ライフサイエンスコーパス: re-epithelialization

1 deficient mice completely restores bronchial re-epithelialization.

2 to delineate the functions of CaSR in wound re-epithelialization.

3 d exposure to estrogen markedly delays wound re-epithelialization.

4 n and dramatically impairs cell motility and re-epithelialization.

5 excisional wounds enhanced the rate of wound re-epithelialization.

6 s suggested a function during the process of re-epithelialization.

7 sPCM accelerated wound re-epithelialization.

8 monstrated that beta-AR agonists delay wound re-epithelialization.

9 orneas before (original) and after (regrown) re-epithelialization.

10 , and ultimately accelerate human skin wound re-epithelialization.

11 ression of MMP9 also contributes to impaired re-epithelialization.

12 arly leukocyte emigration appears to promote re-epithelialization.

13 icosatrienoic acid, had no impact on corneal re-epithelialization.

14 with neutralizing VEGFR-1 antibodies delayed re-epithelialization.

15 enhances keratinocyte migration and promotes re-epithelialization.

16 d induced AD-like lesions, there was delayed re-epithelialization.

17 e in glycoprotein expression occurred during re-epithelialization.

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

19 or eosinophils in negatively affecting wound re-epithelialization.

20 and the resultant phenotypic change directs re-epithelialization.

21 ignaling, impaired angiogenesis, and delayed re-epithelialization.

22 store this lining through a process known as re-epithelialization.

23 interact with nerves and specialize in wound re-epithelialization.

24 betic wounds, and promotes wound closure and re-epithelialization.

25 perivascular cells as active contributors to re-epithelialization.

26 romotes wound edge IGF1R phosphorylation and re-epithelialization.

27 to increased vascular structures and faster re-epithelialization.

28 lls in the uterine stroma also contribute to re-epithelialization.

29 pha SMA and TGF beta, neovascularization and re-epithelialization.

30 ressively returns to a solid-like state with re-epithelialization.

31 nk between LAMC2, improved angiogenesis, and re-epithelialization.

32 and identifies FOSL1 as a critical driver of re-epithelialization.

33 fects of genes and molecules affecting wound re-epithelialization.

34 with AT-RvD3, which also promoted cutaneous re-epithelialization.

35 is leading to increased proliferation during re-epithelialization.

36 peutic penetrating keratoplasty; and time to re-epithelialization.

37 ing amniotic membrane grafting to facilitate re-epithelialization.

38 Keratinocyte migration is critical for wound re-epithelialization.

39 py and require debridement and AMT for rapid re-epithelialization.

40 closure, reduced contraction and accelerated re-epithelialization.

41 dermal fibroblasts are recruited only during re-epithelialization.

42 he local inflammatory response and promoting re-epithelialization.

43 rocesses, including cell migration and wound re-epithelialization.

44 mpairs keratinocyte migration and skin wound re-epithelialization.

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

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

47 g/mL TGF-beta 1 induced a transient delay in re-epithelialization, a reduction in proliferation, and

48 l cytoarchitectural changes and the onset of re-epithelialization after 18 h post-injury.

49 follicular fibroblasts would accelerate skin re-epithelialization after injury faster than interfolli

50 In vivo, TIMP-1 deficiency enhanced airway re-epithelialization after naphthalene injury.

51 roteinases by resident corneal cells impedes re-epithelialization after some types of corneal injury.

52 r increased keratinocyte migration and hence re-epithelialization, although the mechanisms responsibl

53 t day 2-4 postwound, resulting in a complete re- epithelialization and profound granulation tissue fo

54 e with recombinant murine OSM improved wound re-epithelialization and accelerated wound closure by bo

55 aling of diabetic wounds by promoting faster re-epithelialization and angiogenesis, and the enrichmen

56 Eyes were examined for re-epithelialization and clarity throughout the 21-day o

57 ive effects of SPD on keratinocytes in wound re-epithelialization and closure warrant further studies

58 ust be protected to enable appropriate wound re-epithelialization and closure.

59 enhanced wound closure, vascularization and re-epithelialization and confirmed that DRP1 has a vital

60 we demonstrate a beta2-AR-mediated delay in re-epithelialization and decrease in wound-induced epide

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

62 human AM lumican to cultured medium promoted re-epithelialization and enhanced cell proliferation of

63 Re-epithelialization and epithelial cell division were b

64 ng, influencing multiple processes including re-epithelialization and granulation tissue matrix depos

65 tage wound Mos/M s, along with delayed wound re-epithelialization and impaired granulation tissue for

66 mg/mL rTIMP2 significantly promoted corneal re-epithelialization and improved tissue integrity.

