ライフサイエンスコーパス: EPC

1 EPC counts (CD34/KDR) after 24 months were defined as pr

2 EPC cultures issued from embryos that expressed only wil

3 EPC may indeed provide significant clinical protection a

4 EPC measurements in a small sample size were suggestive

5 EPC stimulates transcription factors such as Nrf-1 and h

6 EPC was evaluated on healthy young adults by presenting

7 EPC's showed significant reduction in WT hyperoxic group

8 EPCs and CTCE represent important potential therapeutic

9 EPCs decreased significantly at 1 year in the placebo gr

10 EPCs from Lewis rats exhibited a strong capacity to form

11 EPCs regulate the angiogenic switch via paracrine secret

12 EPCs were independently enumerated using ARCA and FACS w

13 EPCs were injected intravenously into Lewis rats with ar

14 EPCs were isolated from the long bones of Wistar rat bon

15 ormal esophageal squamous epithelium (EPC-1, EPC-2), metaplasia (CP-A) and dysplasia (CP-B) to esopha

16 forming cells (ECFCs) were the most abundant EPC subtype in kidneys, but were not detected in blood o

17 GSK3beta activity contributes to accelerated EPC cellular senescence, an effect reversed by small mol

18 Mice were subjected to CLP and administered EPCs at varying doses, CTCE, or a combination of the two

19 e hypothesized that exogenously administered EPCs are also beneficial in CLP sepsis and that CTCE pro

20 , suppression of miR-10A* and miR-21 in aged EPCs increased Hmga2 expression, rejuvenated EPCs, resul

21 usions: IL-10 deficiency/inflammation alters EPC-derived exosome function, content and therapeutic ef

22 n the BM, and rescued defective LKS cell and EPC mobilization.

23 27, 0.76 and 3.7mA/M/cm(2), while CA, EC and EPC electrode with BQ showed 25, 25, and 60mA/M/cm(2) of

24 41, 47 and 53microW/cm(2), while CA, EC and EPC electrodes with BQ showed 260, 330 and 500microW/cm(

25 densities of biofuel cells using CA, EC and EPC electrodes without BQ were 41, 47 and 53microW/cm(2)

26 CA, EC and EPC of POx on CNTs were used to fabricate enzymatic elec

27 sensor, the sensitivities of the CA, EC, and EPC electrodes without BQ were measured to be 0.27, 0.76

28 e electrodes were prepared using CA, EC, and EPC samples.

29 vitro effect of CTCE on miRNA expression and EPC function were determined.

30 d concentrations, impaired EPC migration and EPC/BM-HC proliferation through a PPARgamma-mediated STA

31 ently recover the known amount of EC-MVs and EPC-MVs from particle-depleted plasma, and to detect the

32 T5 content is crucial for gene targeting and EPC fate.

33 analysis and biomarker discovery of ECs- and EPCs- derived MVs.

34 HMVECs and EPCs from human cord blood were also examined for CXCR6

35 Additionally, HMVECs and EPCs responded to CXCL16 stimulation, but exhibited uniq

36 y activity (toward both isolated kinases and EPCs) remained almost untouched and comparable to the ac

37 r, co-culture of BMP2 gene-modified MSCs and EPCs dramatically increased osteoblast differentiation o

38 and that BMP2 gene modification for MSCs and EPCs dramatically promotes bone regeneration.

39 ne) and BMP2 genetically-engineered MSCs and EPCs in a rat critical-sized (8 mm) caviarial bone defec

40 combination of BMP2 gene -modified MSCs and EPCs in nCS/A dramatically increased the new bone and va

41 sults demonstrated that delivery of MSCs and EPCs with the injectable nCS/A scaffold did not affect c

42 the large nonstructural protein NS1 arrested EPCs at a cell cycle status with a 4 N DNA content, whic

43 row-derived endothelial progenitor cells (BM-EPCs).

44 (TNFR) signaling in RBR was evaluated in BM-EPCs from WT, TNFR1/p55KO, and TNFR2/p75KO mice, in vitr

45 post-IR, indicating a significant RBR in BM-EPCs in vivo.

