ライフサイエンスコーパス: epithelialization

1 sion of MMP9 also contributes to impaired re-epithelialization.

2 local inflammatory response and promoting re-epithelialization.

3 esses, including cell migration and wound re-epithelialization.

4 irs keratinocyte migration and skin wound re-epithelialization.

5 xposure to estrogen markedly delays wound re-epithelialization.

6 sed macrophage recruitment and delayed wound epithelialization.

7 GA on activation of the GR and inhibition of epithelialization.

8 quired to compete a particular step of wound epithelialization.

9 isional wounds enhanced the rate of wound re-epithelialization.

10 uggested a function during the process of re-epithelialization.

11 otes wound edge IGF1R phosphorylation and re-epithelialization.

12 SMA and TGF beta, neovascularization and re-epithelialization.

13 strated that beta-AR agonists delay wound re-epithelialization.

14 eas before (original) and after (regrown) re-epithelialization.

15 nd ultimately accelerate human skin wound re-epithelialization.

16 y leukocyte emigration appears to promote re-epithelialization.

17 satrienoic acid, had no impact on corneal re-epithelialization.

18 h neutralizing VEGFR-1 antibodies delayed re-epithelialization.

19 Ephrin signaling in the regulation of somite epithelialization.

20 e potential of mouse keratinocytes for wound epithelialization.

21 d expression of paraxis implicated in somite epithelialization.

22 shed to near undetectable levels after wound epithelialization.

23 n glycoprotein expression occurred during re-epithelialization.

24 cells did not express Dsc3 or Dsg3 during re-epithelialization.

25 analyzed for rate of cellular migration and epithelialization.

26 of appropriate size rather than a defect in epithelialization.

27 ts of genes and molecules affecting wound re-epithelialization.

28 th AT-RvD3, which also promoted cutaneous re-epithelialization.

29 ances keratinocyte migration and promotes re-epithelialization.

30 leading to increased proliferation during re-epithelialization.

31 nduced AD-like lesions, there was delayed re-epithelialization.

32 ing extracellular matrix proteins to promote epithelialization.

33 tic penetrating keratoplasty; and time to re-epithelialization.

34 amniotic membrane grafting to facilitate re-epithelialization.

35 atinocyte migration is critical for wound re-epithelialization.

36 and require debridement and AMT for rapid re-epithelialization.

37 mal fibroblasts are recruited only during re-epithelialization.

38 ta-catenin, allowing them to progress toward epithelialization.

39 antiseptic therapy significantly accelerated epithelialization.

40 or NPD1 (1 microg) increased the rate of re-epithelialization (65-90%, n = 6-10, p < 0.03) and atten

41 e were examined by IF at times up to full re-epithelialization (96 hours).

42 n vivo, TIMP-1 deficiency enhanced airway re-epithelialization after naphthalene injury.

43 ient for paraxis, a gene required for somite epithelialization, also display defects in the axial ske

44 ncreased keratinocyte migration and hence re-epithelialization, although the mechanisms responsible f

45 , and eplerenone) rescues GC-induced delayed epithelialization and accelerates wound closure in diabe

46 Of note, topical mevastatin stimulated epithelialization and angiogenesis in vivo Mevastatin al

47 MP signaling, whereas N-cadherin inhibits de-epithelialization and BMP signaling.

48 Eyes were examined for re-epithelialization and clarity throughout the 21-day obse

49 nhancing tensile stiffness and/or increasing epithelialization and collagen deposition, as well as by

50 is and provide a framework for understanding epithelialization and complex tissue formation.

51 hanced wound closure, vascularization and re-epithelialization and confirmed that DRP1 has a vital ro

52 stroma both express Wnt4, where it regulates epithelialization and controls smooth muscle fate, respe

53 port the child's clinical progress, tracheal epithelialization and costs over the 4 years.

54 lular matrix signalling, these cells undergo epithelialization and create an apical surface in contac

55 demonstrate a beta2-AR-mediated delay in re-epithelialization and decrease in wound-induced epiderma

56 i-adhesive properties and is felt to promote epithelialization and decrease inflammation, neovascular

57 elays in wound healing parameters, including epithelialization and decreased neovascularization, were

58 that abrogation of this response impairs re-epithelialization and efficient wound closure.

