ライフサイエンスコーパス: mPGES-1

1 mPGES-1 -/- mice developed severe and progressive hypert

2 mPGES-1 -/- mice exhibited a remarkable inhibition of hi

3 mPGES-1 activation, PGE2 production, and edema formation

4 mPGES-1 deficient mice also exhibited attenuation of mec

5 mPGES-1 deletion augmented expression of both prostacycl

6 mPGES-1 inhibited the expression of phosphatase and tens

7 mPGES-1 is a promising target for development of new ant

8 mPGES-1 is overexpressed in human cholangiocarcinoma tis

9 mPGES-1 is widely considered to be the final enzyme regu

10 mPGES-1 null and heterozygous mice exhibited decreased i

11 mPGES-1 promotes experimental cholangiocarcinogenesis an

12 mPGES-1(-/-) LDLR(-/-) plaques were enriched with fibril

13 mPGES-1-derived PGE(2) accelerates atherogenesis in LDLR

14 mPGES-1-expressing cells in tumors from different subtyp

15 mPGES-1-mediated inhibition of PTEN is regulated through

16 ucible COX-2 and microsomal PGE2 synthase 1 (mPGES-1) (1).

17 mice deficient in microsomal PGE synthase 1 (mPGES-1) and in the receptors for PGI2.

18 on of microsomal prostaglandin E synthase 1 (mPGES-1) confers analgesia, attenuates atherogenesis, an

19 tion in microsomal prostaglandin synthase 1 (mPGES-1) expression.

20 on of microsomal prostaglandin E synthase 1 (mPGES-1) in mice attenuates the response to vascular inj

21 Microsomal prostaglandin E synthase 1 (mPGES-1) is a key enzyme of the arachidonic acid cascade

22 Microsomal prostaglandin E synthase 1 (mPGES-1) is an alpha-helical homotrimeric integral membr

23 OX-2, microsomal prostaglandin E synthase 1 (mPGES-1), and EP receptors, was assessed at baseline and

24 minal synthase microsomal PGE(2) synthase 1 (mPGES-1), which is responsible for generating PGE(2), in

25 ) and microsomal prostaglandin E synthase 1 (mPGES-1).

26 n of microsomal prostaglandin E2 synthase-1 (mPGES-1) and 5-lipoxygenase (5-LO) is currently pursued

27 ls of microsomal prostaglandin E synthase-1 (mPGES-1) and elevated levels of PGE2.

28 up-regulation of microsomal PGE synthase-1 (mPGES-1) and L-PGDS.

29 COX-2 and microsomal PGE synthase-1 (mPGES-1) and mPGES-2 are present in postsynaptic dendrit

30 fied microsomal prostaglandin E2 synthase-1 (mPGES-1) as a RET/PTC-inducible gene through subtraction

31 ed both COX-2 and microsomal PGE synthase-1 (mPGES-1) but not COX-1 in the Golgi apparatus.

32 ) and microsomal prostaglandin E synthase-1 (mPGES-1) by a yet unknown mechanism.

33 crosomal prostaglandin (PG) E(2) synthase-1 (mPGES-1) catalyzes isomerization of the cyclooxygenase p

34 Microsomal prostaglandin E synthase-1 (mPGES-1) catalyzes the conversion of cyclooxygenase-deri

35 Microsomal prostaglandin E synthase-1 (mPGES-1) in myeloid and vascular cells differentially re

36 ssing microsomal prostaglandin E synthase-1 (mPGES-1) into the median preoptic nucleus of fever-refra

37 Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme that couples with cyclooxygenas

38 Microsomal prostaglandin E synthase-1 (mPGES-1) is a rate-limiting enzyme that is coupled with

39 Microsomal PGE synthase-1 (mPGES-1) is an inducible enzyme that acts downstream of

40 Microsomal prostaglandin E (PGE) synthase-1 (mPGES-1) is an inducible enzyme that couples with cycloo

41 Microsomal PGE synthase-1 (mPGES-1) is an inducible enzyme that specifically cataly

42 that microsomal prostaglandin E synthase-1 (mPGES-1) is induced in brain vascular cells that also ex

43 hibit microsomal prostaglandin E synthase-1 (mPGES-1) with an IC50 of 17.4 muM.

44 ced expression of microsomal PGE synthase-1 (mPGES-1), a key enzyme in PGE2 biosynthesis.

