ライフサイエンスコーパス: wound closure

1 was required for optimal intestinal mucosal wound closure.

2 coordinates cellular movements and promotes wound closure.

3 osin cable, and these actin structures drive wound closure.

4 nt role for mitochondria in skin quality and wound closure.

5 expression and improved capability to induce wound closure.

6 Hsp90alpha as a potential driver for normal wound closure.

7 of vimentin impairs repair cell function and wound closure.

8 a model to screen for factors implicated in wound closure.

9 g further dermal tissue growth and enhancing wound closure.

10 he eyelids and ocular annexes at the time of wound closure.

11 pha transcription factor is a key feature of wound closure.

12 laboration of vimentin-rich protrusions, and wound closure.

13 otential as exogenous contaminant at time of wound closure.

14 Abelson (Abl) contributes to rapid embryonic wound closure.

15 ce were found to have an accelerated rate of wound closure.

16 antly diminished the PMA-induced increase in wound closure.

17 ophage recruitment, bacterial clearance, and wound closure.

18 s well as reduced proliferation and impaired wound closure.

19 ECs and plays an important role in promoting wound closure.

20 sin cable, a structure that is essential for wound closure.

21 ell-matrix associations, cell migration, and wound closure.

22 esis, and, ultimately, tissue remodeling and wound closure.

23 enty-four of these underwent lower extremity wound closure.

24 presumably to facilitate cell migration and wound closure.

25 EGF and LXA4 increased corneal epithelial wound closure.

26 accelerated, whereas HIF1alpha shRNA delayed wound closure.

27 inase DAPK-1 acts as a negative regulator of wound closure.

28 esulting in increased rates of migration and wound closure.

29 esulted in a significant delay in epithelial wound closure.

30 ounding but instead promotes actin-dependent wound closure.

31 ntact in both in vitro and in vivo models of wound closure.

32 in a lack of bacterial clearance and delayed wound closure.

33 Ischemia complicates wound closure.

34 nted diabetic EPCs also improved the rate of wound closure.

35 s effective than normal EPCs at accelerating wound closure.

36 dermis to identify genes required for normal wound closure.

37 nce indicating tissue hypoxia conflicts with wound closure.

38 k2 signaling potently blocked CXCL12-induced wound closure.

39 caused inhibition of airway epithelial cell wound closure.

40 revealing a non-angiogenic effect of VEGF on wound closure.

41 ed and followed for 30 days after definitive wound closure.

42 deposition, as well as by decreasing time to wound closure.

43 ) and ectocervix (ECX) significantly delayed wound closure.

44 nuated corneal epithelial EGFR signaling and wound closure.

45 age recruitment to the wound-site and impair wound closure.

46 play a conserved autocrine role in epidermal wound closure.

47 erted vortex motion that is maintained after wound closure.

48 ts ligands, Pvf1, are required for epidermal wound closure.

49 3.0 may regulate cell motility and stimulate wound closure.

50 then monthly until week 20 or occurrence of wound closure.

51 aling, including angiogenesis and excisional wound closure.

52 f EGFP-PMN recruitment and the efficiency of wound closure.

53 y absent in a genetic mouse model of delayed wound closure.

54 ole in regulating intestinal epithelial cell wound closure.

55 added HB-EGF and HGF significantly enhanced wound closure.

56 of platelets retards epithelial division and wound closure.

57 n-chaperone function of Hsp90alpha in normal wound closure.

58 eta abolished the effect of PVI treatment on wound closure.

59 working to promote rapid cell migration and wound closure.

60 nflammatory response, poor angiogenesis, and wound closure.

61 migration of SCC cells, leading to decreased wound closure.

62 to predict the hierarchy of factors driving wound closure.

63 le tools to identify the mechanical basis of wound closure.

64 e impairs re-epithelialization and efficient wound closure.

65 panied with persistent inflammation and slow wound closure.

66 l innate immune contributor to IL-10-induced wound closure.

67 d wound re-epithelialization and kinetics of wound closure.

