ライフサイエンスコーパス: myofibroblastic

1 -conditioned medium stimulated HSC to become myofibroblastic.

2 ng phenotypes described as proliferative and myofibroblastic.

3 roblast transition (EMT), but did not affect myofibroblastic activation from interstitial fibroblasts

4 Hepatic stellate cells (HSCs) undergo myofibroblastic activation in liver fibrosis and regener

5 The mechanisms governing myofibroblastic activation remain poorly understood, and

6 rgo phenotypic trans-differentiation called "myofibroblastic activation" in liver fibrogenesis.

7 ated VIC calcification through inhibition of myofibroblastic activation, osteogenic differentiation,

8 n degradation products and TGF-beta1 promote myofibroblastic and osteogenic differentiation in fibrob

9 promotes morphologic transformation toward a myofibroblastic cell phenotype with increased expression

10 including numbers of hepatic progenitors and myofibroblastic cells (both P < 0.03).

11 myoblasts (CT cells) can differentiate into myofibroblastic cells after intramuscular transplantatio

12 tenin signaling occur distinctly in stellate/myofibroblastic cells and hepatoblasts, respectively.

13 ficant increases in both proliferative TDFSM myofibroblastic cells and TDECC cholangiocarcinoma cells

14 It has been recently recognized that myofibroblastic cells are the major contributors to the

15 Notably, our data also show that myofibroblastic cells can differentiate from nephron pro

16 onstrate heterogeneity of gene expression in myofibroblastic cells during active fibrogenesis.

17 -gamma but not in primary rat hepatocytes or myofibroblastic cells exposed to LPS or TNFalpha.

18 Although these myofibroblastic cells had high Yap and Taz accumulation

19 tion of myogenic cells to differentiate into myofibroblastic cells in injured muscle.

20 The myofibroblastic cells in some IMTs contain chromosomal r

21 se myogenic cells were gradually replaced by myofibroblastic cells in the injured muscle.

22 The 3G5 antigen was not present on myofibroblastic cells in the repairing area of a full-th

23 Embryonic stellate/myofibroblastic cells promote beta-catenin activation in

24 (activation) from lipid-storing pericytes to myofibroblastic cells to participate in liver fibrogenes

25 The SMA(+)NG2(+) myofibroblastic cells, F4/80(+) macrophages, and adjacen

26 lKO) and control skin had similar numbers of myofibroblastic cells, suggesting that myofibroblastic d

27 nd promotes accumulation of inflammatory and myofibroblastic cells.

28 creased extracellular matrix deposition, and myofibroblastic changes.

29 The CG treatment also induced myofibroblastic conversion of MCs in the liver.

30 A typically thin mural myofibroblastic cuff was smooth muscle actin positive, w

31 d immunocytochemical changes associated with myofibroblastic dedifferentiation were complete.

32 d incubation in serum-free medium and during myofibroblastic dedifferentiation.

33 erum-free environment and is enhanced during myofibroblastic dedifferentiation.

34 of circulating fibrocytes that show enhanced myofibroblastic differentiation and that are less respon

35 r necrosis factor-alpha (TNF-alpha) modulate myofibroblastic differentiation and the production of EC

36 Portal fibroblast myofibroblastic differentiation can be modeled in cultur

37 ake by lung fibroblasts and their effects on myofibroblastic differentiation have not been establishe

38 I-mediated signaling in pericytes to prevent myofibroblastic differentiation in the tumor microenviro

39 eration, proangiogenic factor secretion, and myofibroblastic differentiation of ASCs.

40 moothened was required for TGF-beta1-induced myofibroblastic differentiation of control fibroblasts,

41 Furthermore, SAB suppressed TGF-beta-induced myofibroblastic differentiation of MRC-5 fibroblasts and

42 oblast EVs (fEVs), suppress TGFbeta1-induced myofibroblastic differentiation of normal and idiopathic

43 bers of circulating fibrocytes, with greater myofibroblastic differentiation potential, were observed

44 t suppresses TbetaRII and TGF-beta dependent myofibroblastic differentiation to constrain tumor growt

45 rs of myofibroblastic cells, suggesting that myofibroblastic differentiation was not responsible for

46 ere also dependent on mechanical tension for myofibroblastic differentiation, and cells cultured on p

47 mEV uptake by lung fibroblasts, which blocks myofibroblastic differentiation, and that mEVs are enric

48 ased mEV uptake and prevented suppression of myofibroblastic differentiation.

