ライフサイエンスコーパス: fibroblast proliferation

1 ferentiation, epithelial cell phenotypes and fibroblast proliferation.

2 ibrosis-related genes in addition to cardiac fibroblast proliferation.

3 has revealed a dose-dependent inhibition of fibroblast proliferation.

4 Polymerized type I collagen suppresses fibroblast proliferation.

5 guanosine monophosphate and inhibits cardiac fibroblast proliferation.

6 by IL-1beta-stimulated fibroblasts enhances fibroblast proliferation.

7 bserved that miR-125b inhibits p53 to induce fibroblast proliferation.

8 sical and novel PKC isozymes does not affect fibroblast proliferation.

9 The C-terminal domain of CTGF mediates fibroblast proliferation.

10 ght-driven H2O2 production and inhibition of fibroblast proliferation.

11 ith P-15 did not have any effect on gingival fibroblast proliferation.

12 d untreated root shavings inhibited gingival fibroblast proliferation.

13 gated the inhibitory effects of IFN-gamma on fibroblast proliferation.

14 rface had synergistic effects in stimulating fibroblast proliferation.

15 produced interferon 1 (IFN1), which inhibits fibroblast proliferation.

16 side synthesis blocked growth factor-induced fibroblast proliferation.

17 ectively bypass the requirement for c-myc in fibroblast proliferation.

18 as a downstream mediator of TGF-beta-induced fibroblast proliferation.

19 th fibroblast-bearing coils showed extensive fibroblast proliferation.

20 iated with osteoclastogenesis inhibition and fibroblast proliferation.

21 important to their synergistic effects on BM fibroblast proliferation.

22 and in synergy with either cytokine induced fibroblast proliferation.

23 tant to elucidate factors regulating cardiac fibroblast proliferation.

24 iac fibroblast-derived) adenosine on cardiac fibroblast proliferation.

25 of endogenous NO synthesis had no effect on fibroblast proliferation.

26 ophy and/or remodeling by modulating cardiac fibroblast proliferation.

27 1c+ CD11b+ CD1c- phagolysosome+) upon dermal fibroblast proliferation.

28 eta resulted in decreased CD11b- dermal cell fibroblast proliferation.

29 omeostatic restraint of primary human dermal fibroblast proliferation.

30 ed Ca(2+) entry, ERK1/2 phosphorylation, and fibroblast proliferation.

31 tion of endothelial cells, and more synovial fibroblast proliferation.

32 emonstrate central roles for LPA and LPA1 in fibroblast proliferation.

33 on indicating the essential role of STAT3 in fibroblast proliferation.

34 harmacological inhibitor of aneuploid murine fibroblast proliferation.

35 eir activation and subsequent stimulation of fibroblast proliferation.

36 atory cell adhesion and migration as well as fibroblast proliferation.

37 dent CTGF expression, which, in turn, drives fibroblast proliferation.

38 ulating Sprouty-1, a protein that suppresses fibroblast proliferation.

39 ed kinase phosphorylation inhibition reduced fibroblast proliferation.

40 bilical vein endothelial cell monolayers and fibroblast proliferation.

41 HAS3 knockdown by shRNA caused inhibition of fibroblast proliferation.

42 hairpin RNA [shRNA]) decreased canine atrial fibroblast proliferation.

43 f dominant-negative FoxO3a augmented control fibroblast proliferation.

44 enced by its enhancement of keratinocyte and fibroblast proliferation.

45 asses of gadolinium chelates stimulate human fibroblast proliferation.

46 her confirmed that histamine inhibited heart fibroblast proliferation.

47 activator (tPA) promotes renal interstitial fibroblast proliferation.

48 a phosphorylation, cyclin D1 expression, and fibroblast proliferation.

49 y synergistically inhibits FoxO3a, promoting fibroblast proliferation.

50 n, proliferation-related gene induction, and fibroblast proliferation.

51 a1 integrin signaling prevented tPA-mediated fibroblast proliferation.