46 NFR2 signaling may prevent delayed RBR in BM-EPCs, conceivably, in bone marrow milieu in general.

47 F-TNFR2 signaling may induce RBR in naive BM-EPCs and that blocking TNF-TNFR2 signaling may prevent d

48 IR conditioned media (CM) of WT and p55KO BM-EPCs largely abolished RBR in both cell types.

49 Full body gamma-IR WT BM-EPCs showed a biphasic response: slow decay of p-H2AX fo

50 essed on ischemic tissue endothelium and BMD-EPC act as double-locks to secure targeted EPC- endothel

51 o induce ischemic tissue endothelium and BMD-EPC to express both E-selectin and its ligands.

52 n and homing of bone marrow-derived EPC (BMD-EPC).

53 findings describe a novel mechanism for BMD-EPC homing and indicate that dual E-selectin/ligand pair

54 Indeed, both EPCs and ECs treated with high glucose (25 mmol/L) in th

55 kidney disease where production by canonical EPCs is compromised.

56 n adheres to epithelioma papillosum of carp (EPC) cells 3 to 5 times more extensively than the wild-t

57 ung EPCs suppressed Hmga2 expression, caused EPC senescence, as evidenced by senescence-associated be

58 METHOD AND RESULTS: Mouse Lin-Sca1(+)CD31(+) EPCs and human CD34(+) cells were treated with inhibitor

59 hat 1) anti-CD105 (EC marker) and anti-CD34 (EPC marker) conjugated-microbeads had the highest sensit

60 helial cell and endothelial progenitor cell (EPC) activation in vitro and ex vivo, respectively.

61 ations affected endothelial progenitor cell (EPC) and bone marrow-derived hematopoietic cell (BM-HC)

62 e properties of endothelial progenitor cell (EPC) and their exosomes on myocardial repair, although t

63 Endothelial progenitor cell (EPC) counts are proposed surrogate markers for vascular

64 We used enteric progenitor cell (EPC) cultures and mice to study the roles of these prote

65 y of endogenous endothelial progenitor cell (EPC) population that limits their recruitment and mobili

66 MVEC) and human endothelial progenitor cell (EPC) recruitment into engrafted human synovium that was

67 (LKS) cell and endothelial progenitor cell (EPC; CD34(+)Flk1(+)) mobilization, and vascular recovery

68 Endothelial progenitor cells (EPC) are able to migrate to tumor vasculature.

69 marrow-derived endothelial progenitor cells (EPC) contribute to the angiogenesis-dependent growth of

70 ic efficacy of endothelial progenitor cells (EPC) from patients with DM.

71 Homing of endothelial progenitor cells (EPC) to the ischemic tissues is a key event in neovascul

72 Endothelial progenitor cells (EPC) were successfully cultured on L-AME functionalized

73 ted protein in endothelial progenitor cells (EPC).

74 recognized reservoir of Epo-producing cells (EPCs), leading to expansion of the erythroid progenitor

75 blood-derived endothelial progenitor cells (EPCs) and bone marrow-derived mesenchymal stem cells (MS

76 cells (MSCs), endothelial progenitor cells (EPCs) and c-Kit(+) cardiac interstitial cells (cCICs) wh

77 bservations on endothelial progenitor cells (EPCs) and endothelial cells (ECs).

78 les (EMPs) and endothelial progenitor cells (EPCs) and evaluated, in 24 preselected patients, in vitr

79 of circulating endothelial progenitor cells (EPCs) and plasma levels of proangiogenic vascular endoth

80 Cs), including endothelial progenitor cells (EPCs) are biologically related to many aspects of cardio

81 d functions of endothelial progenitor cells (EPCs) are increased in patients with acute myocardial in

82 Endothelial progenitor cells (EPCs) are present in the systemic circulation and home t

83 ells (ECs) and endothelial progenitor cells (EPCs) by combining microbeads with fluorescence quantum

84 ld seeded with endothelial progenitor cells (EPCs) can overcome these limitations using an environmen

85 Endothelial progenitor cells (EPCs) contribute to postnatal endothelial repair and reg

86 ified MSCs and endothelial progenitor cells (EPCs) could significantly enhance vascularized bone rege

87 recruitment of endothelial progenitor cells (EPCs) from the bone marrow to the regenerating vasculatu

88 Endothelial progenitor cells (EPCs) have been associated with human sepsis but their r

89 tropism to human erythroid progenitor cells (EPCs) in human bone marrow and the fetal liver.

