous ET-1 caused similar concentration-dependent constriction

69 culosis produces and secretes an enzyme with ET-1 cleavage activity.

70 reased and that Nrf2 silencing increased the ET-1 concentration in the culture media of endothelial c

71 The change in the extracellular ET-1 concentration was dependent on ET-B receptor expres

72 turn mediates the decrease in extracellular ET-1 concentration.

73 Previous studies suggest that endothelin-1 (ET-1) contributes to the pathogenesis of ECM.

74 tment was associated with increases in urine ET-1/creatinine, whereas reduction in pulse-wave velocit

75 did not affect plasma urate, ADMA, or urine ET-1/creatinine, which reflects renal ET-1 production; i

76 ventricular myocytes decreases endothelin-1 (ET-1)-dependent elevation of nuclear calcium and activat

77 ocking Gbetagamma at the Golgi or PM blocked ET-1-dependent cardiomyocyte hypertrophy.

78 in NRVMs, resulting in significantly reduced ET-1-dependent NRVM hypertrophy.

79 Blocking Gbetagamma at the Golgi inhibited ET-1-dependent PI4P depletion and nuclear PKD activation

80 obese subjects and assessed its influence on ET-1-dependent vasoconstrictor tone in obesity.

81 In contrast, ET-1 did not alter surface BKalpha, total beta1, or tota

82 nse to sodium nitroprusside, suggesting that ET-1 diminishes the dilatation capacity of vascular smoo

83 and BeWo choriocarcinoma cells treated with ET-1 displayed an increase in ER stress markers.

84 We show that ET-1 does not modulate methacholine-induced sweating at

85 Endothelin-1 (ET-1) dose and time-dependently up-regulated TRPC6 expre

86 n of profibrotic signals TGF-beta1, CCN2 and ET-1, downstream of angiotensin-II-receptor-1 inhibition

87 -of-function approaches, we demonstrate that ET-1 drastically reduces the rate of remyelination.

88 othelin-A receptor (ET(A)R) by endothelin-1 (ET-1) drives epithelial-to-mesenchymal transition in ova

89 injury molecule-1 (KIM-1) and endothelin-1 (ET-1) during EVKP in a series of discarded human kidneys

90 Furthermore, these results implicate the ET-1/ECE-1/ERK1/2 pathway as a therapeutic target to tre

91 In EOC, the endothelin-1 (ET-1, EDN1)-endothelin A receptor (ETAR, EDNRA) signalin

92 R1 neutralizing antibody partially inhibited ET-1 effects on tube formation.

93 and enhanced transcription of genes, such as ET-1, enhancing the network that sustains chemoresistanc

94 pe I): NF-kappaB target gene expression (ie, ET-1, ET-A and ET-B receptors, vascular cell adhesion mo

95 is patients confirmed an upregulation of the ET-1/ETAR/ECE-1/ERK1/2 axis in patients with chronic itc

96 mokine receptor 1 (CX3CR1), although whether ET-1/ETB receptor activation influences these events is

97 Our aim was to define if ET-1/ETB receptor activation modulates CX3CL1/CX3CR1 sig

98 a novel mechanistic interaction between the ET-1/ETB receptor axis and CX3CL1/CX3CR1 in mediating pu

99 vascular endothelial cells, did not produce ET-1 even when stimulated by antigen-specific T cell act

100 Endothelin 1 (ET-1) evokes histamine-independent pruritus in mammals t

101 esponse mediated by IkappaBbeta/NF-kappaB to ET-1 expression and potentially reveal therapeutic targe

102 ed the consequences of TGF-beta signaling on ET-1 expression and secretion by human trabecular meshwo

103 reciprocal relationship was observed between ET-1 expression and TGF-beta1 expression in human mesoth

104 tion of systemic inflammatory stress-induced ET-1 expression may reveal therapeutic targets.

105 PlGF-mediated ET-1 expression occurs via activation of hypoxia-inducib

106 expression, we demonstrate that LPS-induced ET-1 expression occurs via an NF-kappaB-dependent pathwa

107 ecessary and sufficient to drive LPS-induced ET-1 expression.

108 lpha mRNA and concomitantly led to augmented ET-1 expression.

109 rapidly increased the endothelial release of ET-1 from P1 but not P21 aortas.

110 PlGF-mediated transcription of the ET-1 gene occurs by activation of hypoxia inducible fact

111 recruitment of beta-arr1 and beta-catenin to ET-1 gene promoter.