67 wound closure resulted primarily from faster re-epithelialization and increased formation of granulat

68 Wound closure was associated with improved re-epithelialization and increased neovascularization; a

69 lution (decreased pain and inflammation with re-epithelialization and infiltrate resolution) of 46.9

70 channel involved in calcium influx(3)-during re-epithelialization and inflammation following injury i

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

72 signaling system for wound repair, promoting re-epithelialization and modulating the maturation of th

73 erimental gastric ulcer healing and promoted re-epithelialization and muscle restoration.

74 ient mice exhibited a defect in both corneal re-epithelialization and neutrophil recruitment that cor

75 nt proliferation of cell types that increase re-epithelialization and promote proliferation of kerati

76 serve as a new approach for promoting wound re-epithelialization and provide a platform for further

77 was safe and associated with rapid cutaneous re-epithelialization and recovery in seven patients with

78 nds accelerated wound closure, with improved re-epithelialization and reductions in inflammation and

79 osal wound-healing is characterized by rapid re-epithelialization and remodeling, with minimal scar f

80 smooth muscle cells, which are essential for re-epithelialization and restoration of muscular structu

81 demonstrate that perivascular cells support re-epithelialization and reveal a mechanism regulating t

82 I collagen (COL3) as a critical regulator of re-epithelialization and scar formation during healing o

83 ls acquire a collagenolytic phenotype during re-epithelialization and that contact with different ECM

84 for wound-healing interventions that enhance re-epithelialization and the formation of granulation ti

85 ps, Sol-SPI-Mp nanofibers caused the fastest re-epithelialization and wound healing in a rat model.

86 ical cues are known to regulate keratinocyte re-epithelialization and wound healing; however, the und

87 ate receptors and EAAC1 were observed during re-epithelialization, and alterations in N-methyl-D-aspa

88 t with inflammatory responses, wound healing re-epithelialization, and altered differentiation.

89 oliferation, keratinocyte proliferation with re-epithelialization, and angiogenesis compared with der

90 d healing by stimulating cell proliferation, re-epithelialization, and angiogenesis in a diabetic mic

91 ying diagnoses, previous treatments, days to re-epithelialization, and complications for subsequent a

92 visual acuity, infiltrate/scar size, time to re-epithelialization, and corneal perforation.

93 their ability to mediate cell proliferation, re-epithelialization, and downstream signaling responses

94 t examination, time between the incident and re-epithelialization, and medical and/or surgical manage

95 aling kinetics, including wound contraction, re-epithelialization, and microscopic metrics such as ce

96 heal quicker with less inflammation, faster re-epithelialization, and minimal scarring.

97 the limbus of abraded corneas contributes to re-epithelialization, and P-selectin provides a necessar

98 ffects of exogenous IGF-1 on cell migration, re-epithelialization, and proliferation-essential compon

99 K1-sEVs accelerated wound closure, increased re-epithelialization, and promoted the proliferation of

100 he defect, number of specimens with complete re-epithelialization, and rate of wound closure were eva

101 The primary analysis evaluated health, re-epithelialization, and re-vascularization.

102 f anti-inflammatory cytokine IL-10, promoted re-epithelialization, and restored the epidermal barrier

103 of treatment, durability of the neosquamous re-epithelialization, and safety of the procedure were d

104 hronic skin wounds are characterized by poor re-epithelialization, angiogenesis and granulation.

105 f wound healing, from clot formation through re-epithelialization, angiogenesis and subsequent scar d

106 Surprisingly, wound re-epithelialization, angiogenesis, and collagen synthes

107 healing characterized by impaired or delayed re-epithelialization are a serious medical problem.

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

109 ough HoxD3-treated wounds also show improved re-epithelialization as compared to control db/db wounds

110 This delay included a decreased rate of re-epithelialization as well as a delay in dermal reorga

111 cluded microbiologic cure at 6 days, rate of re-epithelialization, best-corrected visual acuity and i

112 impedes not only epidermal proliferation and re-epithelialization but also capillary and fibroblast r

113 Our method led to faster and more orderly re-epithelialization but unexpectedly did not improve th

114 ngiogenesis, dermal fibroblast function, and re-epithelialization, but had no effect on wound inflamm

115 e mobilization is a critical aspect of wound re-epithelialization, but the mechanisms that control it

116 owth factors and chemokines to promote wound re-epithelialization by increasing migration of skin cel

117 that TIMP-1 overexpression restricts airway re-epithelialization by inhibiting matrilysin activity,

118 ll dynamics after injury, we show that wound re-epithelialization by Lgr6 stem cells is diminished fo

119 ypoxia component of ischemia may limit wound re-epithelialization by stabilizing HIF-1alpha, which in

120 loss, activated parietal cells mediated tuft re-epithelialization by two distinct mechanisms.