45 Microsomal prostaglandin E synthase-1 (mPGES-1), a membrane-associated protein, is critically i

46 Microsomal prostaglandin E(2) synthase-1 (mPGES-1), encoded by the Ptges gene, catalyzes prostagla

47 inducible PGE2, microsomal PGE2 synthase-1 (mPGES-1), has emerged as an interesting drug target for

48 ugh inhibition of microsomal PGE synthase-1 (mPGES-1), not COX-2.

49 lism, microsomal prostaglandin E synthase-1 (mPGES-1), prostaglandin dehydrogenase (PGDH), COX-2 and

50 ) and microsomal prostaglandin E synthase-1 (mPGES-1), which are involved in PGE2 production.

51 f COX enzymes and microsomal PGE synthase-1 (mPGES-1).

52 vels of COX-2 and microsomal PGE synthase-1 (mPGES-1).

53 Microsomal prostaglandin E2 synthase type 1 (mPGES-1) is responsible for the formation of the potent

54 Microsomal PGES-1(-/-) (mPGES-1(-/-)) mice were crossed into low-density lipopro

55 These findings have revealed a mPGES-1/prostaglandin E(2)/NO/cGMP pathway that appears

56 RET/PTC activated mPGES-1 gene transcription.

57 In addition, mPGES-1 null and heterozygous mice showed a marked reduc

58 n experiments using a siRNA directed against mPGES-1.

59 fold up-regulation of TLR4 expression via an mPGES-1-dependent pathway, whereas prolonged shear expos

60 ride, which elevated expression of COX-2 and mPGES-1 and produced PGE2, and this enhancement was inhi

61 IL-1RI positively correlated with COX-2 and mPGES-1 expression in both NM-C and NP-AERD fibroblasts.

62 e capacity of IL-1beta to increase COX-2 and mPGES-1 expression, which results in low PGE2 production

63 roteinase-2 protein and cyclooxygenase-2 and mPGES-1 mRNA expression.

64 IL-1beta increased mRNA levels for COX-2 and mPGES-1, but not for COX-1 or cPGES.

65 ed aortic expression of cyclooxygenase-2 and mPGES-1, increased aortic macrophage recruitment and vas

66 nthetic enzymes cyclooxygenase-2 (COX-2) and mPGES-1 are up-regulated in many cancers.

67 IL-1beta-induced IL-1RI, COX-2, and mPGES-1 expression levels were also lower in these cells

68 Alterations in IL-1RI, COX-2, and mPGES-1 expression that were found in NP-AERD fibroblast

69 cytosolic phospholipase A2alpha, COX-2, and mPGES-1 in the Golgi comprise a dedicated system for COX

70 in this pathway, cPLA2 type IVA, COX-2, and mPGES-1, were dramatically up-regulated at both the tran

71 Induction of COX2 and mPGES-1 expression by TLR2 stimulation or Mtb infection

72 expressed mRNAs of COX-1, COX-2, cPGES, and mPGES-1.

73 functional interaction between PPARgamma and mPGES-1 in controlling the process of pre-adipocyte diff

74 lation of adipogenesis between PPARgamma and mPGES-1.

75 cosanoid metabolism enzymes in wild type and mPGES-1-deficient macrophages.

76 ted insulin secretion equally in both WT and mPGES-1(-/-) islets, indicating that COX-2, not mPGES-1,

77 on was examined in isolated islets of WT and mPGES-1-deficient mice.

78 2, whereas there was no coexpression between mPGES-1 and cyclooxygenase-1.

79 ur findings depict a novel crosstalk between mPGES-1/PGE(2) and EGR1/beta-catenin signaling that is c

80 with in vivo rediversion of PG biosynthesis, mPGES-1-deleted vascular smooth muscle cells generated l

81 iated LPS-induced IL-33 generation from both mPGES-1-null and WT bmMFs, whereas EP1 and EP3 receptor

82 Male mice deficient in both mPGES-1 and LDLR (mPGES-1(-/-) LDLR(-/-)) and littermate

83 ffect on the attenuation of atherogenesis by mPGES-1 deletion in the low-density lipoprotein receptor

84 ane-1,20-dioic acid (PGE-M) was depressed by mPGES-1 deletion.