49 yet attenuated SMAD-dependent signalling and myofibroblastic differentiation.

50 effects on normal and IPF fibroblasts during myofibroblastic differentiation.

51 localization of lipid-raft components during myofibroblastic differentiation.

52 or endogenous hyaluronan in the mediation of myofibroblastic differentiation.

53 st, platelet-derived growth factor inhibited myofibroblastic differentiation.

54 ficient to initiate high-grade sarcomas with myofibroblastic differentiation.

55 ed in vitro, and little is known about their myofibroblastic differentiation.

56 treated primary bovine keratocytes developed myofibroblastic features, including actin stress fibers

57 We suggest a role for stellate/myofibroblastic FGF10 within the liver stem cell niche i

58 cell phenotype with increased expression of myofibroblastic genes Collagen-1alpha1, Fibronectin, and

59 In cirrhotic livers, cholangiocytes, and myofibroblastic hepatic stellate cells (MF-HSC) produce

60 Hepatic accumulation of myofibroblastic hepatic stellate cells (MF-HSCs) is pivo

61 In mouse cholangiocytes, coculture with myofibroblastic hepatic stellate cells, a source of solu

62 bit epithelial and adipocytic features, into myofibroblastic-HSC (MF-HSCs) is a key event in liver fi

63 After transdifferentiation, the myofibroblastic HSCs are incapable of expressing many MM

64 nt and human liver fibrosis, specifically in myofibroblastic HSCs.

65 Navitoclax induced apoptosis in CAF and in myofibroblastic human hepatic stellate cells but lacked

66 Coculturing CCA cells with myofibroblastic human primary hepatic stellate cells or

67 s well as human primary hepatic stellate and myofibroblastic LX-2 cells, for these studies.

68 expressed E-cadherin as well as vimentin, a myofibroblastic marker not usually detected after mesenc

69 ing the expression of the well-characterized myofibroblastic marker S100A4, are functionally relevant

70 gen deposition and ectopic expression of the myofibroblastic markers vimentin and alpha-smooth-muscle

71 culture, the ALCAM(+) cells rapidly acquired myofibroblastic morphology and alpha-SMA expression.

72 thelial marker E-cadherin, transformation of myofibroblastic morphology, and production of interstiti

73 Stimulation of myofibroblastic Muller cells by IGF-I and -II, but not P

74 rom normal retina and from proliferative and myofibroblastic Muller cells did not detect message for

75 ed in all samples, but was least abundant in myofibroblastic Muller cells.

76 interleukin 7 (IL-7) and were identified as myofibroblastic pericytes that expressed integrin alpha(

77 pecific markers and acquire a mesenchymal or myofibroblastic phenotype and express mesenchymal cell p

78 bstructive intimal lesions, showing mainly a myofibroblastic phenotype and variable endothelial/vascu

79 smooth muscle actin, the most used marker of myofibroblastic phenotype and, more important, involved

80 iable stiffness demonstrated an increasingly myofibroblastic phenotype as stiffness increased.

81 efore, attempts to prevent and/or revert the myofibroblastic phenotype could result in novel therapeu

82 ealing corneal wounds, keratocytes exhibit a myofibroblastic phenotype in response to transforming gr

83 In addition, GANT61 treatment reduced the myofibroblastic phenotype of human MSCs isolated from pa

84 oA pathway was essential for the contractile myofibroblastic phenotype present in early cushion forma

85 tor beta(1)-dependent differentiation to the myofibroblastic phenotype was antagonized by the inhibit

86 n I, and fibronectin EDA(+) (markers for the myofibroblastic phenotype) were increased, whereas those

87 n of the organized tubular epithelium to the myofibroblastic phenotype, a process potently driven bot

88 h transdifferentiation of keratocytes to the myofibroblastic phenotype, implicating these cells as th

89 he mutant stromal cells have acquired a more myofibroblastic phenotype, which have been described as

90 a prolonged period of time assume a CAF-like myofibroblastic phenotype.