112 eceptor expression on nociceptors attenuated ET-1 hyperalgesia but had no effect on SIEH, suggesting

113 isense for PKCepsilon did not inhibit either ET-1 hyperalgesia or SIEH, suggesting no role for neuron

114 rocedure eliminated SIEH without attenuating ET-1 hyperalgesia.

115 Next, we performed ET-1 immunohistochemistry on postmortem white matter bra

116 y attenuated alpha-SMA expression induced by ET-1 in fibrocytes from normal participants.

117 Tie2-Cre( + ) mice, which conditionally lack ET-1 in hematopoietic stem cells and vascular endothelia

118 ttle is known about the production source of ET-1 in inflammation and immunity.

119 nclusion, these data support a novel role of ET-1 in linking TLR7 inflammatory signaling to subsequen

120 ed levels of miR-199a2 and reduced levels of ET-1 in lung tissues.

121 Heightened activity of ET-1 in neonatal endothelium probably reflects an early

122 igh levels of ET-1 peptides, rapidly release ET-1 in response to endothelial stimulation, and initiat

123 ar link between miR-199a2 and high levels of ET-1 in SCD.

124 Heightened activity of ET-1 in the neonatal endothelium might contribute to ina

125 to completely understand the contribution of ET-1 in this phenomenon.

126 expression and the release of endothelin-1 (ET-1) in levels sufficient to initiate vasoconstriction

127 er solution (Control), 40 pm, 4 nm or 400 nm ET-1; in Protocol 2 (n = 11) sites were perfused with la

128 Exogenous ET-1 induced a profibrosing phenotype, whereas fibroblas

129 Collectively, the data show that ET-1 induced ER stress in trophoblasts via the ETBR and

130 ET-1 induced Ets-like kinase-1 (Elk-1), signal transduce

131 In murine DRG neurons, ET-1 induced internalization of ETAR within ECE-1-contai

132 Adenovirus-mediated overexpression of ET-1 induced MMT in human mesothelial cells in vitro and

133 ET-1 induced phospho-activation of the ETBR.

134 ide (NO)-mediated dilation and endothelin-1 (ET-1)-induced constriction in retinal arterioles at vari

135 +)](i), and protection against endothelin-1 (ET-1)-induced steady state [Ca(2+)](i) increases in huma

136 MP](i), and [Ca(2+)](i); and did not prevent ET-1-induced [Ca(2+)](i) increases.

137 ), [cGMP](i), and [Ca(2+)](i); and prevented ET-1-induced [Ca(2+)](i) increases.

138 Inhibition of PDE5 by sildenafil suppressed ET-1-induced activation of calcineurin/NFATc4 signaling

139 hibition slowed ETAR recycling yet prolonged ET-1-induced activation of ERK1/2, but not p38.

140 ET-1-induced constriction is mediated by extracellular C

141 kinase (ROCK), and protein kinase C (PKC) to ET-1-induced constriction of porcine retinal arterioles,

142 ET-1-induced ERK activation was Ca(2+) independent.

143 of dominant-negative IkappaBalpha perturbed ET-1-induced integrin alphaV and integrin beta1 expressi

144 Increased Snail expression fostered ET-1-induced migration as confirmed by Snail knockdown e

145 rting enzyme 1 (ECE-1) as a key regulator of ET-1-induced pruritus and neural signaling of itch.

146 tch on sensory nerves by directly regulating ET-1-induced pruritus in humans and mice.

147 Rab11A construct (Rab11A S177A) blocked the ET-1-induced Rab11A phosphorylation, reduction in Rab11A

148 In a murine itch model, ET-1-induced scratching behavior was substantially augme

149 (i), or [Ca(2+)](i) involvement, and prevent ET-1-induced steady state Ca(2+) increases in HTMCs.

150 FATc4 using small interfering RNA suppressed ET-1-induced TRPC6 up-regulation.

151 vasoconstriction to PDBu, but did not alter ET-1-induced vasoconstriction or basal tone.

152 ceptor, xestospongin-C, we demonstrated that ET-1 induces ER stress via the PLC-IP(3) pathway.