85 te that SphK1 regulates PGE(2) production by mPGES-1 expression via the p38 MAPK pathway, independent

86 ular smooth muscle cell and endothelial cell mPGES-1 deletion did not alter blood pressure at baselin

87 ular smooth muscle cell and endothelial cell mPGES-1-deficient mice exhibited a markedly exaggerated

88 In conclusion, myeloid cell mPGES-1 promotes atherogenesis in hyperlipidemic mice, c

89 In primary cultures of CD cells, mPGES-1 expression was significantly increased following

90 By contrast, mPGES-1 in vascular cells does not detectably influence

91 ared with the control (P<0.01); in contrast, mPGES-1 knockdown delayed tumor development and reduced

92 d terminal prostaglandin E synthases (cPGES, mPGES-1, and mPGES-2).

93 We aimed to create mPGES-1 inhibitors by modifying the structure of NSAIDs

94 tudy revealed three modifications dissecting mPGES-1/5-LO inhibition, namely (i) truncation of the ac

95 pro-inflammatory targets of curcumin (i.e., mPGES-1, cyclooxygenases, 12/15-LOs, nuclear factor-kapp

96 (VSMC-mPGES-1-KOs), or endothelial cells (EC-mPGES-1-KOs) were crossed into hyperlipidemic low-densit

97 ad implications for development of efficient mPGES-1 inhibitors, potential anti-inflammatory and anti

98 Compared with WT cells, bmMFs lacking either mPGES-1 or EP2 receptors displayed reduced LPS-induced I

99 In microsomal extracts, mPGES-1 protein was barely detectable in rat islets but

100 The strict structural requirements for mPGES-1 and 5-LO inhibition strongly suggest that specif

101 Furthermore, 26 was selective for mPGES-1 inhibition versus other mechanisms in the prosta

102 itrite biosynthesis using cells derived from mPGES-1 wild-type (WT), heterozygous (Het), and null mic

103 Conditioned medium derived from mPGES-1-deficient macrophages less potently induced vasc

104 ramatic reduction in [3H]PGE2 formation from mPGES-1-/- macrophages compared with controls resulted i

105 lycollate-elicited macrophages isolated from mPGES-1-/- animals and genetically matched wild type con

106 ceptor knockout (LDLR(-/-)) mice to generate mPGES-1(-/-) LDLR(-/-)s.

107 High mPGES-1 expression also corresponded to poor survival of

108 ve determined the crystal structure of human mPGES-1 to 1.2 A resolution.

109 a high-resolution crystal structure of human mPGES-1 was presented, with Ser-127 being proposed as th

110 ch mPGES-1 was silenced, thereby identifying mPGES-1 as a therapeutic target in the regulation of MMP

111 Importantly, mPGES-1 deletion also blocked the nuclear accumulation o

112 Most importantly, mPGES-1 deletion affected neither thrombogenesis nor blo

113 Here, we generated mice deficient in mPGES-1 in vascular smooth muscle cells, endothelial cel

114 Macrophage foam cells were depleted in mPGES-1(-/-) LDLR(-/-) lesions, whereas the total areas

115 lining hyperplasia and tissue destruction in mPGES-1 null mice compared with their wild-type litterma

116 In contrast, we detected in mPGES-1-/- macrophages a >95% reduction in PGE2 producti

117 MCs expressing PGI synthase were enriched in mPGES-1(-/-) LDLR(-/-) lesions.

118 , but not 2,3-dinor-TxB(2), was increased in mPGES-1(-/-) LDLR(-/-)s.

119 ignificantly reduced 4 weeks after injury in mPGES-1 knockout mice compared with wild-type controls (

120 Interest in mPGES-1 inhibition can, in part, be attributed to the po

121 le breakdown product of nitric oxide (NO) in mPGES-1 WT MEFs compared with null MEFs.

122 ly increased in wild-type animals but not in mPGES-1 -/- mice.

123 e redirection of prostaglandin production in mPGES-1-/- cells provides novel insights into how a cell

124 um IgM and IgG were significantly reduced in mPGES-1 null mice.

125 [3H]hydroxyheptadecatrienoic acid release in mPGES-1-/- samples.

126 wever, in neither case did IL-1beta increase mPGES-1 protein levels.

127 Moreover, TNF-alpha induced mPGES-1 by stimulating PC-PLC --> PKC --> NO --> cGMP --

128 , an activator of guanylate cyclase, induced mPGES-1.

129 sion in PCCL3 thyroid cells markedly induced mPGES-1 and COX-2.