121 Impaired re-epithelialization characterized by hyperkeratotic non

122 rin does not significantly alter the rate of re-epithelialization, collagen deposition, or tensile st

123 ard lower M1/M2 macrophage ratio and greater re-epithelialization compared to controls (standard-of-c

124 y naltrexone (NTX) showed an acceleration in re-epithelialization compared to controls.

125 s four times daily significantly accelerated re-epithelialization compared to controls.

126 rane grafting significantly improved corneal re-epithelialization compared with medical therapy alone

127 roved epidermal cellular migration and wound re-epithelialization compared with vehicle-treated STZ-d

128 )-integrins show enhanced wound healing with re-epithelialization complete several days earlier than

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

130 Wound healing consists of re-epithelialization, contraction and formation of granu

131 PKD1-deficient mice exhibited delayed wound re-epithelialization correlated with a reduced prolifera

132 Before re-epithelialization (days 1 and 2) V+, EIIIA+, and EIII

133 After re-epithelialization (days 3 to 42) and reconstitution o

134 ant delay in wound healing with insufficient re-epithelialization, decreased inflammatory reaction, a

135 c wound healing as a consequence of complete re-epithelialization, diminished inflammation, and enhan

136 ha9beta1 is crucial for efficient and proper re-epithelialization during cutaneous wound healing.

137 Cell migration is an integral part of re-epithelialization during skin wound healing, a comple

138 ammation, with reduced revascularization and re-epithelialization during the proliferation phase of h

139 lagenase (MMP-1) expression is important for re-epithelialization during wound healing and indicate t

140 servations suggest that APLP2 contributes to re-epithelialization during wound healing by supporting

141 ad2 in regulating keratinocyte migration and re-epithelialization during wound healing.

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

143 litates cell migration and proliferation and re-epithelialization during wound healing.

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

145 und healing by rapid wound closure, improved re-epithelialization, enhanced extracellular matrix remo

146 directionally into the wound bed to initiate re-epithelialization, essential for wound repair and res

147 Following re-epithelialization, expression of the syndecans return

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

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

150 tinocytes are fully differentiated, to study re-epithelialization following wounding.

151 ired prohealing functions by promoting wound re-epithelialization, formulation of granulation tissue,

152 ion, redox response, inflammation, epidermis re-epithelialization, granulation formation, and proper

153 ic animals, they coacted to accelerate wound re-epithelialization, granulation tissue formation, and

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

155 These studies show that re-epithelialization, granulation tissue formation, incl

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

157 nding that beta-AR antagonists promote wound re-epithelialization in a "chronic" human skin wound-hea

158 eighboring organ can be activated to mediate re-epithelialization in acute colitis.

159 The incidence of complete re-epithelialization in animals given systemic administr

160 e-epithelialization in pig burn wounds (100% re-epithelialization in antagonist-treated wounds vs. ap

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

162 agonist-treated wounds vs. approximately 70% re-epithelialization in control wounds on postburn day 2

163 ted inflammation and significantly increased re-epithelialization in corneal wounds.

164 IL36gamma in epithelial cells promotes rapid re-epithelialization in in vitro wound closure assay.

165 could be involved in the process of abnormal re-epithelialization in lung fibrosis.

166 ular surface burns has efficacy in hastening re-epithelialization in moderate burns.

167 kin-like cells from the anus mediate colonic re-epithelialization in murine colitis.

168 rylation in human skin wounds and a delay in re-epithelialization in murine tail-clip wounds.

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

170 of a synthetic TGF-b antagonist accelerates re-epithelialization in pig burn wounds (100% re-epithel

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

172 cycles of hair follicle regeneration and for re-epithelialization in response to wounding.