68 tion, supports angiogenesis, and accelerates wound closure.

69 t correlation to the observed differences in wound closure.

70 um spp.) significantly prolonged the time to wound closure.

71 s during tissue repair, resulting in delayed wound closure.

72 essential for wound edge actin assembly and wound closure.

73 actin accumulation around wounds and slower wound closure.

74 TPRP-treated wounds reached 90% wound closure 5.6 to 9.5 days earlier than PRP-treated a

75 resulted in significantly increased rates of wound closure (72.3 +/- 14.7% with XAV-939; and 52.1 +/-

76 application of InsP4 accelerate the speed of wound closure, a finding that has potential implications

77 ayers resulted in 5.8+/-0.7-fold increase in wound closure after 24 hours.

78 erogeneity of keratocyte response may impact wound closure after mechanical wounding.

79 that the PKCbetaII-mediated increase in IEC wound closure after PMA stimulation was mediated by incr

80 hed gammadelta T cell activation and delayed wound closure akin to that seen in the absence of gammad

81 GF signalling, which are only required after wound closure, allowing the epidermis outside the wound

82 ivity abrogated the fMLF-induced increase in wound closure and activation of both Rac1 and Cdc42.

83 Percentage wound closure and angiogenesis at 1 week was assessed us

84 le mice exhibited delayed corneal epithelial wound closure and attenuated polymorphonuclear (PMN) leu

85 a novel therapeutic strategy for increasing wound closure and augmenting angiogenesis, which is a ce

86 al precursor to collective cell migration in wound closure and cancer metastasis, respectively.

87 EGF-induced wound closure and cell migration rates of human corneal

88 row to MFG-E8(+/+) mice resulted in impaired wound closure and compromised wound vascularization.

89 s, and local application of RvD1 accelerated wound closure and decreased accumulation of apoptotic ce

90 novel therapeutic agent to improve diabetic wound closure and demonstrate the primary mechanism of i

91 In summary, macrophages seem to promote both wound closure and dermal healing, in part by regulating

92 closure, whereas elevation of mtROS promotes wound closure and enhances survival of mutant animals de

93 ceived wild-type bone marrow showed improved wound closure and improved wound vascularization.

94 AS II promoted wound closure and increased cell proliferation, L-argini

95 nock-out (Has1/3 null) mice show accelerated wound closure and increased numbers of fibroblasts in th

96 tions in cellular phenotype including slowed wound closure and increased transepithelial resistance.

97 Here, we show that S. aureus inhibits wound closure and induces miR-15b-5p in acute human and

98 did promote migration and stimulate in vitro wound closure and invasion.

99 with recombinant PDGF-AA rescued the delayed wound closure and lack of myofibroblast differentiation.

100 onsistent with normal tissue does not affect wound closure and may even lead to highly favorable long

101 VAP-1 enhanced stromal cell spreading and wound closure and modulated expression of profibrotic ge

102 pture the cellular events that contribute to wound closure and morphogenesis of regenerating legs wit

103 proliferation and migration that facilitate wound closure and recovery of the intestinal epithelial

104 hCVAM) has been shown to effectively promote wound closure and reduce wound-related infections.

105 rast, at older ages, Sod2 deficiency delayed wound closure and reduced epidermal thickness, accompani

106 of YAP and TAZ markedly delayed the rate of wound closure and reduced the transforming growth factor

107 ted small interfering RNA (siRNA) to promote wound closure and regeneration.

108 use skin, Smad4-deficient wounds had delayed wound closure and remodeling.

109 ntraction (retraction) is thought to promote wound closure and secure hemostasis while preventing vas

110 y performing time-lapse imaging of planarian wound closure and sequential imaging over days of head r

111 Finally, Dll4-blockade impairs wound closure and severely affects lymphangiogenesis dur

112 yed dermal cell migration leading to delayed wound closure and significantly increased scar size in f

113 d healing process, that is, time to complete wound closure and skin biomechanical properties.