59 an AM lumican to cultured medium promoted re-epithelialization and enhanced cell proliferation of wil

60 Re-epithelialization and epithelial cell division were both

61 These alterations in epithelialization and fusion apparently lead to a loss o

62 e pluripotent state is required for epiblast epithelialization and generation of the pro-amniotic cav

63 , in vivo overexpression of miR-21 inhibited epithelialization and granulation tissue formation in a

64 influencing multiple processes including re-epithelialization and granulation tissue matrix depositi

65 nd closure resulted primarily from faster re-epithelialization and increased formation of granulation

66 s, in addition to its known roles in myocyte epithelialization and intercalated disc formation, N-cad

67 of these cells resulted in delayed wound re-epithelialization and kinetics of wound closure.

68 naling system for wound repair, promoting re-epithelialization and modulating the maturation of the s

69 mental gastric ulcer healing and promoted re-epithelialization and muscle restoration.

70 nocytes and endothelial cells at areas where epithelialization and neovascularization occur.

71 t mice exhibited a defect in both corneal re-epithelialization and neutrophil recruitment that correl

72 l wound-healing is characterized by rapid re-epithelialization and remodeling, with minimal scar form

73 oth muscle cells, which are essential for re-epithelialization and restoration of muscular structures

74 wound-healing interventions that enhance re-epithelialization and the formation of granulation tissu

75 ysically attaches to the duct during de novo epithelialization and tubulogenesis.

76 vity to the pharynx and anterior epidermis ("Epithelialization"), and (3) a concomitant movement of t

77 a cadherin 6B and BMP signaling-mediated de-epithelialization, and a subsequent delamination through

78 receptors and EAAC1 were observed during re-epithelialization, and alterations in N-methyl-D-asparta

79 ith inflammatory responses, wound healing re-epithelialization, and altered differentiation.

80 feration, keratinocyte proliferation with re-epithelialization, and angiogenesis compared with dermal

81 ealing by stimulating cell proliferation, re-epithelialization, and angiogenesis in a diabetic mice e

82 g wound closure by stimulating angiogenesis, epithelialization, and collagen deposition.

83 g diagnoses, previous treatments, days to re-epithelialization, and complications for subsequent anal

84 ual acuity, infiltrate/scar size, time to re-epithelialization, and corneal perforation.

85 ng kinetics, including wound contraction, re-epithelialization, and microscopic metrics such as cell

86 limbus of abraded corneas contributes to re-epithelialization, and P-selectin provides a necessary s

87 cts of exogenous IGF-1 on cell migration, re-epithelialization, and proliferation-essential component

88 defect, number of specimens with complete re-epithelialization, and rate of wound closure were evalua

89 tion showed decreased wound widths, enhanced epithelialization, and reduced numbers of neutrophils an

90 treatment, durability of the neosquamous re-epithelialization, and safety of the procedure were dete

91 nic skin wounds are characterized by poor re-epithelialization, angiogenesis and granulation.

92 Surprisingly, wound re-epithelialization, angiogenesis, and collagen synthesis

93 exhibited lower skin AGE deposits, increased epithelialization, angiogenesis, inflammation, granulati

94 ling characterized by impaired or delayed re-epithelialization are a serious medical problem.

95 we reveal that IGF-1-mediated effects on re-epithelialization are directly mediated by IGF-1R.

96 Impaired cell adhesion and epithelialization are indicated by decreased E-cadherin

97 h HoxD3-treated wounds also show improved re-epithelialization as compared to control db/db wounds, t

98 hat papc is an important regulator of somite epithelialization associated with segmentation.

99 onocyte infiltration, neovascularization and epithelialization at days 3, 5, 7, and 10 postwounding.

100 ocytes undergo many changes that engender an epithelialization behavior.

101 ded microbiologic cure at 6 days, rate of re-epithelialization, best-corrected visual acuity and infi

102 ogenesis, dermal fibroblast function, and re-epithelialization, but had no effect on wound inflammati

103 obilization is a critical aspect of wound re-epithelialization, but the mechanisms that control its p

104 at TIMP-1 overexpression restricts airway re-epithelialization by inhibiting matrilysin activity, con

105 xia component of ischemia may limit wound re-epithelialization by stabilizing HIF-1alpha, which induc

106 s, activated parietal cells mediated tuft re-epithelialization by two distinct mechanisms.

