ライフサイエンスコーパス: fibroblast

1 sensor was tested by using normal human skin-fibroblast.

2 ties of key cells in RA, especially synovial fibroblasts.

3 sed in activated pericytes, a main source of fibroblasts.

4 transcription factor c-JUN in the pathologic fibroblasts.

5 in was significantly upregulated in BD-NFPAs fibroblasts.

6 er accumulation in Ctr1(-/-) mouse embryonic fibroblasts.

7 endent fibro-inflammatory response in dermal fibroblasts.

8 deletion, and is observed in Drp1-deficient fibroblasts.

9 S-derived cardiomyocytes and primary cardiac fibroblasts.

10 sors while favoring the formation of stromal fibroblasts.

11 hesions coordinate the dynamics of spreading fibroblasts.

12 underlie the aberrant mechanobiology of IPF fibroblasts.

13 t for its responsiveness to TGFbeta1 in lung fibroblasts.

14 repression of TGFbeta signaling in the local fibroblasts.

15 val factor in PDGF-activated human and mouse fibroblasts.

16 r, induces the fusion of myomaker-expressing fibroblasts.

17 (ADAM10) is the major ephrin-B2 sheddase in fibroblasts.

18 enhanced ribosome biogenesis in HGPS-derived fibroblasts.

19 ed each other in the extracellular matrix of fibroblasts.

20 lated collagen gene expression by cocultured fibroblasts.

21 old when added to GMT-overexpressing cardiac fibroblasts.

22 r collagen enhancer activation in human lung fibroblasts.

23 senescent (late-passage) human diploid WI-38 fibroblasts.

24 oblast differentiation in primary human lung fibroblasts.

25 in the proliferation and activation of lung fibroblasts.

26 on occurs in separate pools in human primary fibroblasts.

27 cardiogenic activity of AGHMT in adult mouse fibroblasts.

28 which is important for AP-1 activity in lung fibroblasts.

29 h- and low-pressure protrusions like primary fibroblasts.

30 impaired the tumor-supporting properties of fibroblasts.

31 Smad-independent actions in isolated cardiac fibroblasts.

32 o cancer cells and less toxic or nontoxic to fibroblasts.

33 nase (AMPK) as a beta1-integrin inhibitor in fibroblasts.

34 more sensitive to CSE and STE than gingival fibroblasts.

35 comparable to levels of WT IFNAR1 in control fibroblasts.

36 s caveolin-1 function, using patient-derived fibroblasts.

37 and splenocytes and STING N154S SAVI patient fibroblasts.

38 nhibitors of IL-34 expression in RA synovial fibroblasts.

39 cardiomyocyte-specific splicing patterns in fibroblasts.

40 s Smad7 protein expression in primary kidney fibroblasts.

41 assessed with immunofluorescence on cultured fibroblasts.

42 crotubule network architecture phenotypes in fibroblasts.

43 in tetraploid immortalized murine embryonic fibroblasts.

44 All fibroblasts acquired a robust myofibroblast phenotype on

45 Finally, cultured fibroblasts activated IFN-gamma and IL-17A cytokine prod

46 In addition, P311 induced dermal fibroblast activation and proliferation.

47 Fibroblast Activation Protein (FAP) is a membrane-bound

48 Fibroblast activation protein (FAP) is overexpressed by

49 ed dermal fibrosis through the inhibition of fibroblast activation, T helper type 2-skewed immune pol

50 nventional responses were only elicited by a fibroblast-adapted rhesus CMV vector with limited tissue

51 the GLI target PTCH1 was observed in patient fibroblasts after chemical induction of the Hh pathway.

52 n in mice with ablation of GRK2 in activated fibroblasts alone.

53 species, inflammation, and proliferation in fibroblast and smooth muscle cells.

54 ifaceted process that includes activation of fibroblasts and a complex immune response.