52 ll-conditioned media or coculture stimulated fibroblast proliferation, activation, and myofibroblast

53 Analysis of data suggests that increased fibroblast proliferation and a simultaneous decrease in

54 brosis (IPF) is characterized by exaggerated fibroblast proliferation and accumulation of collagens a

55 vere endoluminal coronary injury resulted in fibroblast proliferation and adventitial remodeling.

56 IP-10 did not modulate cardiac fibroblast proliferation and apoptosis but significantly

57 The effects of BMP2 and BMP4 on corneal fibroblast proliferation and apoptosis were also examine

58 ole, the same pathway surprisingly inhibited fibroblast proliferation and cardiac hypertrophy through

59 Conversely, overexpression of FGF2 increased fibroblast proliferation and collagen deposition, accele

60 roblast-bearing coils showed marked interval fibroblast proliferation and collagen formation.

61 K1/2 (MAPKK), and ERK1/2, on CTGF-stimulated fibroblast proliferation and collagen gel contraction wa

62 ibrotic cytokine IL-4 interact in regulating fibroblast proliferation and collagen production, and, i

63 pha expression was associated with increased fibroblast proliferation and collagen production.

64 pharmacological inhibition of c-abl reverses fibroblast proliferation and collagen synthesis to wild-

65 rosis (IPF) through its ability to stimulate fibroblast proliferation and collagen synthesis.

66 Fibrosis, as evidenced by fibroblast proliferation and connective tissue depositio

67 Endothelin-1 induces lung fibroblast proliferation and contractile activity via th

68 at MB was more effective in stimulating skin fibroblast proliferation and delaying cellular senescenc

69 Fibroblast proliferation and differentiation are central

70 Thus, fibroblast proliferation and differentiation are control

71 that in turn regulate underlying mesenchymal fibroblast proliferation and differentiation at least in

72 Moreover, HKL-treatment blocks cardiac fibroblast proliferation and differentiation to myofibro

73 gehog pathway inhibition was assayed by lung fibroblast proliferation and differentiation with and wi

74 ys remodelling at least partly by increasing fibroblast proliferation and differentiation with result

75 TRPC3 channels regulate cardiac fibroblast proliferation and differentiation, likely by

76 26 and causes TRPC3-dependent enhancement of fibroblast proliferation and differentiation.

77 PM7-mediated Ca(2+) signal for its effect on fibroblast proliferation and differentiation.

78 reases epidermal growth factor (EGF)-induced fibroblast proliferation and enhances EGF receptor (EGFR

79 is is a progressive disease characterized by fibroblast proliferation and excess deposition of collag

80 educed the ability of TGF-beta1 to stimulate fibroblast proliferation and expression of alpha-smooth

81 This is accompanied by extensive fibroblast proliferation and extracellular matrix (ECM)

82 redominant source of TGF-beta1, which drives fibroblast proliferation and extracellular matrix deposi

83 dministration suppressed AF while decreasing fibroblast proliferation and extracellular matrix gene e

84 activation of IL-6 trans signaling enhanced fibroblast proliferation and extracellular matrix protei

85 ed protein (LRP) in the regulation of kidney fibroblast proliferation and extracellular signal-regula

86 e pathological consequence of stress-induced fibroblast proliferation and fibroblast-to-myofibroblast

87 les for dermal Wnt signaling/beta-catenin in fibroblast proliferation and in the epidermal hair folli

88 Although excessive fibroblast proliferation and inflammation occur when abn

89 t size, deletion of FGF2 resulted in reduced fibroblast proliferation and interstitial collagen depos

90 ognized function of vimentin in coordinating fibroblast proliferation and keratinocyte differentiatio

91 , IIGP, GTPI, IGTP, Ifi202A), stimulators of fibroblast proliferation and matrix synthesis (interleuk

92 tial fibrosis, which correlated with reduced fibroblast proliferation and matrix synthesis, after nep

93 jor collagen/laminin receptor that regulates fibroblast proliferation and mesangial cell migration an

94 le cell types to coordinate keratinocyte and fibroblast proliferation and migration for epidermal and

95 induced beta-catenin activation, stimulated fibroblast proliferation and migration, collagen gel con

96 ofibroblasts in vitro but potently inhibited fibroblast proliferation and migration.