173 t did not demonstrate a benefit in improving re-epithelialization in severe burns or visual acuity or

174 We found that wound closure by re-epithelialization in the experimental group was 4 day

175 inocytes to stimulate cell proliferation and re-epithelialization in the skin, whereas IL-27 leads to

176 nant Serpinb3a, the mouse ortholog, enhances re-epithelialization in vitro and accelerates wound clos

177 type of oral keratinocytes is altered during re-epithelialization in vitro and that this process is m

178 addition, a deficiency of TNF-alpha delayed re-epithelialization in vivo and this correlated with re

179 Time to corneal re-epithelialization in vivo was significantly delayed i

180 ocytes in vitro, we found no effect on wound re-epithelialization in vivo.

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

182 crucial part in the pathogenesis of retarded re-epithelialization in wound.

183 nocytes from the adjacent epidermis and make re-epithelialization independent of keratinocyte prolife

184 Re-epithelialization involves interactions between kerat

185 Impaired re-epithelialization is a hallmark of these wounds, whic

186 endogenous "wound current" upon injury until re-epithelialization is complete.

187 inocytes late in the regenerative phase when re-epithelialization is completed and matrix maturation

188 cells being located in the basal layer until re-epithelialization is completed.

189 ng a rat thermal injury model suggested that re-epithelialization is impeded by products of resident

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

191 Re-epithelialization is not dependent on DNA synthesis i

192 )-skewed immune response directed at bladder re-epithelialization is observed, with limited capacity

193 onal role of keratinocyte alpha9beta1 during re-epithelialization is unknown and analysis has been pr

194 On re-epithelialization, MCT3 was detected in chick and hfR

195 directionally into the wound bed to initiate re-epithelialization, necessary for wound closure and re

196 was associated with increased proliferation, re-epithelialization, neovascularization, and blood flow

197 Re-epithelialization, neutrophil influx, and platelet ac

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

199 Re-epithelialization occurred in 17 of 20 eyes.

200 Re-epithelialization occurs as keratinocytes are activat

201 Re-epithelialization of 5- to 6-mm-wide rabbit corneal e

202 (HK) migration plays a critical role in the re-epithelialization of acute skin wounds.

203 ay epithelial repair and is required for the re-epithelialization of airway wounds by facilitating ce

204 ed the expression of MCT3 after wounding and re-epithelialization of chick RPE explant and human feta

205 in MCT expression after scratch wounding and re-epithelialization of chick RPE/choroid explant cultur

206 beta signaling would be predicted to enhance re-epithelialization of cutaneous wounds and reduce scar

207 Re-epithelialization of cutaneous wounds in adult mammal

208 nd plays a critical role in coordinating the re-epithelialization of cutaneous wounds.

209 collagenase-1-dependent migration during the re-epithelialization of epidermal wounds.

210 ulation of extracellular matrix and aberrant re-epithelialization of fibrotic lung parenchyma.

211 tinocytes in intact skin and is required for re-epithelialization of human skin wounds.

212 cyte motility plays an important role in the re-epithelialization of human skin wounds.

213 rate that L. rhamnosus GG lysate accelerates re-epithelialization of keratinocyte scratch assays, pot

214 ancer cells in the brain by facilitating the re-epithelialization of metastatic breast cancer cells a

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

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

217 Re-epithelialization of partial- or full-thickness skin

218 the proliferation of cell types that promote re-epithelialization of skin following injury.

219 Re-epithelialization of skin wounds depends upon the mig

220 otes neovascularization, resulting in faster re-epithelialization of skin wounds in diabetic mice.

221 al utility of BETi in promoting keratinocyte re-epithelialization of skin wounds.

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

223 Delayed re-epithelialization of the cornea after injury usually

224 ring with opioid-receptor interaction during re-epithelialization of the cornea in the rat using both

225 The data revealed that re-epithelialization of the corneal epithelium is not de

226 , and 4 weeks after surgery for the complete re-epithelialization of the palatal wound (CWE), the alt

227 healed wounds while simultaneously promoting re-epithelialization of the remaining provisional wound.

228 The mean best-corrected visual acuity after re-epithelialization of the shield ulcer was 20/30, 20/3

229 oglobulin therapy was successful in complete re-epithelialization of the skin.

230 ard of care wound closure endpoint calls for re-epithelialization of the wound with no discharge for

231 flammation and by enhancing angiogenesis and re-epithelialization of the wound, thereby reversing the

232 ation to form a thick granulation tissue and re-epithelialization of the wounds.

233 Re-epithelialization of treated monolayers was compared

234 y, unlike galectin-3, galectin-7 accelerated re-epithelialization of wounds in both gal3(-/-) and gal

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

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

237 d suggest a potential mechanism for enhanced re-epithelialization of wounds under low oxygen tensions

238 o different models of corneal wound healing, re-epithelialization of wounds was significantly slower

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

240 drate-binding proteins galectins-3 and -7 in re-epithelialization of wounds.