114 of dermal wounds with isoxazole accelerates wound closure and suppresses the inflammatory response.

115 chment points for the actomyosin ring during wound closure and that Rho-kinase is required for locali

116 f keratinocytes is an essential component of wound closure and the development of epidermal tumors.

117 mensional (2-D) migration that occurs during wound closure and three-dimensional (3-D) migration thro

118 2 to 4 days after the injury coincided with wound closure, and by 8 days the expression reached near

119 njured patients, early surgical excision and wound closure, and general advances in the intensive car

120 tion and activation in wounded skin, delayed wound closure, and increased proinflammatory macrophage

121 nin-driven epithelial cell proliferation and wound closure, and it interfered with ATII-to-ATI cell t

122 This was associated with a reduced growth, wound closure, and migration capacity.

123 i.e., exocytotic glutamate release, in vitro wound closure, and proliferation), whereas Ca(2+) wave p

124 rected dermal-epidermal separation, improved wound closure, and reduced blister formation.

125 ufficient to mediate accelerated dorsal skin wound closure, and the effects are lost in mice that are

126 Cell-mediated remodeling and wound closure are critical for efficient wound healing,

127 ntin protein expression, cell migration, and wound closure are prevented by a pharmacological inhibit

128 expression in cultures caused inhibition of wound closure as a result of 60% to 75% decrease in epit

129 of Hsp90alpha-Delta mutant protein promoted wound closure as effectively as the full-length wild-typ

130 e organ culture model and by scratch-induced wound closure assay.

131 olon cancer (HT29) cells was assessed with a wound-closure assay in the presence of a mitotic inhibit

132 In a wound-closure assay, GRK6(-/-) mice showed enhanced myel

133 associated with decreased cell migration in wound closure assays, and the inhibitory effect of miR-1

134 EMD and P2 significantly promoted early wound closure at day 1 (P <0.001 and P = 0.004, respecti

135 on-to-treat, was proportion of patients with wound closure at week 20.

136 icant enhancement in the rate and quality of wound closure both clinically and histologically relativ

137 age depletion during this period resulted in wound closure but permanent failure of limb regeneration

138 facilitate nursing care and delayed primary wound closure but the evidence to support its use is poo

139 SMalphaA) and normally function to assist in wound closure, but have been implicated in pathological

140 We show that COL7A1 is instrumental for skin wound closure by 2 interconnected mechanisms.

141 hat mbGR inhibits keratinocyte migration and wound closure by activating a Wnt-like phospholipase (PL

142 -1 induced epithelial cell proliferation and wound closure by activating epithelial pro-proliferative

143 to a cutaneous wound, where they accelerate wound closure by inducing myofibroblast differentiation

144 mtROS can promote wound closure by local inhibition of Rho GTPase activity

145 ve surgical debridement as well as secondary wound closure by means of skin grafting.

146 conclude that topical mevastatin accelerates wound closure by promoting epithelialization via multipl

147 usion, ADV/VEGF is effective in accelerating wound closure by stimulating angiogenesis, epithelializa

148 Normal wound closure can be restored in rapamycin-treated mice

149 nalysis of single-cell migration and scratch-wound closure clearly demonstrated that hERG1-expressing

150 The effect of miR-125b was analyzed in wound closure, colony formation, migration, and invasion

151 howed significantly accelerated and enhanced wound closure compared with a clinically approved collag

152 enhanced neutrophil recruitment, and faster wound closure compared with GRK6(+/+) animals.

153 < 0.05) and significantly improved diabetic wound closure compared with sham-treated controls (32.9

154 ne treatment results in a marked decrease in wound closure, compromised wound integrity, and increase

155 C3 attenuated spontaneous and HB-EGF-induced wound closures, confirmed by delayed wound healing in ce

156 tide that in preclinical studies accelerated wound closure, decreased inflammation and granulation ti

157 a cell monolayer, we quantified the rate of wound closure driven by a contractile circumferential ac

158 n PLGA nanoparticles (PLGA-LL37 NP) promotes wound closure due to the sustained release of both LL37

159 er the full complement of genes required for wound closure during larval epidermal wound healing.