90 roliferation of esophageal progenitor cells (EPCs) in the developing murine esophagus.

91 corporation of endothelial progenitor cells (EPCs) into microvessels contributes to the vascularizati

92 corporation of endothelial progenitor cells (EPCs) into newly developing blood vessels contributes to

93 properties of endothelial progenitor cells (EPCs) is not known.

94 Endothelial progenitor cells (EPCs) may be relevant contributors to endothelial cell (

95 s signals within erythroid progenitor cells (EPCs) that are essential for red blood cell production.

96 Endothelial progenitor cells (EPCs) was assayed by flow cytometer.

97 Endothelial progenitor cells (EPCs) were cultured on the V-RDDs-anchoring scaffold and

98 Circulating endothelial progenitor cells (EPCs) were quantified at baseline and 1 year.

99 ed to quantify endothelial progenitor cells (EPCs), circulating endothelial cells (CECs), and endothe

100 Endothelial progenitor cells (EPCs), defined as CD34(+)VEGR2(+) using traditional fluo

101 les (EMPs) and endothelial progenitor cells (EPCs), respectively.

102 of circulating endothelial progenitor cells (EPCs), which has been attributed to their defective mobi

103 lial cells and endothelial progenitor cells (EPCs).

104 ition to the generation of endothelial cells/EPCs from pluripotent stem cells, direct reprogramming o

105 gramming of fibroblasts to endothelial cells/EPCs is becoming an important source of regenerative vas

106 This extrapolated point charge (EPC) method assigns effective point charges in a consist

107 Circulating EPC and levels of VEGF, HIF-1alpha and EPO were signific

108 ature serve as docking sites for circulating EPC, which express counterpart E-selectin ligands.

109 Circulating EPCs (CD34(+)/KDR(+)), angiogenic T cells (CD3(+)/CD31(+

110 Numbers of blood circulating EPCs were assessed by flow cytometry.

111 In parecoxib-treated mice, blood circulating EPCs were higher, but numbers of recruited EPCs in endom

112 ndicate that bone marrow-derived circulating EPCs do not engraft into blood vessels, but that such ci

113 S988A)-expressing mice have more circulating EPCs than their wild-type counterparts.

114 rtery tonometry), and numbers of circulating EPCs and EMPs (by using flow cytometry) were assessed.

115 bunit) that leads to deficits of circulating EPCs and impaired vascular repair, which could be revers

116 tensities on the mobilization of circulating EPCs over 24 hours in women.

117 In vivo, numbers of circulating EPCs were not affected by estrogen.

118 marrow, decreased the number of circulating EPCs, resulting in angiogenesis suppression and impaired

119 GFP(+)/Tie2(+) EPCs, numbers of circulating EPCs, vascularization, cell proliferation, apoptosis, an

120 Synechococcus clades, Eastern Pacific Clade (EPC) 1 and EPC2, were identified.

121 coating (EC) and enzyme precipitate coating (EPC).

122 coating (EC) and enzyme precipitate coating (EPC).

123 e efficient enhancer-promoter communication (EPC); however, the role of chromatin structure and dynam

124 on microscopy and confocal imaging confirmed EPC-matrix adhesion.

125 The Enhanced PVS Contrast (EPC) was achieved by combining T1- and T2-weighted image

126 porting the association between baseline CPC/EPC levels, future cardiovascular events, and death.

127 Overall, reduced CPC/EPC levels were associated with a approximately 2-fold i

128 ies reporting the prognostic role of the CPC/EPC measure on cardiovascular outcomes and death.