153 Endothelin-1 (ET-1) induces matrix-associated gene expression through

154 ound that IL-6 was a key cytokine underlying ET-1 induction mediated by IgG from women with PE in hum

155 Vasoconstrictors, including endothelin-1 (ET-1), inhibit myocyte BK channels, leading to contracti

156 ET-1 inhibited single BK channels and transient BK curre

157 Test the hypothesis that ET-1 inhibits BK channels by altering BKalpha and beta1

158 These findings reveal that ET-1 is a negative regulator of OPC differentiation and

159 Using iontophoresis, we demonstrated that ET-1 is a potent, partially histamine-independent prurit

160 blood-brain barrier leakage, indicating that ET-1 is involved in the genesis of brain microvascular a

161 in-1 (ET-1) is induced by OA-NO2 Inasmuch as ET-1 is one of the key regulators of vascular tone, we c

162 in control subjects, suggesting that, in MS, ET-1 is released from the brain to the cerebral circulat

163 Endothelin-1 (ET-1) is a 21-amino acid vasoactive peptide that plays a

164 Endothelin-1 (ET-1) is a potent endothelial-derived vasoconstrictor th

165 Although endothelin-1 (ET-1) is a potent vasoconstrictor peptide implicated in

166 The vasoconstrictor peptide endothelin-1 (ET-1) is a transcriptional target of TGF-beta1 and media

167 Elevated circulating endothelin-1 (ET-1) is associated with the disease.

168 Since endothelin-1 (ET-1) is implicated in blood pressure (BP) regulation, w

169 r vascular endothelial-derived endothelin-1 (ET-1) is important for skin Na(+) buffering.

170 ng the vasodilatory effects of endothelin-1 (ET-1) is induced by OA-NO2 Inasmuch as ET-1 is one of th

171 ry or subarachnoid hemorrhage, endothelin-1 (ET-1) is induced resulting in cerebral vasospasm, ischem

172 Endothelin-1 (ET-1) is involved in the pathogenesis of cardiac and ren

173 her the potent vasoconstrictor endothelin-1 (ET-1) is involved.

174 jor source of TGFbeta and that endothelin-1 (ET-1) is one of the key components responsible for the p

175 3 distinct isoforms exist, and endothelin 1 (ET-1) is the most abundant and the best-characterized is

176 Endothelin-1 (ET-1) is unique among a broad range of hyperalgesic agen

177 esize that a balance between Zmp1 control of ET-1 levels and ETA/ETB signaling can allow M. tuberculo

178 tagonists are a possibility because elevated ET-1 levels are associated with adverse cardiovascular e

179 ranscription with a concomitant reduction in ET-1 levels in cultured endothelial cells.

180 e found that, compared with controls, plasma ET-1 levels in patients with MS were significantly eleva

181 y elevated plasma and tissue lactoferrin and ET-1 levels in patients with TNBC compared with those in

182 ET-1 levels increase after isograft implantation, and ET

183 Furthermore, ET-1 levels increased in the syncytiotrophoblast of expl

184 ates miR-648 expression leading to increased ET-1 levels that are known to induce PHT in SCA.

185 In the present study, we found that ET-1 levels were significantly elevated in patients with

186 reoxygenation explants also contained higher ET-1 levels, which induced ER stress in JEG-3 cells that

187 expression can ameliorate PH by reduction of ET-1 levels.

188 Increased endothelin-1 (ET-1) levels, disordered thiol protein status, and eryth

189 Endothelin 1 (ET-1), mainly produced from vascular endothelial cells,

190 ET-1 may also play a significant role in cardiac allogra

191 neous blood flow and sweating and infer that ET-1 may attenuate the heat loss responses of cutaneous

192 lator reactivity and increased endothelin 1 (ET-1)-mediated vasoconstriction, two abnormalities contr

193 , rapidly release ET-1 and initiate powerful ET-1-mediated constriction.

194 nse to endothelial stimulation, and initiate ET-1-mediated endothelium-dependent constriction.

195 Understanding ET-1-mediated events at the molecular level may lead to

196 constriction, we studied the consequences of ET-1-mediated vasoconstriction of the middle cerebral ar

197 obesity, where it is accompanied by reduced ET-1-mediated vasoconstriction.

198 r, there is a paucity of knowledge about how ET-1 mediates drug resistance.

199 t gland, although it remains unclear whether ET-1 modulates cholinergic sweating.

200 /ALK-5 receptor, elicits marked increases in ET-1 mRNA content and ET-1 secretion from cultured prima

201 nd osmolarity were associated with increased ET-1 mRNA in vascular tissue.

202 cs showed that miR-648 targets the 3' UTR of ET-1 mRNA.

203 ress in JEG-3 cells that was abolished by an ET-1-neutralizing antibody.

