ライフサイエンスコーパス: HETE

1 ther chiral monoepoxides and bis-allylic 10S-HETE.

2 formation of prostaglandins, 15-HETE, and 11-HETE but did not inhibit HepsilondGuo-adduct formation.

3 nificant decreases in 8-HETE, 9-HETE, and 11-HETE compared to placebo.

4 ostaglandins, thromboxane B2, 15-HETE and 11-HETE in cerebellar samples of knockin knockout mice.

5 The level of 11-HETE, a nonenzymatic oxidation product of arachidonic (2

6 12-HETE acts in diverse cellular processes, including catec

7 -LOX) to 12-hydroxyeicosatetraenoic acid (12-HETE) and has an important role in the regulation of ang

8 late and 12-hydroxyeicosatetraenoic acid (12-HETE) were detected in mice with NASH.

9 olecule, 12-hydroxyeicosatetraenoic acid (12-HETE), indicating a tunneling mechanism.

10 (ALOX12)-12-hydroxyeicosatetraenoic acid (12-HETE)-G-protein-coupled receptor 31 (GPR31) signaling ax

11 roxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12-HETE).

12 tabolic reprogramming involving an ALOX12-12-HETE-GPR31 axis that functionally determines hepatic IR

13 ible for facilitating lung metastasis and 12-HETE production in breast tumors.

14 and organic solute transporter beta), and 12-HETE synthesis (arachidonate 12-lipoxygenase) were signi

15 cat/ K m) on the presence of 12-HPETE and 12-HETE, indicate that the allosteric site, previously iden

16 Most strikingly, blocking 12-HETE accumulation effectively attenuated all pathologies

17 Notably, blocking 12-HETE production inhibits IR-induced liver dysfunction, i

18 o provided proof of concept that blocking 12-HETE production is a promising strategy for preventing a

19 cytes showed increased VEGF expression by 12-HETE.

20 ), which can be reduced to the eicosanoid 12-HETE (12-hydroxyeicosatetraenoic acid).

21 raenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic acids (H

22 asured by LC-MS/MS the formation of HXB3, 12-HETE, 8-HETE, and 15-HETE from arachidonic acid (AA) at

23 PEDF expression was reduced in 12-HETE-treated rMCs, astrocytes, and the retinal pigment e

24 2/15-lipoxygenase (12/15-LOX) metabolites 12-HETE and 12-HPETE at 300 nM, block axon extension in neu

25 Furthermore, the addition of 12-HETE lowers the observed k(cat)/K(M) SIE from 2.2 to 1.4

26 The effects of 12-HETE on VEGF and PEDF expression were evaluated in Mulle

27 Finally, the allosteric binding of 12-HETE to 15-hLO-1 decreases the K(M)[O(2)] for AA to 15 m

28 present studies, agonist-induced platelet 12-HETE production was decreased in the patient.

29 in hepatocytes during ischemia to promote 12-HETE accumulation and that 12-HETE then directly binds t

30 obilization in human platelets and reduce 12-HETE in beta-cells.

31 to promote 12-HETE accumulation and that 12-HETE then directly binds to GPR31, triggering an inflamm

32 pidly taken up and converted primarily to 12-HETE-T.

33 15-HETE production was reduced in EGCs from patients with C

34 such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) an

35 recursor 15-hydroxyeicosatetraenoic acid (15-HETE) in esterified form within membrane phospholipids,

36 bolites, 15-hydroxyeicosatetraenoic acid (15-HETE), to regulate the permeability of the IEB.

37 cosatetraenoic acid (5-HETE), 8-HETE, and 15-HETE characterized progression from normal to NAFL to NA

38 e formation of HXB3, 12-HETE, 8-HETE, and 15-HETE from arachidonic acid (AA) at baseline and in the p

39 -hydroxyeicosatetraenoic acids (HETE) and 15-HETE from arachidonic acid in the testes were significan

40 The effects of human EGCs and 15-HETE on permeability and transepithelial electrical resi

41 Levels of 5,6-EET and 15-HETE were increased in colons of mice with, but not with

42 ations of prostaglandins, thromboxane B2, 15-HETE and 11-HETE in cerebellar samples of knockin knocko

43 We used immunostaining to identify 15-HETE-producing enzymes in EGCs and tissues.

44 eicosatetraenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic

45 Inhibiting 15-HETE production in rats increased the permeability of th

46 Anti-inflammatory metabolite 15-HETE shows later expression, peaking at 72 h.

47 elevated and a linear increasing trend of 15-HETE concentrations was detected with doses of PFOS.