129 neity among studies and according to the CPC/EPC phenotype was generally high.

130 In studies of cultured EPCs and mice, we found that control of differentiation

131 We found that culturing EPCs in high glucose media increased adhesion to bone ma

132 ro (using the epithelioma papulosum cyprini [EPC] fish cell line) and in vivo (using rainbow trout fr

133 chanisms of IL-10 (interleukin-10) deficient-EPC-derived exosome dysfunction in myocardial repair and

134 Zeb2(Delta/+) EPCs had increased neuronal differentiation compared to

135 Overexpression of EDNRB in Zeb2(Delta/+) EPCs restored inhibition of neuronal differentiation, si

136 Incubation of Zeb2(Delta/+) EPCs with EDN3, on the other hand, resulted in only part

137 heterozygous for the mutation (Zeb2(Delta/+) EPCs) were exposed to EDN3; we analyzed the effects on c

138 bilization and homing of bone marrow-derived EPC (BMD-EPC).

139 ons of macroions interacting via the derived EPC effective potential.

140 Bone marrow-derived EPCs were isolated to monitor their in vivo and in vitro

141 Indeed, wild-type-derived EPCs' injection resulted in a significantly higher blood

142 potential, we investigated whether discrete EPC abnormalities were associated with early nonprolifer

143 DM EPCs also exhibited higher levels of GSK3beta activity r

144 and showed 40% less baseline activity in DM EPCs, an effect reversed by GSKi treatment.

145 Administration of DM EPCs reduced the intima-to-media ratio, an effect that w

146 Proteomic profiling of DM EPCs treated with GSKi identified 37 nonredundant, diffe

147 an effect that was further augmented when DM EPCs were pretreated with GSKi yet absent when cathB was

148 insights on how mechanistically d-PA drives EPC/BM-HC dysfunction in diabetes.

149 PC inhibited sCD146 angiogenic effects, i.e. EPC migration, proliferation, and capacity to form capil

150 A from 25 to 60 bp results in more efficient EPC.

151 e demonstrated that CTCE recruits endogenous EPCs in septic mice.

152 therapy with an angiogenic tissue-engineered EPC construct.

153 termine if hyperglycemic conditions enhanced EPC adhesion.

154 In in vitro analysis, CTCE enhanced EPC proliferation, angiogenesis, and prosurvival signali

155 tion of alcohol consumption, and the ensuing EPC dysfunction, may negatively compete with the benefic

156 ible rare cell identification, can enumerate EPCs in ARMD patients more reliably.

157 used normal esophageal squamous epithelium (EPC-1, EPC-2), metaplasia (CP-A) and dysplasia (CP-B) to

158 e endplate currents (mEPCs) and nerve-evoked EPCs (eEPCs) under voltage-clamp, which, unlike current-

159 othelium interactions by which to facilitate EPC homing and promote neovascularization and tissue rep

160 cell-derived factor (SDF)-1alpha facilitates EPC recruitment and is elevated in murine sepsis models.

161 Patients with DM had fewer EPCs and increased rates of apoptosis.

162 target gene Hmga2 as critical regulators for EPC senescence.

163 D34(+)VEGR2(+) may have predictive value for EPC enumeration in future ARCA studies.

164 Furthermore, EPCs from the transgenic mice exhibited augmented adhesi

165 TEBVs fabricated from HGPS iSMCs and hCB-EPCs show reduced vasoactivity, increased medial wall th

166 od-derived endothelial progenitor cells (hCB-EPCs) from a separate, healthy donor.

167 IH in vitro had similar effects on healthy EPC functions.

168 We observed higher EPC levels (group difference: 1.64%; 95% CI: 0.79-2.13,

169 CXCR6 was prominently expressed on human EPCs and HMVECs, and its expression on HMVECs could be u

170 In primary human EPCs, shRNA knockdown studies confirmed RHEX regulation

171 Estrogen- and vehicle-treated human EPCs were analyzed for migration and tube formation.

172 To identify EPC changes with biomarker potential, we investigated wh

173 ic and stearic acid concentrations, impaired EPC migration and EPC/BM-HC proliferation through a PPAR

174 19(Arf) expression, and resulted in impaired EPC angiogenesis in vitro and in vivo, resembling EPCs d

175 p16(Ink4a)/p19(Arf) expression, and improved EPC angiogenesis in vitro and in vivo.