160 OSM treatment also improved wound closure during the early inflammatory phase of hea

161 Proliferation assays and in vitro wound closure experiments were also performed in the pre

162 ualizing the processes involved in cutaneous wound closure, facilitating the dissection of direct fro

163 Whereas the kinetics of wound closure following acute skin injury was similar in

164 ble protein, leading to potent inhibition of wound closure following PMN-MP binding to IECs.

165 ll monolayers, we observed distinct steps in wound closure from time-lapse images of myosin distribut

166 fication and classification of postembryonic wound closure genes has yet to be developed.

167 our results identify a new set of conserved wound closure genes, determine putative functional roles

168 wounds were induced, and careful analysis of wound closure, granulation tissue formation, and angioge

169 ilage regeneration (H2=26%; P=0.006) and ear wound closure (H2=53%; P<0.00001) were significantly her

170 Although applying adhesive strips to a wound closure has been shown to have outcomes equivalent

171 f epithelial sheets during embryogenesis and wound closure; however, the mechanisms are poorly unders

172 fusion models, this model predicts a partial wound closure if lamellipod formation is inhibited at th

173 ted third-degree burn wound healing by rapid wound closure, improved re-epithelialization, enhanced e

174 rimental and theoretical model for epidermal wound closure in 3D, negating the previously proposed co

175 diethylenetriaamine NONOate markedly reduced wound closure in an in vitro scratch injury model, prima

176 also found to accelerate corneal epithelial wound closure in an in vivo murine model without affecti

177 netic deletion of IL-17A resulted in delayed wound closure in animals.

178 Th2 cytokines also impaired wound closure in BEC monolayers.

179 Loss of CX3CR1 function delayed wound closure in both CX3CR1 knockout (KO) mice and in w

180 eting the fragment-5 region disrupted normal wound closure in both wild-type Hsp90alpha and Hsp90alph

181 ed delayed epithelialization and accelerates wound closure in diabetic animals by targeting epithelia

182 Significantly delayed wound closure in diabetic animals was associated with di

183 We validate MEDUSA by quantifying wound closure in Drosophila embryos, and we show that th

184 ecretion of a neutrophil chemokine and slows wound closure in HBE cells.

185 the Toll/NF-kappaB pathway is essential for wound closure in late Drosophila embryos.

186 administration of synthetic NATs accelerates wound closure in mice and stimulates repair-associated r

187 n of F-5 peptide promoted acute and diabetic wound closure in mice far more effectively than did PDGF

188 Acceleration of infected wound closure in NO-treated groups was clinically shown

189 sts were also functionally less effective at wound closure in nude mice.

190 ulfate dressing versus a control dressing on wound closure in patients with neuroischaemic diabetic f

191 s transfected with PTP1B siRNA showed faster wound closure in response to VEGF.

192 ioengineered skin substitutes can facilitate wound closure in severely burned patients, but deficienc

193 Consistent with these findings, wound closure in T cell- and B cell-deficient Rag1-/- mi

194 Although rescue of epidermal wound closure in the absence of macrophages promotes bla

195 ously added TGF-beta3 accelerated epithelial wound closure in type 2 rat and type 1 mouse DM corneas

196 Accelerated wound closure in vitro induced by anti-miR-200c was asso

197 dification as well as a delay in the rate of wound closure in vitro.

198 ion to fibronectin, and an increased rate of wound closure in vitro.

199 n, tight junction stabilization and impaired wound closure in vitro.

200 Inhibition of GC synthesis accelerated wound closure in vivo, providing the evidence that modul

201 ng that CD301b-depleted mice exhibit delayed wound closure in vivo, which could be rescued by topical

202 ivery vehicle, and this resulted in enhanced wound closure in vivo.

203 which contributes to the effect of Dkk-1 on wound closure in vivo.