107 Mean time to complete (>/=95%) epithelialization (CE) for patients that did and did not

108 l redistribution of beta-catenin, aspects of epithelialization characteristic of cells at somite boun

109 ects of the wound healing cascade, including epithelialization, collagen deposition, and cell migrati

110 does not significantly alter the rate of re-epithelialization, collagen deposition, or tensile stren

111 altrexone (NTX) showed an acceleration in re-epithelialization compared to controls.

112 our times daily significantly accelerated re-epithelialization compared to controls.

113 ed epidermal cellular migration and wound re-epithelialization compared with vehicle-treated STZ-diab

114 ntegrins show enhanced wound healing with re-epithelialization complete several days earlier than in

115 Inhibition of Wnt signalling after re-epithelialization completely abrogates this wounding-ind

116 Wound healing consists of re-epithelialization, contraction and formation of granulat

117 D1-deficient mice exhibited delayed wound re-epithelialization correlated with a reduced proliferatio

118 ound healing as a consequence of complete re-epithelialization, diminished inflammation, and enhanced

119 beta1 is crucial for efficient and proper re-epithelialization during cutaneous wound healing.

120 fish, neural progenitors undergo progressive epithelialization during neurulation, and thus provide a

121 Cell migration is an integral part of re-epithelialization during skin wound healing, a complex p

122 vations suggest that APLP2 contributes to re-epithelialization during wound healing by supporting epi

123 ates cell migration and proliferation and re-epithelialization during wound healing.

124 Keratinocyte migration is a key aspect of re-epithelialization during wound healing.

125 in regulating keratinocyte migration and re-epithelialization during wound healing.

126 OR 2AT4 is involved in human keratinocyte re-epithelialization during wound-healing processes.

127 healing by rapid wound closure, improved re-epithelialization, enhanced extracellular matrix remodel

128 ectionally into the wound bed to initiate re-epithelialization, essential for wound repair and restor

129 nd are thereby inhibited from undergoing the epithelialization event that culminates in the formation

130 f tarsal conjunctiva trauma with lamellar de-epithelialization, followed by re-epithelialization to f

131 epithelial T cells (DETCs), which promote re-epithelialization following injury.

132 nts, or DETCs are silenced in young skin, re-epithelialization following wounding is perturbed.

133 d prohealing functions by promoting wound re-epithelialization, formulation of granulation tissue, an

134 , redox response, inflammation, epidermis re-epithelialization, granulation formation, and proper wou

135 Healing was induced by rapid re-epithelialization, granulation tissue formation, and acc

136 animals, they coacted to accelerate wound re-epithelialization, granulation tissue formation, and syn

137 These studies show that re-epithelialization, granulation tissue formation, includi

138 er MIC was associated with slower time to re-epithelialization (hazards ratio, 0.92; 95% CI, .86-.97;

139 ng that beta-AR antagonists promote wound re-epithelialization in a "chronic" human skin wound-healin

140 skin explant culture system to better assess epithelialization in a wound-like environment.

141 hich blocks FPP formation, not only promotes epithelialization in acute wounds but also reverses the

142 Both miR-21 and miR-130a delayed epithelialization in an acute human skin wound model.

143 The incidence of complete re-epithelialization in animals given systemic administrati

144 pithelialization in pig burn wounds (100% re-epithelialization in antagonist-treated wounds vs. appro

145 The significant impairment in corneal re-epithelialization in AQP3-deficient mice results from di

146 nist-treated wounds vs. approximately 70% re-epithelialization in control wounds on postburn day 26)

147 inflammation and significantly increased re-epithelialization in corneal wounds.

148 ation in human skin wounds and a delay in re-epithelialization in murine tail-clip wounds.

149 keratinocyte cell line and enhances wound re-epithelialization in ob/ob mice.

150 anted into rabbit corneas to determine their epithelialization in organ culture.

151 a synthetic TGF-b antagonist accelerates re-epithelialization in pig burn wounds (100% re-epithelial

152 does not appear to be required for proper re-epithelialization in response to injury, potentially bec

153 les of hair follicle regeneration and for re-epithelialization in response to wounding.

