ライフサイエンスコーパス: HETE

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

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

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

4 5-hydroxyeicosatetraenoic acid (HETE) and 11-HETE were significantly higher in those with hyperplasti

5 ETrE]) or auto-oxidative reactions (i.e., 11-HETE), this may indicate that lipoxygenase activity and

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

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

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

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

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

14 hibited the production of 12-HETE-LPC and 12-HETE-LPE in activated platelets.

15 ted production of 2-AA-LPC, 2-AA-LPE, and 12-HETE-lysophospholipids in mouse platelets.

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 purported G-protein-coupled receptor for 12-HETE, largely phenocopies both the depletion and the inh

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

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

24 is accompanied by significant changes in 12-HETE-LPC in murine serum that were also markedly attenua

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

26 he activation of 12/15-lipoxygenase (LOX)/12-HETE signaling, altering neuronal morphology and affecti

27 2/15-lipoxygenase (12/15-LOX) metabolites 12-HETE and 12-HPETE at 300 nM, block axon extension in neu

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

29 The adjusted mean concentration of 12-HETE, a LOX pathway product, was 56.2% higher (95% credi

30 significantly inhibited the production of 12-HETE-LPC and 12-HETE-LPE in activated platelets.

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

32 abolism, and alongside its major product, 12-HETE, plays a key role in promoting inflammatory signali

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

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

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

36 ed via a signaling axis that includes the 12-HETE receptor GPR31.

37 15-HETE production was reduced in EGCs from patients with C

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

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

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

41 ion, since oxylipids such as 5-, 12-, and 15-HETE are signaling molecules involved in inflammation re

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

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

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

45 11-hydroxyeicosatraenoic acid (HETE), and 15-HETE was absent in both platelet- and global-COX-1-ko mi

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

47 tion by lipoxygenases (i.e., 5-, 12-, and 15-HETE, and 15- hydroxyeicosatrienoic acid [HETrE]) or aut

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

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

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

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

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

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

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

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

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

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

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

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

60 15-lipoxygenase (the enzyme that produces 15-HETE); colons were collected and permeability was measur

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

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

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

64 20-HETE is significantly more potent than its COX-mediated

65 20-HETE synthesis was measured in parallel experiments in c

66 20-HETE; furthermore, administration of a 20-HETE antagonist normalized BP.

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

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

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

70 20-Hydroxyeicosatetraenoic acid (20-HETE) has an important role in the regulation of renal t

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

72 20-Hydroxyeicosatetraenoic acid (20-HETE) is a cytochrome P-450 4A/4F-derived metabolite of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 4A genes responsible for the formation of 20-HETE from the Brown Norway (BN) rat onto the SS genetic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 xide release to suppress vasoconstricting 20-HETE synthesis.

143 .1 vs. 1.6 +/- 0.5 tubes/field) that were 20-HETE dependent and associated with up-regulation of proo

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

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

146 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

147 to the relocalization of cPLA(2)alpha and 5-HETE biosynthetic enzymes to the cytoplasm and cytoplasm

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

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

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

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

152 Specifically, an increase in 5-HETE enhanced dermal fibroblast migration and collagen d

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

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

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

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

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

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

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

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

161 8R-hydroxyeicosatetraenoic acid (8R-HETE), the hydroxy analog of the natural substrate, norm

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

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

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

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

166 ntrations of 5-hydroxyeicosatetraenoic acid (HETE) and 11-HETE were significantly higher in those wit

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

168 shed that 2-15-hydroxyeicosatetraenoic acid (HETE) ether-LPC sn-1 esterification is markedly activate

169 ding bioactive hydroxyeicosatetraenoic acid (HETE) metabolites.

170 nce of certain hydroxyeicosatetraenoic acid (HETE) species.

171 ) F(2alpha) , 11-hydroxyeicosatraenoic acid (HETE), and 15-HETE was absent in both platelet- and glob

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

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

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

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

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

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

178 Arachidonic acid-derived HETEs were significantly associated with colon polyp typ

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

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

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

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

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

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

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

186 12-LOX and its product HETE are important regulators of retinal NV through modu

187 selective with 12(S)-HETE favored over 12(R)-HETE.

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

189 in COX-2 not only triggers formation of 15 R-HETE but also allows oxygenation and cyclization of arac

190 rms 15 R hydroxy-eicosatetraenoic acid (15 R-HETE) as alternate product.