204 GF, whereas LXA4 stimulation induced similar wound closure in wild-type and knockout mice.

205 +)-dependent signaling cascade that promotes wound closure, in parallel to the innate immune response

206 , in young mice, Sod2 deficiency accelerated wound closure, increasing epidermal differentiation and

207 ysis of protein localization dynamics during wound closure indicates that the rapid contraction of me

208 y facing the lesion participated directly in wound closure, indicating that closure is driven by move

209 Treatment with biliverdin accelerated wound closure, inhibited neovascularization and reduced

210 angiogenesis was associated with compromised wound closure, insufficient granulation tissue formation

211 cells, proepithelin additionally stimulated wound closure, invasion, and promotion of cell growth in

212 Throughout wound healing and after wound closure, InvEE macrophages demonstrated sustained

213 Based on our findings, epidermal wound closure is a process in which cell behavior is orc

214 Therefore, rapid wound closure is crucial for proper tissue function and

215 We find that wound closure is faster in early embryos, where, in addi

216 A key aspect of wound closure is the migration of keratinocytes across t

217 Interestingly, although dispensable for wound closure, keratinocyte AR promoted re-epithelializa

218 AS II to assess cell proliferation, scratch wound closure, L-arginine uptake, cationic amino acid tr

219 sNAG membranes profoundly accelerated wound closure mainly by reepithelialization and increase

220 Effective wound closure mechanisms are essential for maintenance o

221 Early operative intervention and wound closure, metabolic interventions, early enteral nu

222 F within the wound significantly accelerated wound closure more effectively than an equal dosage of f

223 fect by these distinct inflammatory drivers, wound closure occurred at a rate similar to the saline-t

224 After 20 weeks, wound closure occurred in 60 patients (48%) in the sucro

225 sed in EM and CX epithelial cells even after wound closure occurred.

226 octasulfate dressing significantly improved wound closure of neuroischaemic diabetic foot ulcers wit

227 guides, we achieve a full thickness (>10 mm) wound closure of porcine skin, which represents approxim

228 A secondary outcome assessed wound closure of topically treated erosions.

229 n cell dynamics, including increased rate of wound closure on SPRY4-IT1 overexpression, suggest that

230 In contrast, TAF had no inhibitory effect on wound closure or tight junction formation following inju

231 increased bacterial colonization and delayed wound closure over time compared with young mice.

232 To follow airway-epithelial wound closure over time, we lesioned small areas of the

233 ism that modulates inflammation and promotes wound closure; pharmacologic amplification of this syste

234 own of beta-catenin underwent evaluation for wound closure, proliferation, and bleomycin-induced cyto

235 5 corneas displayed inhibition of epithelial wound closure promoted by EGF, whereas LXA4 stimulation

236 Hsp90alpha-Delta mutant mice showed similar wound closure rate as the wild-type Hsp90alpha mice.

237 loss of HF neogenesis did not correlate with wound closure rate but with a reduction in Lrig1-positiv

238 We observed that macroscopic wound closure rate is accelerated in the absence of comm

239 The results indicate that the overall wound closure rate is determined primarily by the rate a

240 junctions at the wound edge and had a slower wound closure rate than wild type cells.

241 The wound closure rate varies nearly sixfold on the substrat

242 ation of GF mice with CV microbiota restored wound closure rate, neutrophil and macrophage accumulati

243 Although many reports suggest that wound closure rates depend on isolated cell speed and/or

244 mmunication by a Cx mimetic peptide enhanced wound closure rates in keratinocyte monocultures and in

245 Wound closure rates were measured in human corneal epith

246 Wound closure rates, capillary density, and the recruitm

247 lication of recombinant SDF-1alpha increases wound closure rates, neovascularization, and endothelial

248 sufficient for increased cell-migration and wound-closure rates.

249 helial wound healing as evidenced by delayed wound closure, reduced epithelial cell division, reduced

250 The wound closure, reepithelialization, and collagen deposit

251 wound management, appropriate timing of war wound closure remains subjective.