48 f P2X7 results in efficient hydrolysis of 15-HETE from membrane phospholipids by group IVA cytosolic

49 were given intraperitoneal injections of 15-HETE or an inhibitor of 15-lipoxygenase (the enzyme that

50 permeability of the IEB; the addition of 15-HETE restored permeability to levels of control tissues.

51 tients with CD have reduced production of 15-HETE, which controls IEB permeability by inhibiting aden

52 ipoxygenase-2 and produced high levels of 15-HETE, which increased IEB resistance and reduced IEB per

53 LOX15/ALOX5/LTA4H(low) gene and PGE2/PGD2/15-HETE(high) and LXA4(low) eicosanoid profile.

54 o [(3)H]arachidonic acid ex vivo produced 15-HETE as a major eicosanoid and enhanced balloon injury-i

55 15-lipoxygenase (the enzyme that produces 15-HETE); colons were collected and permeability was measur

56 blocked the formation of prostaglandins, 15-HETE, and 11-HETE but did not inhibit HepsilondGuo-adduc

57 We found that 15-HETE regulates IEB permeability by inhibiting an adenosi

58 LOX, which leads to LXA(4) synthesis via 15-HETE production, reduced (>90%) the ability of AjA to en

59 ntains the oxygenase activity to produce 15R-HETE from arachidonate.

60 20-HETE is significantly more potent than its COX-mediated

61 20-HETE synthesis was measured in parallel experiments in c

62 20-HETE; furthermore, administration of a 20-HETE antagonist normalized BP.

63 Notably, treatment with a 20-HETE antagonist or agents that normalized BP without aff

64 Administration of a 20-HETE antagonist prevented and reversed the effects of di

65 reased BP by 40%, and administration of a 20-HETE antagonist prevented this increase.

66 rease in 20-hydroxyeicosatetraenoic acid (20-HETE) and Nox oxidases.

67 20-Hydroxyeicosatetraenoic acid (20-HETE) has an important role in the regulation of renal t

68 ncreased 20-hydroxyeicosatetraenoic acid (20-HETE) in kidney and urine.

69 20-Hydroxyeicosatetraenoic acid (20-HETE) is a cytochrome P-450 4A/4F-derived metabolite of

70 kidney, 20-hydroxyeicosatetraenoic acid (20-HETE) is a primary cytochrome P450 4 (Cyp4)-derived eico

71 dins and 20-hydroxyeicosatetraenoic acid (20-HETE), a potent vasoconstrictive and proinflammatory ara

72 20-Hydroxyeicosatetraenoic acid (20-HETE), a primarily metabolized product of arachidonic ac

73 -hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE), a primary cytochrome P450 4 (Cyp4)-derived eicosa

74 role of 20-hydroxyeicosatetraenoic acid (20-HETE), an endogenous cytochrome P450 metabolite of arach

75 strictor 20-hydroxyeicosatetraenoic acid (20-HETE), and that this mechanism explains cortical vasocon

76 TIONALE: 20-Hydroxyeicosatetraenoic acid (20-HETE), one of the principle cytochrome P450 eicosanoids,

77 level of 20-hydroxyeicosatetraenoic acid (20-HETE), which correlates with a significantly shorter tai

78 acid to 20-hydroxyeicosatetraenoic acid (20-HETE).

79 th an effect size sequence of adenosine = 20-HETE > angiotensin II > thromboxane = superoxide > renal

80 Losartan, HET0016, and 20-HETE antagonists each normalized SGK1 mRNA expression.

81 identify elevated P450 4A11 activity and 20-HETE as potential risk factors for salt-sensitive human

82 without affecting Cyp4a12 expression and 20-HETE biosynthesis also ameliorated diabetes-mediated ren

83 Levels of CYP4A12 and 20-HETE in preglomerular microvessels of doxycycline-treate

84 P and induced both Cyp4a12 expression and 20-HETE levels in preglomerular microvessels.

85 d androgen-mediated Cyp4a12 synthesis and 20-HETE production, normalized BP, and ameliorated renal da

86 evoked vasoconstriction, whereas K(+) and 20-HETE signaling blockade showed no effect.