97 negative effects mediated by PGE2 on tendon fibroblast proliferation and MMP production, which may l

98 TRPC3 blockade or Ca(2+) removal inhibited fibroblast proliferation and myofibroblast differentiati

99 t CTGF blockade suppressed TGF-beta1-induced fibroblast proliferation and myofibroblast differentiati

100 poptosis have been implicated in the rampant fibroblast proliferation and pannus formation characteri

101 n a critical role to FKN and its receptor in fibroblast proliferation and pannus formation in RA.

102 Normally, polymerized collagen suppresses fibroblast proliferation and serves as a physiological r

103 may be important for both mitogen-stimulated fibroblast proliferation and skeletal muscle cell differ

104 d regeneration after injury, and stimulating fibroblast proliferation and the production of FN and co

105 olysaccharide hyaluronan (HA) in influencing fibroblast proliferation and thereby affecting wound hea

106 y dermis, whereas S100A9 was shown to induce fibroblast proliferation and to enhance fibroblast CCN2

107 nonreceptor c-abl tyrosine kinase regulates fibroblast proliferation and, by this means, is a costim

108 and this effect may be due to suppression of fibroblast proliferation and/or suppression of matrix de

109 Finally, in TACC2-deficient embryonic fibroblasts, proliferation and cell cycle progression as

110 sive disorder characterized by inflammation, fibroblast proliferation, and accumulation of extracellu

111 Ac-SDKP on monocyte/macrophage infiltration, fibroblast proliferation, and collagen deposition in the

112 lting in immune activation, vascular injury, fibroblast proliferation, and collagen deposition.

113 mechanism by which PTEN inhibits alpha-SMA, fibroblast proliferation, and collagen production.

114 rdiac remodeling which involves hypertrophy, fibroblast proliferation, and extracellular matrix produ

115 ssion, activation of integrin/FAK signaling, fibroblast proliferation, and fibrosis.

116 ed in post-infarct heart, stimulates cardiac fibroblast proliferation, and is induced by the proinfla

117 Some of its functions-angiogenesis, fibroblast proliferation, and stimulation of BM progenit

118 f the diarthroidial joints, characterized by fibroblast proliferation, angiogenesis, and perivascular

119 ration-dependent manner, FCS-induced cardiac fibroblast proliferation as assessed by DNA synthesis ([

120 pocellular dermis and a deficiency in dermal fibroblast proliferation as embryos.

121 ay also have deleterious effects on gingival fibroblast proliferation as well as collagen and non-col

122 ine the effects of chlorhexidine on gingival fibroblast proliferation as well as collagen and non-col

123 acid and gadolinium trichloride) stimulated fibroblast proliferation at a concentration of 0.01 mmol

124 meglumine) produced a maximum stimulation of fibroblast proliferation at a concentration of 0.1 mmol/

125 doteridol) produced a maximum stimulation of fibroblast proliferation at a concentration of 5 mmol/L.

126 monstrate that PGE2 can stimulate or inhibit fibroblast proliferation at clinically relevant concentr

127 etween P2 and P50 there was no difference in fibroblast proliferation at the wound site but Wnt signa

128 Results indicate that the degree of fibroblast proliferation, attenuated by extracellular ma

129 reduced Ang II-induced VSMC and adventitial fibroblast proliferation but had no effect on myoendothe

130 reated IL-5(-/-) mice were able to stimulate fibroblast proliferation but not alpha-smooth muscle act

131 rom KGF-treated subjects inhibited pulmonary fibroblast proliferation, but increased alveolar epithel

132 ast growth factors, all strong activators of fibroblast proliferation, but not by epidermal growth fa

133 onstrate that polymerized collagen represses fibroblast proliferation by a mechanism involving the fo

134 lagen suppresses G(1)/S phase transition and fibroblast proliferation by a novel mechanism involving

135 IF2alpha and reduced BeWo cell and placental fibroblast proliferation by approximately 50%.

136 l 20 amino acids of caveolin-1 in modulating fibroblast proliferation by dampening Smad signaling and

