ライフサイエンスコーパス: re-epithelialization

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

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

3 romotes wound edge IGF1R phosphorylation and re-epithelialization.

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

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

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

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

8 arly leukocyte emigration appears to promote re-epithelialization.

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

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

11 e in glycoprotein expression occurred during re-epithelialization.

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

13 or eosinophils in negatively affecting wound re-epithelialization.

14 and the resultant phenotypic change directs re-epithelialization.

15 enhances keratinocyte migration and promotes re-epithelialization.

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

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

18 is leading to increased proliferation during re-epithelialization.

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

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

21 ing amniotic membrane grafting to facilitate re-epithelialization.

22 Keratinocyte migration is critical for wound re-epithelialization.

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

24 dermal fibroblasts are recruited only during re-epithelialization.

25 he local inflammatory response and promoting re-epithelialization.

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

27 mpairs keratinocyte migration and skin wound re-epithelialization.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 Re-epithelialization and epithelial cell division were b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 Following re-epithelialization, expression of the syndecans return

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 Re-epithelialization involves interactions between kerat

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

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

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

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

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

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

135 Re-epithelialization is not dependent on DNA synthesis i

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

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

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

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

140 Re-epithelialization, neutrophil influx, and platelet ac

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

142 Re-epithelialization occurred in 17 of 20 eyes.

143 Re-epithelialization occurs as keratinocytes are activat

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

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

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

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

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

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

150 Re-epithelialization of cutaneous wounds in adult mammal

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

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

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

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

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

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

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

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

159 Re-epithelialization of skin wounds depends upon the mig

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

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

162 Delayed re-epithelialization of the cornea after injury usually

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

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

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

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

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

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

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

170 Re-epithelialization of treated monolayers was compared

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

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

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

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

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

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

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

178 3 after injury (28 +/- 5% versus 79 +/- 14% re-epithelialization, P < 0.005).

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

180 Re-epithelialization, patterns of neutrophil influx and

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

182 Re-epithelialization progressed as a gradient of cell la

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

184 The re-epithelialization rate was similar among treatment gr

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

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

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

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

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

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

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

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

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

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

195 Re-epithelialization time and best-corrected visual acui

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

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

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

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

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

201 Wound re-epithelialization was also significantly faster in be

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

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

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

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

206 Re-epithelialization was delayed with a deficient deline

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

208 Re-epithelialization was rapid and complete within 3 day

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

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

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

212 Re-epithelialization was significantly delayed in mice w

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

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

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

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

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

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

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

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

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

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

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

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