87 were up-regulated via NADPH oxidase- and 20-HETE-dependent mechanisms.

88 on prevented blood pressure elevation and 20-HETE-mediated increases in angiotensin-converting enzyme

89 utyl-2-methylphenyl)formamidine) to block 20-HETE synthesis.

90 ncreased by rofecoxib administration, but 20-HETE production increased in vitro with the addition of

91 pathophysiological functions mediated by 20-HETE in hypertension and cardiovascular diseases.

92 inhibitor of CYP4A, and were mimicked by 20-HETE.

93 In cultured human endothelial cells, 20-HETE binding to GPR75 stimulated Galphaq/11 protein diss

94 ransgenic mice, which express the CYP4A12-20-HETE synthase under the control of a doxycycline-sensiti

95 hophysiological effects of CYP4F2-derived 20-HETE in the vasculature.

96 Although CYP4A-derived 20-HETE is known to have prohypertensive and proangiogenic

97 reases 20-HETE production, CYP4F2-derived 20-HETE mediates EC proliferation and angiogenesis via VEGF

98 To date, a receptor/binding site for 20-HETE has been implicated based on the use of specific ag

99 A pro-hypertensive role for 20-HETE was implicated by normalization of BP and reversal

100 Furthermore, 20-HETE but not rofecoxib significantly increases rat plate

101 In vascular smooth muscle cells, GPR75-20-HETE pairing is associated with Galphaq/11- and GPCR-kin

102 E(4)), HETEs (e.g. 5(S)-HETE, 12(S)-HETE, 20-HETE), lipids (e.g. arachidonic acid, PAF), and biogenic

103 whether androgen-independent increases in 20-HETE are sufficient to cause hypertension, we studied Cy

104 gs suggest that CSD-induced increments in 20-HETE cause the reduction in CBF after CSD and that the a

105 hypothesis that this dramatic increase in 20-HETE is attributable to inhibition of its metabolism and

106 S/MS analysis revealed 2-foldincreases in 20-HETE levels in tissues and endothelial cells (ECs), rela

107 n, and the time course of the increase in 20-HETE paralleled the reduction in CBF after CSD in vivo.

108 T0016 blocked the CSD-induced increase in 20-HETE synthesis and ameliorated the persistent reduction

109 CSD increased 20-HETE synthesis in brain slices for 120 min, and the time

110 ately doubled, correlating with increased 20-HETE-dependent sensitivity to phenylephrine-mediated vas

111 that human CYP4F2 significantly increases 20-HETE production, CYP4F2-derived 20-HETE mediates EC prol

112 tension due to increased Cyp4a12-mediated 20-HETE production.

113 eneration of ROS by CYP4A monooxygenases, 20-HETE, and Nox oxidases is involved in podocyte apoptosis

114 Neither 20-HETE biosynthesis nor cytochrome P4A-like immune reactiv

115 For evaluation of the role of 20-HETE as a mediator of epithelial cell proliferation, pri

116 er a deficiency in the renal formation of 20-HETE enhances the susceptibility of Dahl salt-sensitive

117 4A genes responsible for the formation of 20-HETE from the Brown Norway (BN) rat onto the SS genetic

118 rease in the renal and urinary content of 20-HETE in clock-deficient mice.

119 Increased levels of 20-HETE in experimental animals and in humans are associate

120 f this study was to determine the role of 20-HETE in modulating the reflex sympathetic responses to a

121 a genetic deficiency in the formation of 20-HETE increases the susceptibility of SS rats to ischemic

122 sponses were examined after injections of 20-HETE into the arterial blood supply of the hindlimb musc

123 The s.c. infusion of 20-HETE shortened the tail bleeding time dramatically.

124 he results show that arterial infusion of 20-HETE significantly enhanced the RSNA and MAP responses t

125 We suggest that blockade of 20-HETE synthesis may be clinically relevant to ameliorate

126 ministration of HET-0016, an inhibitor of 20-HETE synthesis, significantly reduced kidney size by hal

127 We observed a similar contribution of 20-HETE to myogenic tone in the mesenteric microvasculature

128 Blockade of the synthesis of 20-HETE with HET0016 reversed the renoprotective effects in

129 rofecoxib exposure and that inhibition of 20-HETE's degradation by rofecoxib is a partial explanation

130 matic system involved in the formation of 20-HETE, a powerful regulator of renal sodium excretion, re

131 GPR75 knockdown in a mouse model of 20-HETE-dependent hypertension prevented blood pressure ele

132 The discovery of 20-HETE-GPR75 pairing presented here provides the molecular

133 receptor (GPCR), as a specific target of 20-HETE.