55 y-three patients were included for whom skin fibroblasts and data on disease course and mutation anal

56 tin architecture in migrating human foreskin fibroblasts and found that network organization varied f

57 segments and variants in primary human lung fibroblasts and HEK293T cells, we show that FLIL33, but

58 of murine fibroblast cell lines and primary fibroblasts and human epithelial cell lines or primary h

59 n of vimentin was analysed in ARSACS patient fibroblasts and in cells where sacsin expression was red

60 us growth requires a close interplay between fibroblasts and keratinocytes.

61 cular approaches and validated in mouse lung fibroblasts and macrophages, and in IPF lung fibroblasts

62 gene the liver X receptor (LXR)alpha in lung fibroblasts and macrophages.

63 uced premature senescence in mouse embryonic fibroblasts and normal human bronchial epithelial cells.

64 morphologic transformation of NIH 3T3 mouse fibroblasts and of WT KRAS to rescue the growth defect o

65 the switching expression of MMP-3 in stromal fibroblasts and prostate cancer cells during tumor progr

66 n immortalization of primary mouse embryonic fibroblasts and recapitulates early steps of cell transf

67 unized BALB/c mice with senescent mouse lung fibroblasts and screened for antibodies that recognized

68 In vitro differentiation into fibroblasts and smooth muscle cells (SMCs) is also descr

69 is a recently discovered globin expressed in fibroblasts and smooth muscle cells with unknown functio

70 ly mild up-regulation of ISGs in STING N153S fibroblasts and splenocytes and STING N154S SAVI patient

71 rillin-1 containing microfibrils in cultured fibroblasts and suppresses fibrillin-2 (FBN2) incorporat

72 specific origins of mouse and human synovial fibroblasts and synovial tissues.

73 ecreased accumulation of bone marrow-derived fibroblasts and TGF-beta expression.

74 flects the mechanical cross-talk between the fibroblasts and the underlying fibrous material on which

75 duced proliferation and migration of cardiac fibroblasts and the up-regulation of CTGF and fibronecti

76 green monkey kidney epithelial), 3T12 (mouse fibroblast), and RAW 264.7 (mouse macrophage) cell lines

77 ast cells, the recruitment and activation of fibroblasts, and angiogenesis in the granulation tissue.

78 TGFbeta1 induction of CDH2 in normal and IPF fibroblasts, and antagomiR-630 abrogated the effect of m

79 raction among megakaryocytes, myeloid cells, fibroblasts, and endothelial cells.

80 iency in flies, mouse cells, patient-derived fibroblasts, and induced pluripotent stem cell-derived d

81 ophages, dermal dendritic cells, mast cells, fibroblasts, and lymphatic endothelium, but keratinocyte

82 PDL fibroblasts appear to be more sensitive to CSE and STE t

83 Activated fibroblasts are deemed the main executors of organ fibro

84 We found that mice lacking ephrin-B2 in fibroblasts are protected from skin and lung fibrosis an

85 hese findings support the use of human CMT1A fibroblasts as a platform for therapy testing.

86 rded efficient transfection in primary human fibroblasts as well as mesenchymal and embryonic stem ce

87 se expression is often elevated in activated fibroblasts associated with tissue remodeling in various

88 ically, loss of Smad2/3 from tissue-resident fibroblasts attenuated injury-induced cellular expansion

89 entiated cells, with reminiscent features of fibroblasts being visible both in chromatin accessibilit

90 In 3D collagen matrix, RhoA knockout reduced fibroblast branching and meshwork formation and resulted

91 l types, i.e., neutrophils, macrophages, and fibroblasts, but IL-1R2 deficiency on neutrophils increa

92 rescued in FKBP65-deficient murine embryonic fibroblasts by reconstitution with wild-type but not mut

93 ntin-pulp engineering strategies that target fibroblast C5L2 to induce pulp innervation.