176 ential therapeutic intervention in improving EPC-mediated angiogenesis and vascular repair.

177 Silencing angiomotin in EPC inhibited sCD146 angiogenic effects, i.e. EPC migrat

178 ant strain does not replicate efficiently in EPC cells and fails to replicate in J774A.1 macrophages.

179 Ex vivo, there was a significant increase in EPC number and AF intensity of individual EPCs from CVD

180 d RA SF exhibited a significant reduction in EPC recruitment.

181 Reductions in EPC levels do not seem to explain the increased risk of

182 The change in EPCs from baseline to 6 hours post-exercise was correlat

183 The change in EPCs from baseline was greatest in the 80% group (P < 0.

184 imilar molecular events could be detected in EPCs isolated from type 2 diabetic patients.

185 g tissues and lineages, RHEX was elevated in EPCs, occurred as a plasma membrane protein, was rapidly

186 e experiments using transgenes expression in EPCs from retroviral vectors.

187 miR-126, -125b, -34a, and -155 expression in EPCs.

188 tensities promoting the highest increases in EPCs and angiogenic factors.

189 Moreover, beta2AR stimulation results in EPCs proliferation, migration, and differentiation, enha

190 in EPC number and AF intensity of individual EPCs from CVD patients concomitant with enhanced PECAM-1

191 previously reported that SDF-1alpha-induced EPC homing is mediated by a panel of adhesion molecules

192 as potential mechanisms for exercise-induced EPCs mobilization.

193 f loss of function of exosomes from inflamed EPCs is still obscure.

194 , and prosurvival signaling while inhibiting EPC senescence.

195 Median (interquartile range [IQR]) EPC counts at baseline and month 24 were 6 (2-9) and 3 (

196 35a; 2) anti-CD144 (EC marker) and anti-KDR (EPC marker) conjugated-Q-dots exhibited the best sensiti

197 ) was highly enriched in both IL-10 knockout EPC-derived exosome as well as TNFalpha (tumor necrosis

198 -type EPC-derived exosome and IL-10 knockout EPC-derived exosome contain different protein expression

199 ntriguingly, ILK knockdown in IL-10 knockout EPC-derived exosome significantly rescued their reparati

200 I neovascularization, whereas IL-10 knockout EPC-derived exosome treatment showed diminished and oppo

201 olated from wild-type EPC and IL-10 knockout EPC.

202 s as compared with not treated or beta2AR KO EPC-treated mice.

203 ion was observed when beta2AR knock out (KO) EPCs were injected.

204 Low EPC levels are associated with a higher risk of subseque

205 We analyzed the major EPC subtypes in murine kidneys, blood, and spleens after

206 The mean EPC levels (+/- standard error of the mean) were 1.4 +/-

207 also provide in vivo data that d-PA-mediated EPC dysfunction could be rescued by PPARgamma blockade.

208 d 5 x 10(5) rat osteogenic transformed MSCs (EPC/otMSCs) were fixed to the exposed calvaria.

209 the groups of nCS/A, nCS/A+MSCs, nCS/A+MSCs+EPCs and nCS/A+BMP2 gene-modified MSCs, the combination

210 ro-CT demonstrated that cotransplantation of EPC/otMSCs significantly improved bone formation and min

211 can differentially affect the efficiency of EPC, suggesting that gene regulation over a distance cou

212 Improved enzyme loading of EPC resulted in 6.5 and 4.5 times higher activity per we

213 re/dynamics and, in turn, affect the rate of EPC in vitro and in silico.