241 3 after injury (28 +/- 5% versus 79 +/- 14% re-epithelialization, P < 0.005).

242 l structures as sources of keratinocytes for re-epithelialization, particularly the sweat apparatus.

243 Re-epithelialization, patterns of neutrophil influx and

244 ct wound healing is characterized by a rapid re-epithelialization process and a muted inflammatory re

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

246 tinocyte differentiation and accelerates the re-epithelialization process.

247 Re-epithelialization progressed as a gradient of cell la

248 Presence of desmosomes throughout re-epithelialization raises the question of how migratin

249 The re-epithelialization rate was similar among treatment gr

250 filtrate/scar size, corneal perforation, and re-epithelialization rates stratified by culture positiv

251 Deletion of CD80 in HFSCs impaired re-epithelialization, reduced accumulation of peripheral

252 uch macrophage depletion resulted in delayed re-epithelialization, reduced collagen deposition, impai

253 In addition, re-epithelialization requires long-range epithelial rear

254 Collective processes such as wound re-epithelialization result from the integration of indi

255 They contribute to inflammation, histolysis, re-epithelialization, revascularization and cell prolife

256 ect keratinocyte migration, proliferation or re-epithelialization, suggesting that the effect of bery

257 l transduction pathway responsible for wound re-epithelialization, the primary mechanism underlying w

258 e capacity to migrate and contribute to this re-epithelialization: the less differentiated cells of t

259 with calcimimetic NPS-R568 accelerated wound re-epithelialization through enhancing the epidermal Ca(

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

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

262 als were sacrificed at day 3 before making a re-epithelialization time analysis with fluorescein stai

263 Re-epithelialization time and best-corrected visual acui

264 main outcome measures: Re-epithelialization time and best-corrected visual acui

265 h lamellar de-epithelialization, followed by re-epithelialization to form an epithelialized tunnel as

266 n response to manual debridement wounds when re-epithelialization took more than 24 hours.

267 icroRNAs may be implicated in limiting wound re-epithelialization under hypoxia, a major component of

268 nt evidence revealed that DAMPs also trigger re-epithelialization upon kidney injury and contribute t

269 Complete re-epithelialization was achieved by day 7 in all patien

270 Wound re-epithelialization was also significantly faster in be

271 f AQP3-facilitated cell migration to corneal re-epithelialization was assessed using an organ culture

272 erproliferative in response to wounding, and re-epithelialization was complete by 24 h.

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

274 of TGF-beta receptor immunoreactivity until re-epithelialization was completed by day 7 after woundi

275 Re-epithelialization was delayed with a deficient deline

276 moval of the corneal epithelium by scraping, re-epithelialization was followed by fluorescein stainin

277 Re-epithelialization was rapid and complete within 3 day

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

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

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

281 Re-epithelialization was significantly delayed in mice w

282 However, although time to complete re-epithelialization was similar with the three methods,

283 n of marapsin, which closely correlated with re-epithelialization, was virtually absent in a genetic

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

285 esent the most promising targets to engineer re-epithelialization, we examined collective and individ

286 e keratinocyte behavior and phenotype during re-epithelialization, we have investigated this process

287 fect resolution and time to complete corneal re-epithelialization were considered primary outcome mea

288 the wound and a concomitant acceleration of re-epithelialization were identified as the underlying m

289 Revascularization and re-epithelialization were observed and the immunological

290 Therefore, targeting re-epithelialization, which mainly involves keratinocyte

291 e monolayer scratch assay was used to assess re-epithelialization; which comprises keratinocyte proli

292 al expansion of Treg cells, thereby enabling re-epithelialization while still kindling inflammation o

293 for wound closure, keratinocyte AR promoted re-epithelialization, while fibroblast AR suppressed it.

294 lactosidase transgene (n = 4) impaired wound re-epithelialization with an epithelial gap of 5.11 +/-

295 ced soft tissue wound opening and more rapid re-epithelialization with MaR1 delivery versus vehicle o

296 kin from Smad7 tg mice exhibited accelerated re-epithelialization, with increased activation of extra

297 reuteri significantly increased the rate of re-epithelialization, with L. rhamnosus GG being the mos

298 ) mice displayed significantly delayed wound re-epithelialization, with the greatest delay at day 3 a

299 l inflammatory milieu concomitant with rapid re-epithelialization within 24 hours.

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