204 n depletion were stimulated with endothelin (ET-1), norepinephrine, insulin-like growth factor-1 (IGF

205 ions of the vasoactive protein endothelin-1 (ET-1) occur in the setting of systemic inflammatory resp

206 In this study, we characterize the role of ET-1 on ECM vascular dysfunction.

207 -1) were utilized to assess the influence of ET-1 on the dilatation capacity of vascular smooth muscl

208 ropose that SIEH is produced by an effect of ET-1 on vascular endothelial cells, sensitizing its rele

209 udy investigated the effect of endothelin-1 (ET-1) on cholinergic mechanisms of end-organs (i.e. skin

210 nhibitor of NO production, and endothelin-1 (ET-1) oppose the actions of NO, suggesting that ET-1 rec

211 zed red blood cells were treated with either ET-1 or saline from 2 to 8 days postinfection (dpi).

212 antly blunted after administration of 400 nm ET-1 (P < 0.05).

213 ET-1 peptide content in skin tissue was increased in flo

214 ndothelin (ppET)-1 mRNA content and secreted ET-1 peptide were quantified by real-time PCR and ELISA,

215 T(A)R, leading to secretion of the bioactive ET-1 peptide.

216 born central arteries express high levels of ET-1 peptides and, in response to endothelial stimulatio

217 Endothelial expression of ET-1 peptides, as assessed by immunofluorescence analysi

218 orn endothelial cells express high levels of ET-1 peptides, rapidly release ET-1 in response to endot

219 ls increase after isograft implantation, and ET-1 plays a key role in CNI-induced renal vasoconstrict

220 Given the central role that ET-1 plays in these patients and to identify the downstr

221 Here, we show a novel example of ET-1 posttranscriptional regulation by PlGF via action o

222 izumab on VEGF induced vasoactive changes on ET-1 pre-contracted vessels.

223 rterioles under normal tone or endothelin-1 (ET-1) pre-contracted conditions and determines the influ

224 Immunocytostaining showed that ET-1-producing cells emerged only in PBMCs stimulated wi

225 uses dying with CHB revealed the presence of ET-1-producing mononuclear cells in the septal region in

226 However the molecular basis of increased ET-1 production and its role in PE are unknown.

227 ling is a key mechanism underlying increased ET-1 production and subsequent maternal features.

228 el causative factor responsible for elevated ET-1 production and that increased TNF-alpha/IL-6 signal

229 ice, demonstrating that autoantibody-induced ET-1 production contributes to pathophysiology.

230 ative factors, pathological role of elevated ET-1 production in PE, and the underlying mechanisms.

231 F-alpha signaling, contributing to increased ET-1 production in pregnant mice.

232 ypothesis that increased extrarenal vascular ET-1 production in response to HS intake is mediated by

233 nstrates the existence of an immune-mediated ET-1 production induced by T cells upon activation throu

234 Here, we studied whether T cell-mediated ET-1 production system exists and operates independent o

235 Finally, ET-1 production was elevated in response to increasing e

236 This ET-1 production was inhibited by anti-IFN-gamma and/or T

237 ET-1 production was readily detectable in the culture su

238 l factors and signaling cascades involved in ET-1 production, subsequent disease symptom development,

239 urine ET-1/creatinine, which reflects renal ET-1 production; in contrast, sitaxentan led to statisti

240 ET-1 promoted podocyte migration via ET(A)R activation a

241 Using pharmacologic inhibitors, ET-1 promoter luciferase assays, and by silencing and ov

242 Endothelin-1 (ET-1) promotes renal damage during cardiovascular diseas

243 dial ET type A (but not type B) receptor and ET-1 protein levels were increased compared with the non

244 amp) are induced in the brain in response to ET-1, providing a novel target in the treatment of multi

245 s the primary source of elevated circulating ET-1, rather than the endothelium as previously proposed

246 ET-1 receptor antagonism did not affect responses to thr

247 support of the therapeutic effectiveness of ET-1 receptor antagonist to completely block the lactofe

248 was inhibited by endothelial-denudation, by ET-1 receptor antagonists (BQ123 plus BQ788) or by inhib

249 udies are needed to explore the role of dual ET-1 receptor antagonists in patients with HFpEF.