214 positively or negatively affect the rate of EPC, depending upon the length and location of the DNA r

215 p the microRNA/gene expression signatures of EPC senescence, we performed microRNA profiling and micr

216 that precipitation and crosslinking steps of EPC have an important role in maintaining enzyme activit

217 Furthermore, ethanol-mediated suppression of EPC biology was endothelial nitric oxide synthase-depend

218 , proliferative and angiogenic capacities of EPCs, angiogenic T-cell numbers, and vascular endothelia

219 n of MSCs and endothelial differentiation of EPCs in vitro.

220 In vitro, exposure of EPCs to ethanol suppressed E2-induced proliferation, sur

221 ce results in reduced number and function of EPCs, potentially contributing to increased cardiac risk

222 educed E2-induced mobilization and homing of EPCs to injured myocardium compared with the E2-alone gr

223 e cell cycle arrest during B19V infection of EPCs, we analyzed the cell cycle change using 5-bromo-2'

224 rogressively decreased circulating levels of EPCs positive for both Flk-1 and Sca-1 (Flk-1(+)/Sca-1(+

225 copy demonstrated a significant migration of EPCs from the construct to the myocardium, suggesting a

226 nin stimulated transendothelial migration of EPCs in a concentration-dependent manner.

227 ontitis is associated with a mobilization of EPCs from the bone marrow, apparently in response to sys

228 trogen significantly increased the number of EPCs incorporated into the lesions' microvasculature, re

229 ish-oil supplementation increased numbers of EPCs and reduced numbers of EMPs relative to those with

230 When subthreshold numbers of EPCs were coadministered with CTCE in CLP mice they syne

231 ificantly suppressed synovial recruitment of EPCs and hyperproliferation of synovial cells.

232 rt a key role for YAP in the self-renewal of EPCs and stratification of the esophageal epithelium.

233 study, we investigated the potential role of EPCs in renal EC repair.

234 velopment of therapeutic strategies based on EPC in the treatment of ischemic diseases.

235 conversion to TAC has no favorable effect on EPC.

236 rch avenues to move forward our knowledge on EPC biology.

237 The effect of tacrolimus (TAC) on EPC is unknown.

238 We aimed to evaluate the role of beta2AR on EPCs' function.

239 nalysis showing the expression of beta2AR on EPCs.

240 significant increase of Flk-1 expression on EPCs as assessed by fluorescence-activated cell sorter.

241 cells, tissue-resident endothelial cells or EPCs may primarily drive the restoration of vascular fun

242 ELISA protein profiling of WT and p55KO EPC gamma-IR-CM over 5 days showed significant increases

243 layed RBR (3-5 days) were amplified in p55KO EPCs, suggesting a possible role for TNFR2/p75 signaling

244 mation of p-H2AX foci in nonirradiated p55KO EPCs.

245 BR (1-5 h) were inhibited in p55KO and p75KO EPCs, whereas delayed RBR (3-5 days) were amplified in p

246 both hormesis and exercise preconditioning (EPC).

247 ogenic potential was assessed by quantifying EPC cell migration and vascular differentiation.

248 [CNT]) or beta-TCP mixed with 5 x 10(5) rat EPCs and 5 x 10(5) rat osteogenic transformed MSCs (EPC/

249 1); among patients with MDS, those receiving EPC had greater rates of depression response at 12 weeks

250 g EPCs were higher, but numbers of recruited EPCs in endometriotic lesions were significantly lower w

251 ndothelial response, associated with reduced EPCs, and increased PTH in RTRs; the evaluation of endot

252 We found that Yap deficiency reduces EPC proliferation and stratification whereas persistent

253 miR-10A* and miR-21 regulate EPC senescence via suppressing Hmga2 expression and modu

254 med to determine whether microRNAs regulated EPC senescence and, if so, what the underlying mechanism

255 EPCs increased Hmga2 expression, rejuvenated EPCs, resulting in decreased senescence-associated beta-

256 ate differentiation conditions, reprogrammed EPCs showed efficient differentiation into cardiomyocyte

257 lts suggest that epigenetically reprogrammed EPCs display a safe, more plastic phenotype and improve

258 ngiogenesis in vitro and in vivo, resembling EPCs derived from aged mice.

