ライフサイエンスコーパス: collagen I

1 platelet-derived growth factor receptor, and collagen I).

2 ion or fibrosis occurs, mostly consisting of collagen I.

3 ll adhesion to bone marrow stromal cells and collagen I.

4 ss endothelial cells and through Matrigel or collagen I.

5 tracellular matrix (ECM) proteins, including collagen I.

6 ustained dissemination, but exclusively into collagen I.

7 beta1 integrins lack the major receptors for collagen I.

8 s enhanced, resembling the binding of VWF to collagen I.

9 hibited OC (3.4-fold), Runx2 (2.8-fold), and collagen I (2.6-fold).

10 After T3-SCI, the MCA had more collagen I (42%), collagen III (24%), transforming growt

11 Collagen is a biological macromolecule capable of second

12 We now show that type IV collagen is a component within the morphological DEJ of

13 Fibrosis with excessive amounts of type I collagen is a hallmark of many solid tumours, and fibros

14 Overexpression of collagen is a hallmark of organ fibrosis.

15 Normal type I collagen is a heterotrimer triple-helical molecule consi

16 gether, these findings indicate that type VI collagen is a key regulator of dermal matrix assembly, c

17 Type IV collagen is a major and crucial component of basement me

18 Type VI collagen is a nonfibrillar collagen expressed in many co

19 We recently demonstrated that type VII collagen is a novel component of the inner enamel organi

20 Plastic compressed collagen is a superior biomaterial in terms of its speed

21 Collagen is a triple-helical protein that forms various

22 he NC2 domain (only 35-50 residues) of FACIT collagens is a potent trimerization domain.

23 s of the extracellular matrix, in particular collagens, is a hallmark of idiopathic pulmonary fibrosi

24 how alignment occurs in biopolymers such as collagen-I (a major component of the ECM).

25 Following myocardial infarction (MI), collagen I, a major component of cardiac ECM, is cleaved

26 MMP-1 promoted MLE12 cell migration through collagen I, accelerated wound closing, and protected cel

27 Furthermore, fibronectin (not collagen-I) accumulates in the tendons of Mmp14-null mic

28 We found that lung epithelial cell-derived collagen I activates fibroblast collagen receptor discoi

29 site (Pro-986) in the alpha1-chain of type I collagen is almost completely 3-hydroxylated in every ti

30 ycin lung injury, and activate expression of collagen-I(alpha)1 and the myofibroblast marker alphaSMA

31 A collagen-I(alpha)1-expressing mesenchymal population of

32 n, our studies suggest a distinct lineage of collagen-I(alpha)1-expressing resident fibroblasts that

33 We studied collagen-I(alpha)1-producing cells in normal and disease

34 e and decreased expression of fibronectin-1, collagen I, alpha-smooth muscle actin, connective tissue

35 , higher expression levels of fibronectin-1, collagen I, alpha-smooth muscle actin, CTGF, and PAI-1,

36 Photochemical cross-linking of corneal collagen is an evolving treatment for keratoconus and ot

37 istep self-assembly of the fibrillar protein collagen is an important design challenge in biomimetic

38 Collagen is an insoluble protein that widely distributes

39 pressed fibromodulin increased expression of collagen I and alpha-smooth muscle actin, indicating inc

40 analysis together with a RT-PCR detection of collagen I and collagen II gene expression to show that

41 In collagen I and collagen IV (targets for MMP1 and MMP3, r

42 r epithelial cell differentiation, excessive collagen I and elastin deposition, and hypercellularity

43 olithographic 3D printing, and the effect of collagen I and fibrin extracellular matrix proteins and

44 onectin-deficiency reduced the expression of collagen I and fibronectin.

45 eta1/Smad2/3 inhibitor, eliminated excessive collagen I and III accumulation induced by AAT1 knockdow

46 downregulation of alpha-smooth muscle actin, collagen I and III and decreased migration and different

47 but AAT1 knockdown mimicked the increase in collagen I and III expression, TGF- beta1 expression and

48 AAT1 overexpression blocked the increase in collagen I and III expression, transforming growth facto

49 downregulated SO2/AAT1 pathway and increased collagen I and III protein expression.

