ライフサイエンスコーパス: ET-1

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

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

3 d levels of ATF3 and increased expression of 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 nicotine-induced increases in NGF, FN1, and ET-1.

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

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

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

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

12 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

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

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

15 Here, we report that Endothelin-1 (ET-1), a molecular component of the postnatal SVZ, promo

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

17 Thus, ET-1, acting through the ET(A) receptors, contributes to

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

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

20 ET-1 administration also increased endothelial tube form

21 injection of vasoconstrictive endothelin-1 (ET-1) along with Abeta toxicity on CNS pathogenesis; dri

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

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

24 Higher levels of plasma ET-1 and Ang II and elevated expression of ET-1 mRNA in

25 OSAHS-induced elevated levels of ET-1 and Ang II may be attributed to myocardial structur

26 was negatively correlated with the levels of ET-1 and Ang II.

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

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

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

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

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

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

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

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

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

36 Endothelin 1 (ET-1) and ET-2 activate two G protein-coupled receptors

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

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

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

40 ), endothelin-1 (EDN1, herein referred to as ET-1), and collagen (COL1A1 and COL3A1) were measured in

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

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

43 )-9, reported to be potentially regulated by ET-1, and MMP-8, considered as neutrophil collagenase, a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 o hyperglycemia increased vitreous levels of ET-1 but not thromboxane B(2) In conclusion, both in vit

60 The regulation of ET-1 by iron was also demonstrated in healthy humans exp

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

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

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

64 Exogenous ET-1 caused similar concentration-dependent constriction

65 eages, including the environmentally adapted ET-1 clade, as noted previously for these genes.

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

67 posed controls, nicotine increased NGF, FN1, ET-1, COL1A1, and COL3A1 expression in human and mouse L

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

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

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

71 Furthermore, the finding that ET-1 constrains the blood flow response to exercise sugg

72 ET-1 contributes to vasoconstriction, vascular and cardi

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

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

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

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

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

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

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

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

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

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

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

89 r, the cerebral damage induced by the 6 pmol ET-1 (E6), Abeta and E6 + Abeta rats was not detrimental

90 days of treatment, a high dose (60 pmol) of ET-1 (E60) alone caused the greatest increase in neuroin

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

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

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

94 r mRNA levels of the vasoconstrictor peptide ET-1 (endothelin-1) and higher levels of the 2 potent va

95 The levels of ET-1(endothelin-1) and Ang II (Angiotensin II) in the pl

96 he endothelin axis components [endothelin-1 (ET-1), endothelin-3 (ET-3), endothelin receptor A (EdnrA

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

98 transforming growth factor beta/Smad2/3 and ET-1/Erk1/2 signaling in Acta2(-/-) HSCs.

99 und endothelin axis component (EdnrA, EdnrB, ET-1, ET-3) expression in developing extramedullary hema

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 ET-1 has been shown to promote degeneration of optic ner

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

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

120 rocedure eliminated SIEH without attenuating ET-1 hyperalgesia.

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

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

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

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

125 monstrated reduced vasodilatory responses to ET-1 in lean AE-PCOS (logED(50) , 0.59 +/- 0.08) versus

126 nicotine-induced increases in NGF, FN1, and ET-1 in LFs.

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

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

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

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

131 in health, little is known about the role of ET-1 in the cardiovascular response to exercise in hyper

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

133 Lastly, high levels of ET-1 in the SVZ of patients with Cathepsin A-related art

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

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

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

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

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

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

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

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

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

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

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

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

146 Troglitazone blunted ET-1-induced contraction of UtA in hypoxic and normoxic

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

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

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

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

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

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

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

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

155 We propose that the attenuated ET-1-induced vasodilatation in AE-PCOS is a consequence

156 ET(B) R inhibition decreased ET-1-induced vasodilatation in AE-PCOS women (logED(50)

157 tically observed at the cellular level, with ET-1-induced, DAF-FM-measurable endothelial cell NO prod

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

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

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

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

162 mary RGCs and in vivo following intravitreal ET-1 injection in rats.

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

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

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

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

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

168 We also show that ET-1 is required for increased neural stem cell and OPC

169 ET-1 is the most potent vasoconstrictor in the human car

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

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

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

173 Endothelin-1 (ET-1) is a vasoactive peptide that is elevated in aqueou

174 Endothelin-1 (ET-1) is an indicator of endothelial injury and dysfunct

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

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

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

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

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

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

181 3 distinct isoforms exist, and endothelin 1 (ET-1) is the most abundant and the best-characterized is

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

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

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

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

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

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

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

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

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

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

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

193 ented the cutaneous vasodilating response to ET-1(logED(50) 0.29 +/- 0.21, 0.47 +/- 0.09, P < 0.05 fo

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

195 Log[ET-1]-%maxCVC dose-response curves demonstrated reduced

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

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

198 A-seq analysis was used to assess changes in ET-1 mediated gene expression in primary RGCs, which rev

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

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

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

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

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

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

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

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

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

208 a ET-1 and Ang II and elevated expression of ET-1 mRNA in cardiac tissue were detected in Group OSAHS

209 The expression of ET-1 mRNA in heart tissue was detected by RT-PCR.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 ry during low dose intradermal microdialysis ET-1 perfusions (1, 3, 4, 5 and 7 pmol) with either lact

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

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

229 Our results demonstrate that ET-1 produced a decrease in expression of vital componen

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

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

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

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

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

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

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

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

238 itric oxide and downregulating endothelin-1 (ET-1) production, has been implicated in IUGR.

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

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

241 oenergetics and suggest a mechanism by which ET-1 promotes neurodegeneration of RGCs in glaucoma.

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

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

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

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

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

252 ical analysis revealed enhanced staining for ET-1 receptors in the placental labyrinthine zone in hyp

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

254 s levels of angiotensin II, aldosterone, and ET-1; reduces ammoniagenesis; and diminishes inflammatio

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

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

257 an increased number of SVZ OPCs, suggesting ET-1's role as a regulator of glial progenitor prolifera

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

259 Loss of ET-1 signaling increases neurogenesis and reduces oligod

260 ET-1 signaling therefore presents a potential new therap

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

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

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

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

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

273 giotensin II, aldosterone, and endothelin-1 (ET-1) that mediate the immediate benefit of increased ki

274 enules from euglycemic pigs to endothelin-1 (ET-1), thromboxane analog U46619, and norepinephrine wer

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

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

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

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

281 ET-1 treatment significantly decreased protein expressio

282 ET-1 treatment significantly induced CX3CL1 production i

283 Parasitemia was not affected by ET-1 treatment.

284 te of mitochondrial ATP production following ET-1 treatment.

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

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

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

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

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

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

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

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

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

297 t to recapitulate increases in NGF, FN1, and ET-1, whereas treatment with a miR-98 mimic significantl

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 ression of the vasoconstrictor endothelin-1 (ET-1) within PASMCs.