94 ctional studies identified cancer-associated fibroblast (CAF)-derived EVs (from patients and xenograf

95 Cancer-associated fibroblasts (CAFs) are major components of the carcinoma

96 lecular mechanism by which cancer-associated fibroblasts (CAFs) confer chemoresistance in ovarian can

97 ormal and prostate cancer-associated stromal fibroblasts (CAFs) derived from a coculture cell model a

98 d two distinct subtypes of cancer-associated fibroblasts (CAFs).

99 primarily expressed in the cancer-associated fibroblasts (CAFs).

100 t RNAs localized in protrusions of migrating fibroblasts can be distinguished in two groups, which ar

101 protects from stressor-induced cell death in fibroblasts, cardiomyoblasts, neuronal cells, and primar

102 es of a mitochondrion from a mouse embryonic fibroblast cell line (NIH3T3) were visualized by tomogra

103 ganelle contacts in live cells from a monkey fibroblast cell line.

104 ung pathology and in vitro culture of murine fibroblast cell lines and primary fibroblasts and human

105 ary fibrotic and 7 non-fibrotic conjunctival fibroblast cell lines from patients with and without pre

106 es of FXN deficiency in patient-derived FRDA fibroblast cell models, the FRDA mouse model KIKO, and i

107 phototoxicity for cancer cells versus normal fibroblast cells (MRC5).

108 ic effects on SHSY5Y, MRC5, and human dermal fibroblast cells compared with the dissolved PhIP but cl

109 We reprogrammed 32 skin fibroblast cells from families of donors into human indu

110 itro studies on the response of human dermal fibroblast cells toward pristine titania nanotubes fabri

111 tion in the ATP-induced calcium responses of fibroblast cells, using a vectorial, or multi-time-point

112 on (30-40%) of the 26S in WT mouse embryonic fibroblast cells.

113 bout whether T cells directly impact cardiac fibroblasts (CFBs) to promote cardiac fibrosis (CF) in n

114 1 protein level and C-P4H activity in dermal fibroblasts compared to age-matched control samples.

115 Normal lung but not skin fibroblasts consistently elongated and aligned with unde

116 nsisting of tumor-associated macrophages and fibroblasts contribute to treatment tolerance through a

117 zed that downstream effectors of TGFbeta1 in fibroblasts could be attractive therapeutic targets and

118 Furthermore, we observed that cultured lung fibroblasts could internalize live NTHi.

119 rescue the growth defect of mouse embryonic fibroblasts deficient in all Ras genes.

120 tro studies using Gal-3 knockdown in cardiac fibroblasts demonstrated that Gal-3 regulates cell survi

121 expression levels in lymphoblastic lines and fibroblasts derived from affected individuals were decre

122 Fibroblasts derived from an affected individual and ACTB

123 ar size correlates with donor age in primary fibroblasts derived from healthy individuals and that ri

124 we found no evidence for collagen-producing fibroblasts derived from hematopoietic or bone marrow li

125 insoluble protein fraction were observed in fibroblasts derived from patients with the mutations p.(

126 iferation, impaired scar remodeling, reduced fibroblast-derived collagen synthesis, and perturbed ali

127 hat involves macrophage-derived IL-1beta and fibroblast-derived CXCR2 ligands.

128 We used fibroblast-derived induced pluripotent stem cells to gen

129 Surprisingly, cardiac fibroblasts did not appear to contribute appreciably to

130 IPF and normal lung fibroblasts differentially expressed and responded to VE

131 lso found that collagen-expressing precursor fibroblasts differentiate into white adipocytes in the e

132 and mechanical strain that promote resident fibroblast differentiation into contractile and extracel

133 ggest that SHP2 is an important regulator of fibroblast differentiation, and its loss as observed in

134 The patients' fibroblasts displayed impaired GINS complex assembly, ba

135 Collagen-I and alphaSMA(+) fibroblasts do not correlate with paucity in T-cell accu

136 of lipogenic or myogenic populations of lung fibroblasts during fibrosis formation and resolution.