134 These results point to a potential 20-HETE dependence of intrarenal angiotensinogen production

135 CR-kinase interacting protein-1 prevented 20-HETE-mediated endothelial growth factor receptor phospho

136 the SS genetic background increased renal 20-HETE levels after ischemia and reduced plasma creatinine

137 These data suggest 20-HETE as a marker of rofecoxib exposure and that inhibiti

138 Here, we demonstrate that 20-HETE both activates and sensitizes mouse and human TRPV1

139 aken together, these results suggest that 20-HETE both mediates androgen-induced hypertension and can

140 These results indicate that 20-HETE has a protective role in renal IR injury by maintai

141 Our data suggest that 20-HETE plays a role in modulating muscle afferent-mediated

142 n mRNA increases by administration of the 20-HETE antagonists 2-((6Z,15Z)-20-hydroxyicosa-6,15-dienam

143 dulates renal function and identifies the 20-HETE synthesis pathway as one of its principal renal tar

144 of the functional outcomes attributed to 20-HETE in vitro and in vivo.

145 hypertension is the major contributor to 20-HETE-driven diabetes-mediated kidney injury.

146 of MaxiKbeta, linking GPR75 activation to 20-HETE-mediated vasoconstriction.

147 ce, produced increased levels of vascular 20-HETE; furthermore, administration of a 20-HETE antagonis

148 xide release to suppress vasoconstricting 20-HETE synthesis.

149 .1 vs. 1.6 +/- 0.5 tubes/field) that were 20-HETE dependent and associated with up-regulation of proo

150 study, we defined the mechanisms whereby 20-HETE affects the progression of diabetic nephropathy.

151 ndertaken to identify a receptor to which 20-HETE binds and through which it activates a signaling ca

152 ienes (e.g. LTB(4), LTC(4), LTD(4), LTE(4)), HETEs (e.g. 5(S)-HETE, 12(S)-HETE, 20-HETE), lipids (e.g

153 bolites 5(S)-hydroxyeicosatetraenoic acid (5-HETE), 8-HETE, and 15-HETE characterized progression fro

154 d the ratio of ARA/LA, leukotriene B4, and 5-HETE but no effect on levels of cyclooxygenase products.

155 reased 12-LOX expression and 12-, 15-, and 5-HETE production.

156 glutamyl peptides, GGT, leukotriene B4 and 5-HETE.

157 acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic acids (HODEs), i

158 course of HK formation paralleled that of 5-HETE and LTB4, implying the availability of the 5S-HETE

159 A23187 resulted in the formation of PGE2, 5-HETE, and LTB4 as the principal metabolites of COX-2 and

160 levels were similar to PGE2, but less than 5-HETE and LTB4 The time course of HK formation paralleled

161 ation of 5S-hydroxyeicosatetraenoic acid (5S-HETE).

162 Platelets did not form HKs from exogenous 5S-HETE, implying that COX-1 is not involved.

163 nd LTB4, implying the availability of the 5S-HETE substrate as a limiting factor in biosynthesis rath

164 (S)-hydroxyeicosatetraenoic acid (5-HETE), 8-HETE, and 15-HETE characterized progression from normal

165 y LC-MS/MS the formation of HXB3, 12-HETE, 8-HETE, and 15-HETE from arachidonic acid (AA) at baseline

166 s associated with significant decreases in 8-HETE, 9-HETE, and 11-HETE compared to placebo.

167 8R-hydroxyeicosatetraenoic acid (8R-HETE), the hydroxy analog of the natural substrate, norm

168 acid was converted to two major products, 8R-HETE and 8R,9S-eicosatrienoic acid (8R,9S-EET), plus oth

169 The enantiomer, 8S-HETE, was epoxidized stereospecifically, although with l

170 ated with significant decreases in 8-HETE, 9-HETE, and 11-HETE compared to placebo.

171 2-, and 8-monohydroxy-eicosatetraenoic acid (HETE) are elevated from 4 to 72 h, in association with p

172 (S)-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE).