130 Chronic salt loading remarkably induced mPGES-1 protein expression exclusively in the distal nep

131 athione-based analog, providing insight into mPGES-1 flexibility and potential for structure-based dr

132 This perspective introduces mPGES-1 as a key player within the network of eicosanoid

133 Mice lacking mPGES-1 (and therefore PGE2) developed arthritis normall

134 Mice lacking mPGES-1 (ptges(-/-) mice) and wild-type C57BL/6 controls

135 Mice lacking mPGES-1 conditionally in myeloid cells (Mac-mPGES-1-KOs)

136 Mice lacking mPGES-1 showed lower IL-33 levels and attenuated lung in

137 ale mice deficient in both mPGES-1 and LDLR (mPGES-1(-/-) LDLR(-/-)) and littermate LDLR(-/-) mice we

138 d pirinixic acids represent potent dual 5-LO/mPGES-1 inhibitors with an attractive pharmacological pr

139 ured pirinixic acid derivatives as dual 5-LO/mPGES-1 inhibitors with improved potency (exemplified by

140 mPGES-1 conditionally in myeloid cells (Mac-mPGES-1-KOs), vascular smooth muscle cells (VSMC-mPGES-1

141 vealed markedly reduced atherogenesis in Mac-mPGES-1-KOs, which was concomitant with a reduction in o

142 e to vascular injury, implicating macrophage mPGES-1 as a cardiovascular drug target.

143 erapeutic rationale for targeting macrophage mPGES-1 in inflammatory cardiovascular diseases.

144 nship and pharmacological potential of major mPGES-1 inhibitor classes in light of recent insights fr

145 Mechanistically, mPGES-1-induced HCC cell proliferation, invasion and mig

146 Compared with WT mice, mPGES-1 null mice exhibited a significant reduction of h

147 In a mouse tumor xenograft model, mPGES-1-overexpressed cells formed palpable tumors at ea

148 antibody that specifically recognizes mouse mPGES-1 and dual-labeling for cell-specific markers, we

149 We therefore suggest that the CD14/NFAT/mPGES-1 pathway represents a possible target for antiinf

150 ES-1(-/-) islets, indicating that COX-2, not mPGES-1, mediates IL-1beta-induced PGE(2) production and

151 The absence of mPGES-1 reduced the size and number of preneoplastic abe

152 lonocytes, resulting in increased amounts of mPGES-1 mRNA and protein.

153 Increased amounts of mPGES-1 were detected in inflamed intestinal mucosa from

154 as applied to characterize this new class of mPGES-1 inhibitors.

155 report, we characterize the contribution of mPGES-1 to cellular PGH2 metabolism in murine macrophage

156 strate for the first time that deficiency of mPGES-1 inhibits the development of collagen-induced art

157 Deletion of mPGES-1 also depressed urinary PGE-M, whereas it augment

158 Deletion of mPGES-1 decreased both the incidence (87.5% versus 27.3%

159 We show that deletion of mPGES-1 depressed PGE(2) expression, augmented PGI(2) ex

160 able, however, mice with genetic deletion of mPGES-1 have been generated that have given insight into

161 for the first time that genetic deletion of mPGES-1 in Apc-mutant mice results in marked and persist

162 Deletion of mPGES-1 in mice attenuates neointimal hyperplasia after

163 Deletion of mPGES-1 in the vasculature and myeloid cells differentia

164 the response to vascular injury, deletion of mPGES-1 in VSMCs, ECs, or both had no detectable phenoty

165 Deletion of mPGES-1 modulates experimentally evoked pain and inflamm

166 monstrates the effect of genetic deletion of mPGES-1 on the developing immunologic responses and its

167 Deletion of mPGES-1 protects against abdominal aortic aneurysm forma

168 Deletion of mPGES-1 reduced plaque burden in fat-fed LDLR(-/-)s but

169 The results show that genetic deletion of mPGES-1 results in a dramatic decrease in PGE2 productio

170 Indeed, deletion of mPGES-1 retards atherogenesis and angiotensin II-induced

171 edly suppressed by myeloid cell depletion of mPGES-1 with decreased hyperplasia, leukocyte infiltrati

172 To determine whether the effect of mPGES-1 and PGE2 was localized to hematopoietic or nonhe

173 din E2 accounts for the protective effect of mPGES-1 deletion in atherosclerosis, augmentation of PGI

174 We also examined the effect of mPGES-1 deletion on carcinogen-induced colon cancer.

175 ld facilitate investigation of the effect of mPGES-1 genetic deletion on prostanoid biosynthesis in f

176 The effects of mPGES-1 on human cholangiocarcinoma cells were determine

177 cular injury, reflecting distinct effects of mPGES-1-derived PGE2 in these cell types on discrete cel

178 re standing at the threshold of a new era of mPGES-1-targeting anti-inflammatory drugs.