137 Adipocytes formed from human keloid fibroblasts either when treated with BMP or when placed

138 ymal stem cells, committed progenitor cells, fibroblasts, endothelial cells, and immune cells.

139 se with potent neutralizing activity against fibroblast entry, while all antibodies that neutralized

140 ty, and neutralized both epithelial cell and fibroblast entry.

141 iously shown that patient-derived VCP mutant fibroblasts exhibit lower mitochondrial membrane potenti

142 a genome-wide shRNA screen in primary human fibroblasts expressing OSKM.

143 proapoptotic transcription factor, protected fibroblasts from 5-aza only when the cytotoxicity was ex

144 s not present at the primary cilium and that fibroblasts from affected individuals did not display ci

145 show transcriptomic differences in synovial fibroblasts from different joint locations and that HOX

146 TPase (IRGM1) was overexpressed in embryonic fibroblasts from dynamin1 like (DNM1L) protein-knockout

147 e found that the HTTexon1 mRNA is present in fibroblasts from juvenile HD patients and can also be re

148 We investigated the bioenergetic profiles of fibroblasts from LOAD patients and healthy controls, as

149 tissues from patients with CD and embryonic fibroblasts from mice, along with enteroids and human IE

150 ltured mesoderm explants and mouse embryonic fibroblasts from null mutants shows that the mesoderm mi

151 f NEMO-containing structures was impaired in fibroblasts from patients with IP carrying the truncated

152 demonstrate unexpectedly that primary dermal fibroblasts from pre-symptomatic mutation carriers recap

153 Primary dermal fibroblasts from R258C patients exhibited increased prol

154 ate alignment and migration of skin and lung fibroblasts from SSc patients and healthy controls.

155 potential role for the pentamer in promoting fibroblast fusion.

156 integrin beta3 and paxillin in rat embryonic fibroblasts growing on two different extracellular matri

157 Activating mutations in fibroblast growth factor (FGF) receptor 3 and inactivati

158 These treatments lead to activation of the fibroblast growth factor (FGF) receptor, phospholipase C

159 Fibroblast growth factor (Fgf) receptors have a recogniz

160 Fibroblast Growth Factor (FGF) signaling promotes self-r

161 cription of glycolytic enzymes downstream of fibroblast growth factor (FGF) signaling.

162 Fibroblast growth factor (FGF) signalling in the distal

163 We found that the loss of an intracellular fibroblast growth factor (FGF), FGF13, in the mouse DRG

164 ollicle patterning, identifying a network of fibroblast growth factor (FGF), wingless-related integra

165 ockout of FXR were given daily injections of fibroblast growth factor (FGF)19.

166 Fibroblast Growth Factor 19 (FGF19) is one of the most f

167 eptor and TGR5, the BA-induced gut hormones, fibroblast growth factor 19 and glucagon-like peptide 1,

168 Fibroblast growth factor 2 (FGF2) has previously been im

169 Fibroblast growth factor 2 (FGF2) is crucial for the dev

170 es, markers of inflammation, serum levels of fibroblast growth factor 21 (FGF21), and activation of s

171 nsulin resistance with increased circulating fibroblast growth factor 21 (FGF21), elevated Fgf21 mRNA

172 these effects require the metabolic hormone fibroblast growth factor 21 (FGF21).

173 Interestingly, fasting induction of fibroblast growth factor 21 in liver was attenuated.

174 Circulating levels of fibroblast growth factor 23 (FGF23) increase during the

175 Circulating levels of bone-derived fibroblast growth factor 23 (FGF23) increase early durin

176 Elevated fibroblast growth factor 23 (FGF23) levels, measured at

177 a precise and dynamic expression pattern of fibroblast growth factor 8 (Fgf8) in the HAA anlage, whi

178 terior to posterior (AP) patterning, whereas fibroblast growth factor 8 (Fgf8) is produced by the api

179 at muscle fibers secrete and concentrate the fibroblast growth factor binding protein 1 (FGFBP1) at N

180 ithelial cells resulted in a higher level of fibroblast growth factor receptor (FGFR) activation and

181 d growth factor receptor alpha (PDGFRA), and fibroblast growth factor receptor 1 (FGFR1) to cell prol

182 The regulatory mechanism of one such RTK, fibroblast growth factor receptor 2 (FGFR2) kinase, is s

183 is caused by a gain-of function mutation in fibroblast growth factor receptor 3 (FGFR3).