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

192 The effects of the abundance of 12(S)-HETE and its contribution to several chronic inflammator

193 phospholipids as well as nonesterified 12(S)-HETE are potent lipid mediators that activate THP-1 huma

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

195 of 2-12(S)-HETE-lysophospholipids and 12(S)-HETE by their ability to release TNFalpha and activate N

196 dysfunction in endothelial cells, and 12(S)-HETE effects were absent in endothelial cells from TRPV1

197 ease TNFalpha was stereoselective with 12(S)-HETE favored over 12(R)-HETE.

198 Both 12(S)-HETE in concentrations found in diabetic patients and TR

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

200 was 2.1 nm, whereas the EC(50) of free 12(S)-HETE was 23 nm Additionally, lipid extracts of activated

201 RP-HPLC demonstrating the coelution of 12(S)-HETE with fractions initiating TNFalpha release.

202 s of lipoxygenase-derived metabolites [12(S)-HETE, 15(S)-HETE] and a decrease in the concentrations o

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

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

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

206 nce, we found that a peptide targeting 12(S)-HETE-induced TRPV1 interaction at the TRPV1 TRP box amel

207 -hydroxyeicosatetraenoic acid-induced [12(S)-HETE-induced] activation of the intracellularly located

208 downstream 12-LOX oxidation products, 12(S)-HETE-LPC and 12(S)-HETE-LPE, in calcium ionophore (A2318

209 oxidation products, 12(S)-HETE-LPC and 12(S)-HETE-LPE, in calcium ionophore (A23187)-stimulated murin

210 Furthermore, the EC(50) of 2-12(S)-HETE-lysophosphatidylcholine in activating THP-1 cells w

211 estern blotting analyses revealed that 12(S)-HETE-lysophospholipids activated the phosphorylation of

212 e the potent signaling properties of 2-12(S)-HETE-lysophospholipids and 12(S)-HETE by their ability t

213 Herein, we demonstrate that 2-12(S)-HETE-lysophospholipids as well as nonesterified 12(S)-HE

214 vealing a previously unknown role of 2-12(S)-HETE-lysophospholipids in mediating inflammatory respons

215 Moreover, TNFalpha release induced by 12(S)-HETE-lysophospholipids was inhibited by the TNFalpha con

216 kably, low nanomolar concentrations of 12(S)-HETE-lysophospholipids, but not other oxidized signaling

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

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

219 he 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] lipid mediator is among inflammatory molecules tha

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

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

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

223 PDAC progression and that ALOX12 and 12-(S)-HETE may be potential stromal targets for interventions

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

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

226 roxy-5,8,10,14-eicosatetraenoic acid (12-(S)-HETE) compared with their younger counterparts.

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

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

229 15(S)-HETE also induced Fra-1 and c-Jun expression in a Rac1-M

230 15(S)-HETE also induced tyrosine phosphorylation of Janus kina

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

232 15(S)-HETE also stimulated macrophage adhesion to the endothel

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

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

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

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

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

238 15(S)-HETE by inducing HMG-CoA reductase expression caused inc

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

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

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

242 15(S)-HETE induced Egr-1 expression in a time-dependent manner

243 15(S)-HETE induced fibroblast growth factor-2 (FGF-2) expressi

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

245 15(S)-HETE induced MMP-2 expression and activity in a time-dep

246 15(S)-HETE induced the production of H(2)O(2) via an NADPH oxi

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

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

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

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

251 15(S)-HETE stimulated Rac1 in a sustained manner in human derm

252 15(S)-HETE stimulated tyrosine phosphorylation of EGFR in a ti

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

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

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

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

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

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

259 15(S)-Hydroxyeicosatetraenoic acid (15(S)-HETE), the major 12/15-LO metabolite of arachidonic acid

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

261 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE), the major product of human 15-LOXs 1 and 2, induc

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

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

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

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

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

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

268 15(S)-HETE-induced Egr-1 expression requires Src activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 enase-derived metabolites [12(S)-HETE, 15(S)-HETE] and a decrease in the concentrations of amino acid

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

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

294 rix, we show that a shallow gradient of 12-S-HETE enhances chemotaxis towards low concentrations of S

295 These results suggest that 12-S-HETE might be an autocrine signaling molecule exported b

296 ntial homolog of the human receptor for 12-S-HETE, gpr31, is expressed on GSCs and differentiating va

297 scued by addition of the 12-Lox product 12-S-HETE.

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

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

300 d iPLA2gamma activity channels AA into toxic HETEs.