91 Those with myofibroblastic phenotypes produce more type I collagen

92 ls, Hh-pathway activation, EMT, expansion of myofibroblastic populations, and liver fibrosis occurred

93 acute/chronic (SA/C) vasculitis, and luminal myofibroblastic proliferation (LMP).

94 Evaluation of myofibroblastic proliferation should provide indirect ev

95 g hydroxyproline accumulation and inhibiting myofibroblastic proliferation.

96 Myofibroblastic RPE (35 days in culture) express cytoker

97 the predominant binding protein produced by myofibroblastic RPE cells.

98 Early reactive and myofibroblastic RPE have detectable levels of message fo

99 on is limited to the area demarcated by this myofibroblastic scaffold and occurs independently of epi

100 ng experiments suggest that the SMA(+)NG2(+) myofibroblastic scaffold originates from choroidal peric

101 with subsequent formation of a SMA(+)NG2(+) myofibroblastic scaffold, into which endothelial cells t

102 nt number of genes, including S100A4, in the myofibroblastic signature; however, DNA copy number vari

103 Snail1-depleted CAF failed to acquire myofibroblastic traits in response to TGFbeta, including

104 Hepatic stellate cells (HSCs) undergo myofibroblastic trans-differentiation in liver fibrogene

105 , vitamin A-storing liver pericytes, undergo myofibroblastic trans-differentiation or "activation" to

106 Hepatic stellate cells (HSCs) undergo myofibroblastic transdifferentiation (activation) to par

107 vated receptor gamma (PPARgamma) accompanies myofibroblastic transdifferentiation of hepatic stellate

108 antibodies against glycoprotein M6a, undergo myofibroblastic transdifferentiation.

109 st activation, increased ECM deposition, and myofibroblastic transformation of dermal fibroblasts.

110 paB activity selectively in REPs resulted in myofibroblastic transformation, indicating that NFkappaB

111 s pericyte recruitment to tumor vasculature, myofibroblastic transformation, tumor angiogenesis, and

112 pathway-dependent mechanisms that stimulated myofibroblastic transition of HSCs and enhanced MF-HSC v

113 PM3-ALK in a clinical biopsy of inflammatory myofibroblastic tumor (IMT) carrying the t(1;2)(q21;p23)

114 resistance in a patient with an inflammatory myofibroblastic tumor (IMT) harboring a RANBP2-ALK trans

115 Inflammatory myofibroblastic tumor (IMT) is a distinctive mesenchymal

116 Inflammatory myofibroblastic tumor (IMT) is a rare, but distinctive m

117 Inflammatory myofibroblastic tumor (IMT) is a relatively rare soft ti

118 Inflammatory myofibroblastic tumor (IMT), also known as inflammatory

119 n the nonhematopoietic neoplasm inflammatory myofibroblastic tumor (IMT), and some are present in bot

120 MR) imaging features of hepatic inflammatory myofibroblastic tumor (IMT).

121 large-cell lymphoma (ALCL) and inflammatory myofibroblastic tumor (IMT).

122 ymphoma kinase (ALK)-rearranged inflammatory myofibroblastic tumor, cedarinib for alveolar soft part

123 gastrointestinal stromal tumor, inflammatory myofibroblastic tumor, congenital fibrosarcoma and mesob

124 trointestinal stromal tumor and inflammatory myofibroblastic tumor.

125 Inflammatory myofibroblastic tumors (IMTs) are characterized by myofi

126 PURPOSE OF REVIEW: Inflammatory myofibroblastic tumors (IMTs) are indolent mesenchymal n

127 Inflammatory myofibroblastic tumors (IMTs) are neoplastic mesenchymal

128 large cell lymphomas (ALCL) and inflammatory myofibroblastic tumors (IMTs).

129 plastic large-cell lymphoma and inflammatory myofibroblastic tumors.

130 roblastoma, three of seven with inflammatory myofibroblastic tumour, and one of two with NSCLC).

131 plastic large-cell lymphoma and inflammatory myofibroblastic tumours, and that further investigation

132 anaplastic large-cell lymphoma, inflammatory myofibroblastic tumours, non-small-cell lung cancer (NSC

133 ity lipoprotein (oxLDL), in turn, stimulated myofibroblastic VIC differentiation and secretion of num