184 Activation of the fibroblast growth factor receptor FGFR4 by FGF19 drives

185 enerate mMSCs by utilizing hypoxia and basic fibroblast growth factor supplementation.

186 mple tests to quantify angiogenesis factors (fibroblast growth factor, vascular endothelial growth fa

187 fference in VAT activity was associated with fibroblast growth factor-2 (FGF2) levels.

188 demonstrated increased expression levels of fibroblast growth factor-2, transforming growth factor-b

189 ietic KDR(+)CD235a(-) mesoderm in a WNT- and fibroblast growth factor-dependent manner.

190 oss of kinase activity upon stimulation with fibroblast growth factor.

191 larization of the graft bed by agarose-basic fibroblast growth factor.

192 d in PC3 or DU145 (prostate cancer), NIH3T3 (fibroblast), H23 (lung cancer), and A-172 (glioblastoma

193 In ARSACS patient fibroblasts HSP70, ubiquitin and the autophagy-lysosome

194 GF)-beta1-induced spatial differentiation of fibroblasts, ii) spatiotemporal interactions between bre

195 iators and shedding new light on the role of fibroblasts in chronic inflammation.

196 d by the accumulation of apoptosis-resistant fibroblasts in the lung.

197 phils increased the IL-1-induced response of fibroblasts in trans.

198 a PI3K-dependent manner in normal human lung fibroblasts in vitro Mechanistically, TRPV4 modulated ma

199 No antibodies inhibited CMV spread in fibroblasts, including those with potent neutralizing ac

200 on of these factors from normal human breast fibroblasts increased proliferation of co-cultured breas

201 o assays applying macrophages and peritoneal fibroblasts indicated that this effect was cooperatively

202 describes how to isolate and infect primary fibroblasts; induce reprogramming and observe iCPC colon

203 expression of constitutively active ARF1 in fibroblasts induced formation of putative podosome precu

204 RhoA knockout in fibroblasts induced vimentin intermediate filament reorg

205 METHODS AND Deletion of IPMK in fibroblasts induces angiogenesis in both in vitro and in

206 oviral-GMT in reprogramming resident cardiac fibroblasts into iCMs in mouse infarct hearts.

207 s, Gata4, Mef2c, and Tbx5 (GMT), can convert fibroblasts into induced cardiomyocyte-like cells, albei

208 Oct4 during reprogramming of mouse embryonic fibroblasts into iPSCs.

209 itochondrial proteins in Nox4-deficient lung fibroblasts is inhibited by silencing of nuclear factor

210 und that loss of one allele of TSC2 in human fibroblasts is sufficient to increase p53 levels and imp

211 sebocyte differentiation, its role in dermal fibroblasts is unclear.

212 ovascular endothelial cells, melanocytes and fibroblasts isolated from 36 human skins ranging from ne

213 Fibroblasts isolated from the post-TKA fibrotic infrapat

214 receptor, is downregulated in the PTEN-null fibroblasts leading to a loss in the paracrine activatio

215 ages, with preferential differentiation into fibroblast-like cells but not into cardiomyocytes.

216 growth factor beta, which activates stromal fibroblast markers.