137 on with polymerized collagen inhibits normal fibroblast proliferation by suppression of the phosphoin

138 It increases BEC and fibroblast proliferation by up-regulating TGFbeta signal

139 , and the inhibitive effects of histamine on fibroblast proliferation could be blocked by JAK3/STAT6

140 d function of the skin secondary to impaired fibroblast proliferation, decreased collagen synthesis,

141 d function of the skin secondary to impaired fibroblast proliferation, decreased collagen synthesis,

142 Fibroblast proliferation, differentiation into myofibrob

143 are present in renal fibroblasts and control fibroblast proliferation, differentiation, and activatio

144 brought much attention to the regulation of fibroblast proliferation, differentiation, extracellular

145 g preparation enhanced IGF-stimulated 3T3-L1 fibroblast proliferation, due to the presence of a co-pu

146 echanical support of the ECM also stimulates fibroblast proliferation, expands vasculature, and incre

147 by PPM1A-depleted epithelial cells augmented fibroblast proliferation (>50%) compared with controls.

148 t size but were associated with unrestrained fibroblast proliferation, impaired scar remodeling, redu

149 nective tissue growth factor (CTGF), driving fibroblast proliferation in a paracrine fashion.

150 ces a paracrine p53 response that suppresses fibroblast proliferation in associated stroma.

151 activates ERK, and promotes inflammation and fibroblast proliferation in bleomycin-induced lung injur

152 Regulation of fibroblast proliferation in cultures of myocardial cells

153 rosis than wild-type mice due to 1) enhanced fibroblast proliferation in response to growth factors (

154 on induced by SV40 large T antigen supported fibroblast proliferation in the absence of betacyto-acti

155 Fibroblast proliferation in the presence of concentratio

156 phage-CSF, or type I collagen production, or fibroblast proliferation in this culture system.

157 We discovered that myostatin stimulated fibroblast proliferation in vitro and induced its differ

158 shown that angiotensin II induces human lung fibroblast proliferation in vitro via activation of the

159 of BAL fluid (BALF) to stimulate human lung fibroblast proliferation in vitro was examined in relati

160 r epidermal growth factor potentiated Nf1+/- fibroblast proliferation in vitro, demonstrating abnorma

161 d transforming growth factor-beta-stimulated fibroblast proliferation in vitro.

162 AII to stimulate fetal and adult human lung fibroblast proliferation in vitro.

163 rsten isoform is key in the control of renal fibroblast proliferation in vitro.

164 Similar to Col1 expression, fibroblast proliferation increased following physiologic

165 3- and TUNEL-positive fibroblasts, decreased fibroblast proliferation, increased nuclear translocatio

166 Fibroblast proliferation induced by tPA was associated w

167 Fibroblast proliferation is an early feature of progress

168 VSMC and fibroblast proliferation is AT1 receptor-dependent, wher

169 Further studies revealed that the effect of fibroblast proliferation is biphasic, with the promitoge

170 However, how interstitial fibroblast proliferation is controlled remains ambiguous

171 While fibroblast proliferation is necessary for hair follicle

172 pothesis that, in fibrotic gingival lesions, fibroblast proliferation is stimulated and apoptosis is

173 however, the effect of adenosine on cardiac fibroblast proliferation is unknown.

174 tPA as a mitogen that promotes interstitial fibroblast proliferation, leading to expansion of these

175 These activated T cells stimulate fibroblast proliferation, leading to fibroblast-associat

176 Extracellular ATP stimulates cardiac fibroblast proliferation, lung inflammation, and fibrosi

177 We find that ORC and ONRC inhibit fibroblast proliferation, migration and matrix contracti

178 ocesses involved in wound healing, including fibroblast proliferation, migration, adhesion, and the a

179 wth factors significantly increased gingival fibroblast proliferation, migration, and cell adhesion o

180 Such amplification results in fibroblast proliferation, myofibroblast differentiation,

181 Significantly enhanced fibroblast proliferation observed in NCaPP-PDGF-B-treate

182 gulation may underlie the increased gingival fibroblast proliferation observed.