154 brane (AM) transplantation facilitates rapid epithelialization in severe neurotrophic corneal ulcers.

155 LIMK1 induces de-epithelialization in the neural tube and dominant negati

156 cytes to stimulate cell proliferation and re-epithelialization in the skin, whereas IL-27 leads to su

157 and ZGA inhibited keratinocyte migration and epithelialization in vitro and ex vivo.

158 dition, a deficiency of TNF-alpha delayed re-epithelialization in vivo and this correlated with reduc

159 iation, which recapitulates the hallmarks of epithelialization in vivo in a synchronized rather than

160 Time to corneal re-epithelialization in vivo was significantly delayed in A

161 tes in vitro, we found no effect on wound re-epithelialization in vivo.

162 these cells may also contribute to wound re-epithelialization in vivo.

163 cial part in the pathogenesis of retarded re-epithelialization in wound.

164 way mediates non-canonical BMPRII induced de-epithelialization, in response to either cadherin-6B or

165 a subset of the transcripts associated with epithelialization, including Pax8, cyclin D1 (Ccnd1) and

166 e VEGF-treated wounds demonstrated increased epithelialization, increased matrix deposition, and enha

167 ytes from the adjacent epidermis and make re-epithelialization independent of keratinocyte proliferat

168 lation deficient mutated cofilin inhibits de-epithelialization induced by cadherin-6B as well as LIMK

169 Furthermore, de-epithelialization induced by cadherin-6B was found to be

170 ube and dominant negative LIMK1 decreases de-epithelialization induced by either cadherin-6B or BMP.

171 Impaired re-epithelialization is a hallmark of these wounds, which i

172 Rescue of epithelialization is accompanied by restoration of kerat

173 ogenous "wound current" upon injury until re-epithelialization is complete.

174 cytes late in the regenerative phase when re-epithelialization is completed and matrix maturation ens

175 ls being located in the basal layer until re-epithelialization is completed.

176 ompatible with metazoans, but the absence of epithelialization is consistent only with a stem-metazoa

177 ed; bone histolysis does not occur, wound re-epithelialization is inhibited and the blastema does not

178 We now find that de-epithelialization is mediated by non-canonical BMP signa

179 Re-epithelialization is not dependent on DNA synthesis in t

180 asticity of keratinocytes (KCs) during wound epithelialization is one of the major goals in epithelia

181 l role of keratinocyte alpha9beta1 during re-epithelialization is unknown and analysis has been precl

182 xpression is up-regulated following vascular epithelialization, is required to prevent the disassembl

183 These nonautonomous aspects of epithelialization may involve interplay of EphA4 with ot

184 On re-epithelialization, MCT3 was detected in chick and hfRPE

185 e A (PKA), through PKA-2, in a specific post-epithelialization morphogenetic step (conversion of the

186 ectionally into the wound bed to initiate re-epithelialization, necessary for wound closure and resto

187 associated with increased proliferation, re-epithelialization, neovascularization, and blood flow.

188 Re-epithelialization, neutrophil influx, and platelet accum

189 In this manner, all re-epithelialization occurred from residual appendageal str

190 Re-epithelialization occurred in 17 of 20 eyes.

191 Re-epithelialization of 5- to 6-mm-wide rabbit corneal epit

192 ced flap with CT graft resulting from the de-epithelialization of a free gingival graft.

193 K) migration plays a critical role in the re-epithelialization of acute skin wounds.

194 epithelial repair and is required for the re-epithelialization of airway wounds by facilitating cell

195 the expression of MCT3 after wounding and re-epithelialization of chick RPE explant and human fetal (

196 MCT expression after scratch wounding and re-epithelialization of chick RPE/choroid explant cultures

197 a signaling would be predicted to enhance re-epithelialization of cutaneous wounds and reduce scarrin

198 Re-epithelialization of cutaneous wounds in adult mammals t

199 lagenase-1-dependent migration during the re-epithelialization of epidermal wounds.

200 ocytes in intact skin and is required for re-epithelialization of human skin wounds.

201 e motility plays an important role in the re-epithelialization of human skin wounds.