250 reatment of BERK sickle transgenic mice with ET-1 receptor antagonists lowered circulating and erythr

251 1) oppose the actions of NO, suggesting that ET-1 receptor antagonists may have a role in cardiovascu

252 In some experiments, TGF-beta or ET-1 receptor antagonists, or Rho G-protein inhibitors,

253 Thus alpha-adrenergic and ET-1 receptor signaling via PKD in adult myocytes featur

254 Interestingly, a therapeutic ET-1 receptor-antagonist blocked lactoferrin-dependent m

255 f TGFbeta was decreased by inhibitors of the ET-1 receptors ETa or ETb or by an anti-ET-1 antibody bu

256 Antagonists to the ET-1 receptors, ET(A) and ET(B), attenuated both initial

257 samples and found that the likely source of ET-1 release are reactive astrocytes in MS plaques.

258 ribute to disease pathogenesis by augmenting ET-1 responses.

259 ts marked increases in ET-1 mRNA content and ET-1 secretion from cultured primary or transformed huma

260 a-mediated increases in ppET-1 mRNA content, ET-1 secretion, and stress fiber organization.

261 nd 100 mm MCh administration relative to the ET-1 site (all P < 0.05).

262 ET-1 stimulated Rab11A phosphorylation, which reduced Ra

263 n of Akt, GIT1 tyrosine phosphorylation, and ET-1-stimulated GIT1-eNOS association but did not affect

264 Gbetagamma inhibition blocked ET-1-stimulated Golgi PI4P depletion in neonatal and adu

265 a separate pathway at the PM is required for ET-1-stimulated hypertrophy, and the efficacy of Gbetaga

266 ET-1 stimulates PKC-mediated phosphorylation of Rab11A a

267 Taken together, our study indicates that ET-1 stimulates TRPC6 expression by activation of calcin

268 n dependent cell contraction, and increasing ET-1 synthesis and secretion, in human TM cells.

269 cal basis for it being a better biomarker of ET-1 synthesis.

270 In conclusion, the ET-1 system is important for the development of tunicamy

271 These studies aimed to determine whether the ET-1 system promotes renal ER stress development in resp

272 n breast cancer, which uses another secreted ET-1 system to confer invasiveness.

273 Restoring CBF by interfering with the ET-1 system warrants further investigation as a potentia

274 These results strongly support a role for an ET-1/TGF-beta1 axis as an inducer of MMT and subsequent

275 METHODS AND ET-1, through activation of PKC (protein kinase C), redu

276 This work studied the contribution of ET-1 to the development of peritoneal damage and failure

277 in-coupled receptor-linked mediators such as ET-1, to activate CRE response genes involved in angioge

278 ET-1-treated PbN-infected mice displayed leukocyte adhes

279 ET-1-treated PbN-infected mice exhibited neurological si

280 These alterations were not present in either ET-1-treated uninfected or saline-treated PbN-infected m

281 In summary, ET-1 treatment of PbN-infected mice induced an ECM-like

282 ET-1 treatment significantly induced CX3CL1 production i

283 Parasitemia was not affected by ET-1 treatment.

284 ower with reciprocally high levels of plasma ET-1, unlike unaffected controls.

285 However, it enhanced ET-1 vasoconstriction and prolonged the increase in bloo

286 Moreover, PlGF induced the expression of ET-1 via hypoxia-inducible factor 1alpha.

287 To determine whether ET-1, via the ET(A) receptor, facilitates T cell infiltr

288 The reduced level of ET-1 was correlated with reduction of microvascular hype

289 ET-1 was induced to a greater extent from HUVECs than fr

290 dilatation in arterioles pre-contracted with ET-1 was significantly inhibited by bevacizumab.

291 muscle to dilate to NO donor or contract to ET-1 was unaffected throughout the study period.

292 n to PKC activator PDBu, vasoconstriction to ET-1 was unaffected.

293 Constriction of retinal arterioles to ET-1 was unaltered at all time periods of hyperglycemia.

294 um creatinine, and higher levels of NGAL and ET-1 were associated with a higher EVKP score (P < 0.05)

295 Urinary levels of NGAL, KIM-1, and ET-1 were measured after EVKP.

296 (n = 8), only two sites (Control and 400 nm ET-1) were utilized to assess the influence of ET-1 on t

297 magnetic beads in the inner chamber produced ET-1 when T cells were activated with antigen or anti-CD

298 us inhibitor of remyelination, Endothelin-1 (ET-1), which is highly expressed in reactive astrocytes

299 strate that reduced CBF in MS is mediated by ET-1, which is likely released in the cerebral circulati

300 ach elicited a robust (>7-fold) secretion of ET-1 while enhancing stress fiber organization.