252 Wound closure requires a complex series of micro-environ

253 Wound closure requires actin polymerization and is negat

254 Wound closure requires the activation of keratinocyte mi

255 Wound closure requires the Cdc42 small GTPase and Arp2/3

256 The accelerated wound closure resulted primarily from faster re-epitheli

257 e in vitro data were consistent with in vivo wound closure studies, and suggest that ANKRD1 is import

258 ling pathway previously implicated in larval wound closure suggests that Pvr signaling leads wound-ma

259 While sutures remain the common wound closure technique, they have many disadvantages.

260 ysteine had beneficial effects on epithelial wound closure, their combination significantly accelerat

261 release at tail fin wounds to initiate rapid wound closure through long-range activation of basal epi

262 PGT inhibition shortened cutaneous wound closure time in diabetic mice from 22 to 16 days.

263 Wound closure timing was compared between IFI and non-IF

264 ared, there was no significant difference in wound closure timing.

265 ells) using a femtosecond laser and followed wound closure up to 6 hours by autofluorescence multipho

266 ffects of succinate-pretreated hMSC enhanced wound closure, vascularization and re-epithelialization

267 The time to 50% wound closure was 11days, 16days, 14days, and 17days for

268 The defect in wound closure was accompanied by impaired removal of E-c

269 IFI wound closure was also assessed according to mold specie

270 Corneal epithelial wound closure was assessed in cultured HCECs and porcine

271 LPA-stimulated and spontaneous wound closure was attenuated by AG1478, GM6001, or CRM19

272 Wound closure was clinically evaluated.

273 Corneal epithelial wound closure was delayed and re-innervation was slow an

274 nged, the formation of these junctions after wound closure was delayed.

275 ines on TJ-mediated BEC barrier function and wound closure was examined by immunoblot, transepithelia

276 Wound closure was found to increase with substrate stiff

277 d an age-dependent expression pattern during wound closure was identified, including miR-31 and miR-2

278 stent cell migration was inhibited such that wound closure was impaired.

279 ersely, NO-mediated inhibition of epithelial wound closure was largely prevented after small interfer

280 The time to wound closure was longer for the IFI wounds (median, 16

281 oth equally impaired barrier function, while wound closure was more sensitive to TFV.

282 t in wound healing as assessed by percentage wound closure was observed only at the highest cell dose

283 FGFR1OP2/wit3.0 -expression vector, the skin wound closure was significantly accelerated, resulting i

284 In excisional wound-healing experiments, wound closure was significantly faster in Has1/3 null th

285 Fourteen days after treatment, wound closure was significantly more complete in AMD3100

286 Delayed wound closure was, in part, attributable to damage of th

287 sms by which AnxA2 promotes IEC movement and wound closure, we used a loss of function approach.

288 bpv(pic)) and LY294002 on cell migration and wound closure were investigated using time-lapse imaging

289 Overall, the times to wound closure were longest for the IFI wounds with Mucor

290 Among the IFI wounds, times to wound closure were significantly longer for wounds with

291 Cellular viability and wound closure were significantly promoted, and cytotoxic

292 n scaffold demonstrated increased percentage wound closure when compared with lower doses.

293 ide-specific antioxidants blocks actin-based wound closure, whereas elevation of mtROS promotes wound

294 expression of ANKRD1, and delayed excisional wound closure, which was characterized by decreased cont

295 C15 administration indirectly accelerates wound closure while altering fibroblast-mediated collage

296 dicted a relatively weak correlation between wound closure with proliferation, and the unexpectedly m

297 -/-) mice with rIL-22 significantly promoted wound closure, with peak epithelial cell division increa

298 bsence of clinical BU specific features' or 'wound closure' within 6 months ("primary cure"), and 'ab

299 l rHDL application rescued diabetes-impaired wound closure, wound angiogenesis, and capillary density

300 Even at 90 days, long after wound closure, wounds in the CXCR3(-/-) mice remained hy