173 oduction of 11-hydroxyeicosatetraenoic acid (HETE) and 15(S)-HETE, in addition to prostanoids such as

174 ding bioactive hydroxyeicosatetraenoic acid (HETE) metabolites.

175 osanoid was 5-hydroxyeicosate traenoic acid (HETE), which demonstrated a diabetes-specific increase (

176 OX-mediated 5-hydroxyeicosatetraenoic acids (HETE) and 15-HETE from arachidonic acid in the testes we

177 xoODEs), and hydroxy-eicosatetraenoic acids (HETEs) were quantified by mass spectrometry in plasma ob

178 tion of toxic hydroxyeicosatetraenoic acids (HETEs) and attenuate the activity of phospholipases that

179 ed intestinal hydroxyeicosatetraenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as h

180 ated dipeptide hydroxyethylthioethyl-CysPro (HETE-CP) derived from the HSA-SM adduct that was detecte

181 rated high affinity binding for 12-(S)-[(3)H]HETE (K(d) = 4.8 +/- 0.12 nm).

182 ores of fibrosis and between the decrease in HETEs and improved lobular inflammation.

183 gnificantly reduced UFP-mediated increase in HETEs, HODEs, AA, PGD2, and LPA.

184 fluential FADS SNP, rs174537 on leukotriene, HETE, prostaglandin, and thromboxane biosynthesis in sti

185 Mechanistically, HETEs activated the Ca(2+)-induced opening of the mPTP i

186 The amounts of HETEs also were significantly higher in the vitreous of

187 ectrometry was used to assess the amounts of HETEs in the murine retina and human vitreous samples.

188 12-LOX and its product HETE are important regulators of retinal NV through modu

189 The ability of 12(R)-HETE to activate AHR target genes required receptor expr

190 ts, have demonstrated the inability of 12(R)-HETE to directly bind or directly activate the AHR to a

191 Z),10(E), 14(Z)-eicosatetraenoic acid [12(R)-HETE], an arachidonic acid metabolite produced by either

192 owever, COX-2 (but not COX-1) can form 15(R)-HETE, which is metabolized to aspirin-triggered lipoxin

193 Treatments with LXA4, 12(S)-, and 15(S)- HETE did not stimulate neurite outgrowth.

194 Pretreatment with 12(S)-HETE also amplified the signaling effects of angiotensin

195 These findings identify 12(S)-HETE as a trigger of platelet MP internalization by neut

196 Mechanistically, 12(S)-HETE is produced through the concerted activity of secre

197 ct 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE) increased AT1R mRNA and protein expression, primar

198 TD(4), LTE(4)), HETEs (e.g. 5(S)-HETE, 12(S)-HETE, 20-HETE), lipids (e.g. arachidonic acid, PAF), and

199 Among 5(S)-HETE, 12(S)-HETE, and 15(S)-HETE, 15(S)-HETE potentially stimulated

200 lites of arachidonic acid 12(S)-HpETE, 12(S)-HETE, HXA(3), or HXB(3) evoked profound, persistent tact

201 ch was rescued by prior treatment with 12(S)-HETE, in a peritonitis model.

202 rophils in the endomembrane system via 12(S)-HETE.

203 ied 12(S)-hydroxyeicosatetranoic acid [12(S)-HETE] as the predominant eicosanoid generated by MPs.

204 ty 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] receptor (12-HETER1).

205 Also, 12-(S)-HETE efficiently and selectively stimulated GTPgammaS co

206 tified high affinity receptor for the 12-(S)-HETE hydroxyl fatty acids.

207 Activating GTPgammaS coupling with 12-(S)-HETE proved to be both regio- and stereospecific.

208 Thus, GPR31 is named 12-(S)-HETE receptor (12-HETER) in this study.

209 down 12-HRTER specifically inhibited 12-(S)-HETE-stimulated cell invasion.