259 Seeded EPCs underwent ex vivo modification with stromal cell-de

260 In coculture studies, EPCs augmented LPS-induced macrophage IL-10 production.

261 D-EPC act as double-locks to secure targeted EPC- endothelium interactions by which to facilitate EPC

262 After 34 days at room temperature, EPC retained 65% of initial activity, while CA and EC ma

263 We found that EPC improves the conspicuity of the PVS and aid resolvin

264 These results demonstrated that EPCs increase new vascular growth, and that BMP2 gene mo

265 esent study provides the first evidence that EPCs express a functional beta2AR.

266 e cylinder, BV/TV and TMD were higher in the EPC/otMSC group compared with CNT (BV/TV: 22.9% +/- 4.4%

267 he three subregions, BV/TV was higher in the EPC/otMSC group compared with CNT (top: 20.25% +/- 2.4%

268 For enrichment of the EPC repertoire from nonendothelial precursors, abundantl

269 he effective pair potential and validate the EPC method by comparing molecular dynamics simulations o

270 POx immobilization and stabilization via the EPC approach can lead us to develop continuous glucose m

271 on and the virial pressure obtained with the EPC model.

272 he EPCs migratory activity, and enhanced the EPCs' ability to promote endothelial cell network format

273 increase of cell proliferation, improved the EPCs migratory activity, and enhanced the EPCs' ability

274 th, cyst formation, homing of GFP(+)/Tie2(+) EPCs, numbers of circulating EPCs, vascularization, cell

275 ming of green fluorescent protein(+)/Tie2(+) EPCs, vascularization, cell proliferation, and apoptosis

276 virulence by reducing bacterial adhesion to EPC cells and facilitating intracellular bacterial repli

277 EseJ inhibits bacterial adhesion to EPC cells from within bacterial cells.

278 Patients assigned to EPC had greater improvements in PHQ-9 scores at 12 weeks

279 In vitro, estrogen-treated EPCs exhibited a higher migratory and tube-forming capac

280 deep sequencing of small RNAs revealed tumor EPC-intrinsic miRNAs including miR-10b and miR-196b, whi

281 Two EPC subtypes with different functions have been characte

282 in cargo of exosomes isolated from wild-type EPC and IL-10 knockout EPC.

283 ass spectrometry analysis revealed wild-type EPC-derived exosome and IL-10 knockout EPC-derived exoso

284 del of myocardial infarction (MI), wild-type EPC-derived exosome treatment significantly improved lef

285 Stimulation of wild-type EPCs with beta-agonist isoproterenol induced a significa

286 The mechanisms underlying EPC senescence are unknown.

287 FRbeta(+) cells as a previously unrecognized EPC reservoir that could be harnessed for augmenting Epo

288 We measured levels of CD34(+)VEGFR2(+) EPCs suggestive of a trend with higher values in patient

289 Interestingly, CD34(+)VEGR2(+) EPC analysis using FACS did not produce similar results

290 versus 35.7% +/- 4.9%, P = 0.02; CNT versus EPC/otMSC, respectively).

291 60.78 +/- 5.8 mgHA/ccm, P = 0.03; CNT versus EPC/otMSC, respectively).

292 In vivo EPC administration in sepsis increased plasma IL-10, sup

293 onsistent with our in vitro results, in vivo EPCs' treatment resulted in an improvement of impaired a

294 eceptor pair that is closely associated with EPC recruitment and blood vessel formation in the RA joi

295 Survival was improved with EPC therapy at a threshold of 10(6) cells.

296 Furthermore, this scaffold laden with EPCs promoted neovascularization in an animal model of h

297 erexpression of miR-10A* and miR-21 in young EPCs suppressed Hmga2 expression, caused EPC senescence,

298 When exposed to EDN3, Zeb2(+/+) EPCs continued expression of ZEB2 but did not undergo an

299 ntiation, similar to incubation of Zeb2(+/+) EPCs with EDN3.

300 hat expressed only wild-type Zeb2 (Zeb2(+/+) EPCs) or were heterozygous for the mutation (Zeb2(Delta/