179 emical analyses to examine the expression of mPGES-1 in formalin-fixed, paraffin-embedded human chola

180 esponse-1 (Egr-1), a transcription factor of mPGES-1.

181 The impact of mPGES-1 deletion on formation of angiotensin II-induced

182 To further assess the importance of mPGES-1 to IL-1beta regulation of an islet physiologic r

183 ility of COX-2 but preserved inducibility of mPGES-1 on gene expression level were confirmed in an in

184 te cyclase activity blocked the induction of mPGES-1 by TNF-alpha.

185 ling as being important for the induction of mPGES-1 by TNF-alpha.

186 Finally, the induction of mPGES-1 was regulated, in part, through a positive feedb

187 The ubiquitous induction of mPGES-1-dependent PGE2 may be crucial for innate immune

188 membrane effects underlie the inhibition of mPGES-1 and 5-LO by curcumin.

189 Inhibition of mPGES-1 has been proposed as a therapeutic strategy for

190 ic potential for pharmacologic inhibition of mPGES-1 in inflammatory conditions.

191 otential efficacy of selective inhibition of mPGES-1 in preventing or retarding aneurysm formation wa

192 Pharmacologic inhibition of mPGES-1 may therefore impact both the inflammation and t

193 Selective inhibition of mPGES-1 might be a promising step to avoid cyclooxygenas

194 Interestingly, selective inhibition of mPGES-1 was also associated with a decrease in LPS-induc

195 Selective inhibition of mPGES-1 with either siRNA or isoform-selective inhibitor

196 Specific inhibitors of mPGES-1 are not yet available, however, mice with geneti

197 Inhibitors of mPGES-1 may be less likely than those selective for cycl

198 se prostaglandins suggest that inhibitors of mPGES-1 may be less likely to cause cardiovascular adver

199 These results suggest that inhibitors of mPGES-1 may retain their antiinflammatory efficacy by de

200 migration and invasion, whereas knockdown of mPGES-1 inhibited these parameters, in vitro.

201 ; in contrast, RNA interference knockdown of mPGES-1 inhibited tumor growth parameters.

202 ma cells with overexpression or knockdown of mPGES-1.

203 Lack of mPGES-1 in bone marrow-derived leukocytes negatively reg

204 modified mice, the cellular localization of mPGES-1 in the mouse brain has not been thoroughly deter

205 Overexpression of mPGES-1 in human cholangiocarcinoma cells increased tumo

206 these results suggest that overexpression of mPGES-1 in IBD is the result of Egr-1-mediated activatio

207 Forced overexpression of mPGES-1 in two HCC cell lines (Hep3B and Huh7) increased

208 r consideration the therapeutic potential of mPGES-1 inhibitors as adjuvant therapy for percutaneous

209 pacity of PGE(2) as measured by the ratio of mPGES-1:PGDH was elevated in sub-acute injury, suggestin

210 f what is known about the functional role of mPGES-1 for these centrally evoked symptoms is based on

211 The role of mPGES-1 in abdominal aortic aneurysm is unknown.

212 In this study, we define the role of mPGES-1 in bone marrow-derived leukocytes in the recover

213 ession of various human cancers, the role of mPGES-1 in carcinogenesis has not been determined.

214 have given insight into the specific role of mPGES-1 in eicosanoid biosynthesis in vivo and in perito

215 dy provides novel evidence for a key role of mPGES-1 in HCC growth and progression.

216 hepatocellular carcinoma (HCC), the role of mPGES-1 in hepatocarcinogenesis is not well established.

217 We investigated the role of mPGES-1 in human cholangiocarcinoma growth.

218 The present study examined the role of mPGES-1 in regulation of sodium balance and blood pressu

219 his study, we further elucidated the role of mPGES-1 in the humoral immune response.