202 yte migration in vitro and accelerates wound epithelialization of human wounds ex vivo.

203 igated the effect of Smad2 overexpression on epithelialization of incision wounds.

204 We previously showed that epithelialization of incisional wounds is accelerated in

205 e that L. rhamnosus GG lysate accelerates re-epithelialization of keratinocyte scratch assays, potent

206 Deficits in the epithelialization of mesenchymal cells were evidenced by

207 er cells in the brain by facilitating the re-epithelialization of metastatic breast cancer cells and

208 that PAM induced senescence and impaired re-epithelialization of oral mucosa.

209 collagenase-1 in ex vivo wounded skin and re-epithelialization of partial thickness porcine burn woun

210 Re-epithelialization of partial- or full-thickness skin wou

211 Cadherin 6B selectively induces the de-epithelialization of PMNCCs, which is mediated by stimul

212 segmentation by altering the CDH2-dependent epithelialization of PSM cells.

213 Re-epithelialization of skin wounds depends upon the migrat

214 s neovascularization, resulting in faster re-epithelialization of skin wounds in diabetic mice.

215 estigated the role of keratin IFs during the epithelialization of skin wounds using a keratin 6alpha

216 progenitor epithelial cells contribute to re-epithelialization of the airway and re-establishment of

217 erely affected embryos have abnormalities in epithelialization of the blastoderm, resulting in loss o

218 g with opioid-receptor interaction during re-epithelialization of the cornea in the rat using both sy

219 The data revealed that re-epithelialization of the corneal epithelium is not depen

220 akdown of coherent clonal growth accompanies epithelialization of the epiblast and is essentially com

221 rovided evidence that cadherin-6B induces de-epithelialization of the neural crest prior to delaminat

222 nd 4 weeks after surgery for the complete re-epithelialization of the palatal wound (CWE), the altera

223 for maximal cell aspect ratio and thus full epithelialization of the posterior somite.

224 ads to loss of Six2 expression and premature epithelialization of the progenitors.

225 led wounds while simultaneously promoting re-epithelialization of the remaining provisional wound.

226 e mean best-corrected visual acuity after re-epithelialization of the shield ulcer was 20/30, 20/30,

227 Somite morphogenesis involves the epithelialization of the somite border cells around a co

228 mmation and by enhancing angiogenesis and re-epithelialization of the wound, thereby reversing the pa

229 on to form a thick granulation tissue and re-epithelialization of the wounds.

230 it was not sufficient to induce appropriate epithelialization of these cells.

231 Re-epithelialization of treated monolayers was compared to

232 unlike galectin-3, galectin-7 accelerated re-epithelialization of wounds in both gal3(-/-) and gal3(+

233 Exogenous galectin-3 accelerated re-epithelialization of wounds in gal3(+/+) mice but, surpr

234 cles (HFs) are able to contribute to this re-epithelialization of wounds in vivo.

235 uggest a potential mechanism for enhanced re-epithelialization of wounds under low oxygen tensions.

236 ifferent models of corneal wound healing, re-epithelialization of wounds was significantly slower in

237 The extent of acceleration of re-epithelialization of wounds with both galectin-3 and gal

238 te-binding proteins galectins-3 and -7 in re-epithelialization of wounds.

239 hicle and P=0.14 vs. cyclosporine A) but not epithelialization (P>0.2 vs. vehicle).

240 after injury (28 +/- 5% versus 79 +/- 14% re-epithelialization, P < 0.005).

241 ed by a masked investigator for lesion size, epithelialization, pain, infection, inflammation, and sc

242 Epithelialization, pain, infection, inflammation, and sc

243 tructures as sources of keratinocytes for re-epithelialization, particularly the sweat apparatus.

244 Re-epithelialization, patterns of neutrophil influx and CXC

245 rotubule defects are associated with altered epithelialization/polarity in renal cells and with prone

246 ture, null keratinocytes exhibit an enhanced epithelialization potential due to increased migration.

247 uccessfully detect increases or decreases in epithelialization potential, and can be useful in the ch

248 the dermal compartment to synchronize the re-epithelialization process.

249 c time-points for markers of interest in the epithelialization process.