183 for smooth muscle cells, myofibroblasts, and fibroblasts, proliferation of which is a hallmark of idi

184 However, P-15 did not enhance fibroblast proliferation on root sections.

185 arily involuting blood elements with minimal fibroblast proliferation or collagen formation.

186 ge in the presence of pulmonary neutrophils, fibroblast proliferation, or collagen gene expression.

187 and aFGF may contribute to angiogenesis and fibroblast proliferation, potentially independently of i

188 Overexpression of pVHL increased lung fibroblast proliferation, protein abundance of fibronect

189 olymerized type I collagen normally inhibits fibroblast proliferation, providing a physiological mech

190 lone, serve to regulate c-Jun expression and fibroblast proliferation rates.

191 ata demonstrate that ATP-induced adventitial fibroblast proliferation requires activation and interac

192 expression of two genes that promote tendon fibroblast proliferation: scleraxis and tenomodulin.

193 embryonic lethality, neuronal apoptosis, and fibroblast proliferation/senescence defects but not lymp

194 the Chaos3 background and impaired embryonic fibroblast proliferation, suggesting that ATM drug inhib

195 ntin orchestrates the healing by controlling fibroblast proliferation, TGF-beta1-Slug signaling, coll

196 ma is associated with enhanced potential for fibroblast proliferation that is related, at least in pa

197 both Xenopus oocyte maturation and mammalian fibroblast proliferation, the underlying mechanisms resp

198 ated that TGF-beta1 inhibited murine cardiac fibroblast proliferation; these antiproliferative effect

199 Fibroblast proliferation, thought to play a central role

200 a potent mitogen that promotes interstitial fibroblast proliferation through a cascade of signaling

201 l 20 amino acids of caveolin-1 in modulating fibroblast proliferation through dampening Smad signalin

202 In conclusion, gangliosides promote fibroblast proliferation through enhancement of growth f

203 ent mitogen that promotes renal interstitial fibroblast proliferation through LDL receptor-related pr

204 summary, HA facilitates TGF-beta1-dependent fibroblast proliferation through promoting interaction b

205 agonists may have a role in pulmonary artery fibroblast proliferation to hypoxia.

206 2 expression in the absence of GILT restores fibroblast proliferation to wild-type levels.

207 Furthermore, NRK-49F fibroblast proliferation triggered by conditioned media

208 he relationship between c-myc expression and fibroblast proliferation using a c-myc antisense oligonu

209 ibroblast-derived adenosine inhibits cardiac fibroblast proliferation via activation of A2B receptors

210 integrin-mediated signaling pathway promotes fibroblast proliferation via FoxO3a suppression.

211 UPAR-/- fibroblast proliferation was 60% inhibited by an ERK kin

212 Lung fibroblast proliferation was analyzed using the Quick Ce

213 Fibroblast proliferation was determined by ELISA which m

214 The selective action of glutamine on fibroblast proliferation was determined by labeling cult

215 gery were mixed with autologous T cells, and fibroblast proliferation was determined.

216 ing intact Agtr1a) were infused with Ang II, fibroblast proliferation was found equally in these card

217 No effect on fibroblast proliferation was found in the presence of il

218 rol animals and demonstrated that peritoneal fibroblast proliferation was highly LPA1 dependent.

219 fibroblasts from an additional patient, and fibroblast proliferation was inhibited by BRAF-specific

220 Enhanced uPAR-/- fibroblast proliferation was reversed by a recombinant n

221 was added to the medium (292 micrograms/ml) fibroblast proliferation was stimulated, and by 5-6 days

222 postmitotic cell proliferation and enhances fibroblast proliferation, whereas overexpressing miR-24

223 fibroblasts by inducing capillary growth and fibroblast proliferation, which secondarily support grea

224 d activation with interstitial inflammation, fibroblast proliferation with extracellular matrix colla

225 bFGF significantly stimulated gingival fibroblast proliferation with or without heparin.

226 evious studies have implicated inhibition of fibroblast proliferation with polymerized collagen-media