210 Also, 12-(S)-HETE/12-HETER interactions lead to activation of ERK1/2,

211 Similarly, 15(S)-HETE activated tyrosine phosphorylation of STAT-5B in a

212 15(S)-HETE also induced Fra-1 and c-Jun expression in a Rac1-M

213 15(S)-HETE also induced monocyte chemoattractant protein-1 (MC

214 15(S)-HETE also induced tyrosine phosphorylation of Janus kina

215 In the arteries of WT mice ex vivo, 15(S)-HETE also induced ZO-1 phosphorylation and endothelial T

216 15(S)-HETE also stimulated macrophage adhesion to the endothel

217 , it inhibits angiogenesis mediated by 15(S)-HETE and did not enhance inhibition of collagen-induced

218 These results reveal 15(S)-HETE as a major platelet cyclooxygenase-1 product with s

219 te for the first time that the 15-Lox1-15(S)-HETE axis activates EGFR via redox-sensitive manner, whi

220 ct evidence for a role of 12/15-Lox-12/15(S)-HETE axis in the regulation of ischemia-induced angiogen

221 s show for the first time that 15-LOX1-15(S)-HETE axis plays a major role in vascular wall remodeling

222 ervations suggest that the 12/15-LO-12/15(S)-HETE axis, in addition to tyrosine phosphorylation of ZO

223 15(S)-HETE by inducing HMG-CoA reductase expression caused inc

224 hibits the production of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1.

225 These findings may suggest that 15(S)-HETE could be a potential endogenous regulator of pathol

226 We found that 15(S)-HETE enhances ZO-1 phosphorylation at Thr-770/772 residu

227 15(S)-HETE induced Egr-1 expression in a time-dependent manner

228 15(S)-HETE induced fibroblast growth factor-2 (FGF-2) expressi

229 The 15(S)-HETE induced interleukin-8 (IL-8) expression in Jak2-STA

230 15(S)-HETE induced MMP-2 expression and activity in a time-dep

231 15(S)-HETE induced the production of H(2)O(2) via an NADPH oxi

232 sure of arteries from WT mice to AA or 15(S)-HETE led to Src-Pyk2-dependent ZO-2 tyrosine phosphoryla

233 unction also attenuated the effects of 15(S)-HETE on HDMVEC migration and tube formation as well as M

234 Consistent with the effects of 15(S)-HETE on the activation of EGFR-Src-Jak2-STAT3 signaling

235 5(S)-HETE, 12(S)-HETE, and 15(S)-HETE, 15(S)-HETE potentially stimulated more vascular smooth muscle

236 Thus, 15(S)-HETE represents a potential target for the development o

237 15(S)-HETE stimulated Rac1 in a sustained manner in human derm

238 15(S)-HETE stimulated tyrosine phosphorylation of EGFR in a ti

239 The 15(S)-HETE stimulated tyrosine phosphorylation of Jak2 in a ti

240 sible for catalyzing the conversion of 15(S)-HETE to 15-oxo-ETE.

241 Furthermore, 15(S)-HETE was metabolized primarily to 15-oxo-ETE.

242 ominant-negative mutant of Src blocked 15(S)-HETE's effects on migration and tube formation of HDMVEC

243 ch 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) activates Rac1 in the induction of angiogenesis, w

244 ch 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) activates signal transducer and activator of trans

245 hat 15(S)-hydroxyeicosatetranoic acid (15(S)-HETE) induces CD36 expression involving STAT1.

246 nd 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) production, indicating an inhibitory action of I3M

247 d, 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE), on vascular smooth muscle cell (VSMC) migration b

248 15(S)-Hydroxyeicosatetraenoic acid (15(S)-HETE), the major 12/15-LO metabolite of arachidonic acid

249 at 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE), the major 15-lipoxygenase 1 (15-LO1) metabolite o

250 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE), the major product of human 15-LOXs 1 and 2, induc

251 in 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE)-induced angiogenesis, we have studied the role of

252 ng 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE)-induced angiogenesis, we have studied the role of

253 Among 5(S)-HETE, 12(S)-HETE, and 15(S)-HETE, 15(S)-HETE potentially stimulated more vascular sm

254 It also interacts with 15(S)-HETE, being the first lipocalin described to date to bin

255 ydroxyeicosatetraenoic acid (HETE) and 15(S)-HETE, in addition to prostanoids such as thromboxane A2

256 ole of 12/15-LO and its AA metabolite, 15(S)-HETE, in high-fat diet-induced endothelial tight junctio

257 ether, these observations suggest that 15(S)-HETE-induced angiogenesis requires Jak2-STAT-5B-dependen

258 f these observations, we conclude that 15(S)-HETE-induced angiogenesis requires Src-mediated Egr-1-de

259 tivated receptor-gamma is required for 15(S)-HETE-induced CD36 expression, oxidized low density lipop

260 15(S)-HETE-induced Egr-1 expression requires Src activation.