250 Re-epithelialization progressed as a gradient of cell layer

251 Presence of desmosomes throughout re-epithelialization raises the question of how migrating c

252 The re-epithelialization rate was similar among treatment group

253 Open wound and epithelialization rates and angiogenesis significantly i

254 trate/scar size, corneal perforation, and re-epithelialization rates stratified by culture positivity

255 macrophage depletion resulted in delayed re-epithelialization, reduced collagen deposition, impaired

256 In addition, re-epithelialization requires long-range epithelial rearran

257 Collective processes such as wound re-epithelialization result from the integration of individ

258 y contribute to inflammation, histolysis, re-epithelialization, revascularization and cell proliferat

259 These findings suggest that the de-epithelialization step of the neural crest EMT by cadher

260 keratinocyte migration, proliferation or re-epithelialization, suggesting that the effect of berylli

261 on begins to occur within hours after somite epithelialization, the identity of the responding tissue

262 apacity to migrate and contribute to this re-epithelialization: the less differentiated cells of the

263 inning, ulceration, and delayed conjunctival epithelialization; there is some evidence of increasing

264 was to determine whether TIMP-1 inhibits re-epithelialization through matrilysin.

265 First, COL7A1 was required for re-epithelialization through organization of laminin-332 at

266 were sacrificed at day 3 before making a re-epithelialization time analysis with fluorescein stainin

267 Re-epithelialization time and best-corrected visual acuity.

268 main outcome measures: Re-epithelialization time and best-corrected visual acuity.

269 amellar de-epithelialization, followed by re-epithelialization to form an epithelialized tunnel as a

270 esponse to manual debridement wounds when re-epithelialization took more than 24 hours.

271 tubule induction and differentiation (i.e., epithelialization, tubular organization and elongation a

272 oRNAs may be implicated in limiting wound re-epithelialization under hypoxia, a major component of is

273 evidence revealed that DAMPs also trigger re-epithelialization upon kidney injury and contribute to e

274 tatin accelerates wound closure by promoting epithelialization via multiple mechanisms: modulation of

275 The mean time to complete epithelialization was 56.7 +/- 14.9, 22.0 +/- 10.2, and

276 Wound re-epithelialization was also significantly faster in betaa

277 QP3-facilitated cell migration to corneal re-epithelialization was assessed using an organ culture mo

278 UB cell epithelialization was augmented in the presence of MM ce

279 By 5 d after wounding, re-epithelialization was complete in all EGFR wild-type wou

280 Re-epithelialization was delayed with a deficient delineati

281 al of the corneal epithelium by scraping, re-epithelialization was followed by fluorescein staining.

282 Re-epithelialization was rapid and complete within 3 days i

283 In the grade 2 group, re-epithelialization was seen in 36 (88%) eyes that receive

284 In the grade 1 group, re-epithelialization was seen in 67 (94%) eyes.

285 In the grade 3 group, re-epithelialization was seen in only 1 (1.7%) eye that rec

286 Re-epithelialization was significantly delayed in mice with

287 Mean time to epithelialization was similar, and there was no signific

288 rimary endpoint, time to complete burn wound epithelialization, was determined by independent, blinde

289 f marapsin, which closely correlated with re-epithelialization, was virtually absent in a genetic mou

290 To address mechanisms of impaired re-epithelialization we examined MMP9 expression in vivo in

291 nt the most promising targets to engineer re-epithelialization, we examined collective and individual

292 Cellular migration and epithelialization were unaffected in the stromelysin-1-d

293 Therefore, targeting re-epithelialization, which mainly involves keratinocytes,

294 onolayer scratch assay was used to assess re-epithelialization; which comprises keratinocyte prolifer

295 r wound closure, keratinocyte AR promoted re-epithelialization, while fibroblast AR suppressed it.

296 tosidase transgene (n = 4) impaired wound re-epithelialization with an epithelial gap of 5.11 +/- 0.6

297 from Smad7 tg mice exhibited accelerated re-epithelialization, with increased activation of extracel

298 uteri significantly increased the rate of re-epithelialization, with L. rhamnosus GG being the most e

299 ice displayed significantly delayed wound re-epithelialization, with the greatest delay at day 3 afte

300 lization, proliferation, human skin wound re-epithelialization, wound-induced ERK phosphorylation, an