217 Herein, we hypothesized that scar-associated fibroblasts may be a source of stress-induced inflammato

218 h aortic smooth muscle cells and adventitial fibroblasts may contribute to development of TAAD and pr

219 Although claudin strand behavior in fibroblasts may not fully recapitulate that of epithelia

220 importance of TGF-beta-Smad2/3 signaling in fibroblast-mediated cardiac fibrosis has not been direct

221 mes more potent, with an IC50 of 5 muM, in a fibroblast-mediated collagen contraction assay, was less

222 (H3K27me3) in both Pten null mouse embryonic fibroblasts (MEFs) and Pten null mouse prostate tissues.

223 sruption of Cul9-p53 binding in mouse embryo fibroblasts (MEFs) by a knock-in mutation in Cul9 (Delta

224 hanistically, Tmem30a-mutant mouse embryonic fibroblasts (MEFs) exhibited diminished PS flippase acti

225 ncer cells and SerpinB2(-/-) mouse embryonic fibroblasts (MEFs) resulted in increased tumour growth,

226 on factor 2alpha (eIF2alpha) mouse embryonic fibroblasts (MEFs); moreover, ECD mRNA levels were incre

227 ient and longer duration changes in synovial fibroblast membrane potential.

228 We aimed to model pathogenic fibroblast migration in SSc in order to identify enhanci

229 red recruitment and activation of peritoneal fibroblasts, mitigated epithelial-mesenchymal-transition

230 ar/molecular mechanisms that account for the fibroblast-myofibroblast differentiation/activation in i

231 Fibroblasts/myofibroblasts are thought to be the major c

232 a lamina propria core with matrix molecules, fibroblasts, nerves, and vessels.

233 67 ovarian CAF samples and 10 normal ovarian fibroblast (NOF) samples were analysed to identify diffe

234 MCA expression in cancer cells compared with fibroblasts, offering a potential explanation for the di

235 e the role of exosomes released by bronchial fibroblasts on epithelial cell proliferation in severe a

236 -like 2 (LOXL2), thereby limiting effects to fibroblasts or cancer cells, the major LOXL2 producers.

237 we show that Rev1-deficiency in mouse embryo fibroblasts or mouse liver tissue is associated with rep

238 s associated with early activation of portal fibroblasts (PFs) that express Thy-1, fibulin 2, and the

239 d that leads to subsequent Src activation in fibroblasts plated on fibrotic matrix, osteopontin.

240 Bronchial fibroblasts play a key role in airway remodelling in ast

241 ubclones and clonal iPSC lines from the same fibroblast population and applied next-generation sequen

242 ctly proportional to the invasion induced by fibroblast populations.

243 Fibroblasts possess the capacity to suppress T cell resp

244 hannels that are expressed in human synovial fibroblast preparations have begun to provide important

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

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

247 ferentiation, epithelial cell phenotypes and fibroblast proliferation.

248 man cancer cells/red blood cells; and rodent fibroblasts/red blood cells.

249 We have identified that in human fibroblasts rendered senescent by stress, replicative ex

250 d to define an association between mtDNA and fibroblast responses in IPF.

251 scle and heart, and less so in the liver and fibroblasts, resulting in the perturbed assembly of the

252 vidual and ACTB siRNA knockdown in wild-type fibroblasts showed altered cell shape and migration, con

253 Deletion of Smad2/3 or Tgfbr1/2 from cardiac fibroblasts similarly inhibited the gene program for fib

254 Fibroblast-specific collagen expression was decreased an

255 Fibroblast-specific knockout of STAT3, or its pharmacolo

256 omyocyte hypertrophy is blunted with cardiac fibroblast-specific loss of beta-catenin after trans-aor

257 We report that fibroblast-specific PTEN deletion greatly restricts mamm

258 Mice with fibroblast-specific Smad3 loss had accentuated adverse r

259 The consequences of fibroblast-specific Smad3 loss were not a result of effe

260 indicated that the majority of COL1-positive fibroblasts stem from a pool of SOX9-expressing cells, a