261 nine phosphorylation of TJ proteins in 15(S)-HETE-induced endothelial TJ disruption and its barrier d

262 anscription start site is required for 15(S)-HETE-induced FGF-2 expression.

263 ts dominant-negative mutant attenuated 15(S)-HETE-induced HDMVEC migration and tube formation as well

264 Down-regulation of alphaPix inhibited 15(S)-HETE-induced HDMVEC migration and tube formation.

265 or depletion of its levels attenuated 15(S)-HETE-induced HDMVEC migration, tube formation, and Matri

266 rence of STAT-5B activation suppressed 15(S)-HETE-induced HRMVEC migration and tube formation and Mat

267 tralizing anti-IL-8 antibodies reduced 15(S)-HETE-induced HRMVEC migration and tube formation and Mat

268 ts dominant-negative mutant attenuated 15(S)-HETE-induced HRMVEC migration and tube formation and Mat

269 hat STAT binding site is essential for 15(S)-HETE-induced IL-8 promoter activity.

270 In addition, 15(S)-HETE-induced MMP-2 expression and activity were mediated

271 scriptional start site is required for 15(S)-HETE-induced MMP-2 expression, and Fra-1 and c-Jun are t

272 n with neutralizing antibodies blocked 15(S)-HETE-induced monocyte migration.

273 These observations indicate that 15(S)-HETE-induced monocyte/macrophage migration and trafficki

274 bitor of HMG-CoA reductase, suppressed 15(S)-HETE-induced Rac1 activation in HDMVECs affecting their

275 Mevalonate rescued 15(S)-HETE-induced Rac1 farnesylation and membrane translocati

276 erference with EGFR activation blocked 15(S)-HETE-induced Src and STAT3 tyrosine phosphorylation, mon

277 art site was found to be essential for 15(S)-HETE-induced Src-STAT-3-mediated MCP-1 expression.

278 factor subunit (FosB) are involved in 15(S)-HETE-induced TF expression.

279 In addition, 15(S)-HETE-induced VSMC migration was dependent on Src-mediate

280 ti-MCP-1 antibodies completely negated 15(S)-HETE-induced VSMC migration.

281 acetic acid (CAY10397) reduced AA- and 15(S)-HETE-mediated formation of 15-oxo-ETE in a dose-dependen

282 cysteine (NAC) and catalase suppressed 15(S)-HETE-stimulated EGFR, Src, Jak2, and STAT3 phosphorylati

283 n response to AA, which was rescued by 15(S)-HETE.

284 bind to MMP-2 promoter in response to 15(S)-HETE.

285 of STAT-5B to this site in response to 15(S)-HETE.

286 eturned by coincubation with exogenous 15(S)-HETE.

287 expression and foam cell formation by 15(S)-HETE.

288 n the regulation of CD36 expression by 15(S)-HETE.

289 11,13-(Z,Z,Z,E)-eicosatetraenoic acid [15(S)-HETE] and 15-oxo-ETE, confirming the role of 15-LO-1 in

290 ng 15(S)-hydroxyeicosatetraenoic acid [15(S)-HETE]-induced angiogenesis, we studied the role of Egr-1

291 Concentrations of 5(S)-HETE increased from 0.07 +/- 0.01 to 45.50 +/- 4.05 pmol

292 ibitor reduced HepsilondGuo-adducts and 5(S)-HETE to basal levels.

293 ,11,14-(E,Z,Z,Z)-eicosatetraenoic acid (5(S)-HETE)).

294 ), LTC(4), LTD(4), LTE(4)), HETEs (e.g. 5(S)-HETE, 12(S)-HETE, 20-HETE), lipids (e.g. arachidonic aci

295 Among 5(S)-HETE, 12(S)-HETE, and 15(S)-HETE, 15(S)-HETE potentially

296 ntrast, aspirin, which had no effect on 5(S)-HETE, blocked the formation of prostaglandins, 15-HETE,

297 hydroxyeicosatetraenoic acid (12[S] or 15[S]-HETE), and nerve growth factor (NGF) as positive control

298 In contrast, structurally similar HETE isomers failed to demonstrate significant activatio

299 odeling metabolically channels AA into toxic HETEs promoting mPTP opening, which induces necrosis/apo

300 d iPLA2gamma activity channels AA into toxic HETEs.