220 The role of mPGES-1 in the response to vascular injury is unknown.

221 the natriuretic and antihypertensive role of mPGES-1 that likely contributes to blood pressure homeos

222 The cell selective roles of mPGES-1 in atherogenesis are unknown.

223 Germinal center formation in the spleen of mPGES-1 null and WT mice were similar after immunization

224 Stimulation of mPGES-1(-/-) VSMC and macrophages with bacterial LPS inc

225 We determined the crystal structure of mPGES-1 bound to four potent inhibitors in order to unde

226 We have also determined the structure of mPGES-1 in complex with a glutathione-based analog, prov

227 ntation (BMT) from either COX-2-deficient or mPGES-1-deficient mice into WT mice or macrophage-specif

228 in brain endothelial cells, but not in other mPGES-1-positive cells, was coexpressed with cyclooxygen

229 mply a widespread synthesis of PGE2 or other mPGES-1-dependent products in the mouse brain that may b

230 Consistently, pharmacological mPGES-1 inhibition directed pre-adipocyte differentiatio

231 The most potent mPGES-1 inhibitor was lonazolac derivative 22 (IC(5)(0)

232 onists emerge as potential therapy to reduce mPGES-1 expression and PGE(2) levels in inflammatory and

233 median preoptic nucleus of fever-refractive mPGES-1 knock-out mice, resulted in a temperature elevat

234 -RAS and MEK1, RET/PTC was found to regulate mPGES-1 through Shc-RAS-MEK-ERK.

235 Increasing evidence reveals mPGES-1 inhibitors as a safe alternative to nonsteroidal

236 The first selective mPGES-1 inhibitors recently entered clinical trials.

237 ssue from mice lacking PPARgamma also showed mPGES-1 up-regulation and increased PGE2 levels.

238 Specifically, mPGES-1-derived PGE(2) induces the formation of EGR1-bet

239 tumor necrosis factor (TNF)-alpha stimulated mPGES-1 transcription in human colonocytes, resulting in

240 Following immune stimulation, mPGES-1 in brain endothelial cells, but not in other mPG

241 Our data show the feasibility of targeting mPGES-1 for cancer chemoprevention with the potential fo

242 vious studies in mice suggest that targeting mPGES-1 may be less likely to cause hypertension or thro

243 We conclude that mPGES-1 and PGE2-dependent phenotypic changes of nonhema

244 We demonstrated that mPGES-1 deficiency in nonhematopoietic cells was the cri

245 In addition, we provide evidence that mPGES-1 deficiency sensitized the hypertensive effect of

246 However, we found that mPGES-1 deficiency was associated with a disorganized va

247 Our data support the hypothesis that mPGES-1 induction in response to an inflammatory stimulu

248 These findings indicated that mPGES-1-derived PGE(2) was not required for allergen sen

249 d burst of PGE(2) production indicating that mPGES-1 mediates LPS-induced PGE(2) production in BMDM.

250 ng for cell-specific markers, we report that mPGES-1 is constitutively expressed in the mouse brain,

251 In addition, we show that mPGES-1 gene deletion and subsequent decrease in PGE2 le

252 Furthermore, we show that mPGES-1 gene deletion results in diversion of prostanoid

253 In summary, our data show that mPGES-1, but not mPGES-2 or c-PGES isomerase, mediates L

254 We showed that mPGES-1 null mice had a significantly reduced incidence

255 with interleukin (IL)-1beta, suggesting that mPGES-1 is critically important for PGE2 production.

256 and limited structural information about the mPGES-1 inhibitor binding site.

257 talytic domain and within a subpocket of the mPGES-1 active site.

258 Binding of Egr-1 to the GC box region of the mPGES-1 promoter was enhanced by treatment with TNF-alph

259 -alpha localized to the GC box region of the mPGES-1 promoter.

260 locked TNF-alpha-mediated stimulation of the mPGES-1 promoter.

261 Thus, mPGES-1 and its product, PGE(2), protect the pulmonary v

262 -1 exhibited efficient catalytic coupling to mPGES-1.

263 ed protein levels of COX-2, but unexpectedly mPGES-1 protein levels were low and unaffected.

264 Vascular mPGES-1 was augmented during atherogenesis in LDLR(-/-)s

265 S-1-KOs), vascular smooth muscle cells (VSMC-mPGES-1-KOs), or endothelial cells (EC-mPGES-1-KOs) were

266 and increased tumor weight (P<.01), whereas mPGES-1 knockdown delayed tumor formation and reduced tu

267 markedly attenuated in macrophages in which mPGES-1 was silenced, thereby identifying mPGES-1 as a t

268 In SCID mice with tumor xenografts, mPGES-1 overexpression accelerated tumor formation and i