261 FAK inhibition was sufficient to decrease fibroblast stiffness and collagen expression, supporting

262 demonstrate that the synthetic TLR2/6 ligand Fibroblast-stimulating lipopeptide (FSL-1) substantially

263 For all fibroblast strains combined, the partial least squares-l

264 , we undertook a unique approach by deriving fibroblast subclones and clonal iPSC lines from the same

265 ression by SFRP2(+), FMO1(+), and COL11A1(+) fibroblasts suggests roles in matrix deposition, inflamm

266 mputation, tph1b(+) joint cells give rise to fibroblasts that distribute across the entire lengths of

267 ools to address the developmental origins of fibroblasts that give rise to new endothelial cells.

268 In this paper, we report that primary fibroblasts that have been isolated from RTT patients di

269 In fibroblasts, the formation of syncytiumlike structures w

270 PTP4A1 promotes TGFbeta signaling in human fibroblasts through enhancement of ERK activity, which s

271 mitogen-activated protein kinase within the fibroblast to program the fibrotic response and myofibro

272 Direct reprogramming of fibroblasts to cardiomyocytes represents a potential mea

273 mediate the increased susceptibility of old fibroblasts to IR and chemotherapy that can be mitigated

274 ly active SHP2 reduced the responsiveness of fibroblasts to profibrotic stimuli, including significan

275 Exposure of cultured fibroblasts to uniaxial cyclic stretch results in an act

276 ression or activity was sufficient to induce fibroblast-to-myofibroblast differentiation in primary h

277 , myeloperoxidase was demonstrated to induce fibroblast-to-myofibroblast transdifferentiation by acti

278 Reducing CircPVT1 levels in proliferating fibroblasts triggered senescence, as determined by a ris

279 depletion (STED) nanoscopy in neurons, human fibroblasts, U2OS, and HeLa cells.

280 ators including proteins and lipids in human fibroblasts upon inflammatory stimulation and subsequent

281 ac progenitor cells (iCPCs) from mouse adult fibroblasts using forced expression of Mesp1, Tbx5, Gata

282 ng Tcf21 (MerCreMer) or in activated cardiac fibroblasts using periostin (Postn) (MerCreMer) .

283 catenin loss of function in resident cardiac fibroblasts using Tcf21 (MerCreMer) or in activated card

284 We analyzed genomic DNA from skin fibroblasts using whole-exome sequencing, and were able

285 fibroblasts and macrophages, and in IPF lung fibroblasts, using loss-and-gain of function assays, and

286 in macrophages, cardiomyocytes, and cardiac fibroblasts via proteinase-activated receptor 1 (PAR-1)

287 cross-talk between chondrocytes and synovial fibroblasts via raised levels of the pro-inflammatory ad

288 luext*46 mutant protein expressed in patient fibroblasts was comparable to levels of WT IFNAR1 in con

289 monstrated that IL-6 secretion from synovial fibroblasts was induced by chondrocyte-derived IL-6.

290 nteraction between rootletin and Nesprin1 in fibroblasts, we demonstrate that multiple isoforms of Ne

291 Using UV-exposed human skin fibroblasts, we found that, at the dose used, a single w

292 PDL and gingival fibroblasts were exposed to various concentrations of CS

293 monstrated that the vast majority of infarct fibroblasts were of epicardial origin and not derived fr

294 nded skin contained abundantly CD26-positive fibroblasts, whereas in gingiva they were rare.

295 single cells and clones derived from primary fibroblasts, which allows us to make the first direct co

296 Propagation of HSV-1 on DHCR24(-/-) fibroblasts, which lack the desmosterol-to-cholesterol c

297 progression are defective in patient-derived fibroblasts, which, similar to mouse neocortical progeni

298 ease in mitochondrial respiration in patient fibroblasts with a homozygous ANKZF1 R585Q mutation, and

299 Transduction of fibroblasts with a lentivirus encoding the wild-type pro

300 Fibroblasts within the mammary tumor microenvironment ar