50 udy sought to determine if serum markers for collagen I and III synthesis, the carboxyl terminal pept

51 ctivated receptor-gamma 1-alpha (PGC1alpha), collagen I and III transcription, and thyroxine decrease

52 on of alpha-smooth muscle actin (alpha-SMA), collagen I and III was significantly higher in the heart

53 ith a downregulation in collagen production (collagen I and III), collagen processing, cleavage, cros

54 histochemistry markers were used to identify collagen I and III, lymphocytes (CD45), proliferation (K

55 IL-6, TGF-beta) and excessive production of collagen I and III.

56 Histologic analyses of four matrix proteins-collagen I and IV, laminin, and fibronectin-in skin biop

57 tro, LA under TGFbeta1 stimulation increased collagen I and lysyl oxidase (LOX), the enzyme that cros

58 matrix and vascular proteins in addition to collagen I and osteocalcin.

59 s with periostin increased the expression of collagen I and stimulated the phosphorylation of FAK, p3

60 nt protein-1, alpha-smooth muscle actin, and collagen I and TIMP1 expression.

61 remodeling, by reducing the stiffer cardiac collagen I and titin n2b expression in the left ventricl

62 qRT-PCR data showed low levels of collagen I and V, as well as keratocan for HKCs, indicat

63 on of miR-199a-3p increased TGFbeta1-induced collagen I and vimentin expression and restored SOCS7 ex

64 reatment induced fibrotic changes, including collagen I and vimentin expression, being associated wit

65 of E-cadherin and zona occludens-1, whereas collagen-I and alpha-smooth muscle actin were increased

66 d murine FL-fibroblasts was reduced, whereas collagen-I and alpha-smooth muscle actin were markedly e

67 n of basal PAI-1 in NL-fibroblasts increased collagen-I and alpha-smooth muscle actin.

68 Collagen-I and alphaSMA(+) fibroblasts do not correlate

69 (Ad-PAI-1) suppressed expression of uPA and collagen-I and attenuated proliferation in FL-fibroblast

70 CV) cirrhotic patients showed coinduction of Collagen-I and cleaved OPN compared to healthy individua

71 tein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation.

72 ce without lung injury also showed increased collagen-I and uPA.

73 linking sites and the MMP-1 cleavage site in collagens I and II.

74 beta1, transforming growth factor-beta2, and collagens I and III in both keloid and normal skin fibro

75 a substrate preference for collagen II over collagens I and III.

76 ession of miR-29 repressed the expression of collagens I and IV at both the mRNA and protein levels b

77 ssion of connective tissue growth factor and collagens I and IV.

78 ofibrotic mediators and effectors, including collagens I and V and alpha-smooth muscle actin, on the

79 ) and minor enrichment of laminin-gamma1 and collagens I and VI.

80 led to increased expression of fibronectin, collagen I, and alpha-smooth muscle actin in the TM in m

81 were identified by their expression of CD45, collagen I, and alpha-smooth muscle actin using flow cyt

82 th high affinity to immobilized fibronectin, collagen I, and collagen V.

83 lpha-actin fiber formation, up-regulation of collagen I, and down-regulation of collagen III.

84 arameters (transforming growth factor-beta1, collagen I, and fibronectin) were increased at baseline.

85 ification showed a dominance of collagen IV, collagen I, and laminin isoforms in the glomerular ECM t

86 e also decreased mRNA expression of osterix, collagen I, and osteocalcin by mesenchymal stem cells at

87 tion rate; decreased expressions of osterix, collagen I, and osteocalcin; but increased trabecular se

88 actor-beta-mediated profibrotic fibronectin, collagen I, and proinflammatory interleukin-6.

89 Cells were seeded onto collagen I, and subsequently treated with differentiatio

90 scle actin, connective tissue growth factor, collagen I, and TGF-beta; and reduced renal macrophage i

91 ctivation and the expression of miR-199a-3p, collagen I, and vimentin during TGF-beta1 treatment.

92 ls to the adhesive ECM proteins fibronectin, collagen-I, and laminin, known to interact with it.

93 eased alpha smooth muscle actin (alpha-SMA), collagen-I, and transforming growth factor beta messenge

94 These collagenases cleave DDR1 and attenuate collagen I- and IV-induced receptor phosphorylation.

95 eases following mesangial cell attachment to collagen I, associated with increased collagen I express

96 s compared with MMP-1, GVSK degraded soluble collagen I at the high but not the low Ca(2+) concentrat

97 he cell surface, and its ectodomain displays collagen I binding with an affinity similar to that of t

98 pressing cells did not demonstrate increased collagen I binding, collagen I-driven motility, or alpha

99 Fibromodulin bound to collagen I, but the binding did not prevent collagen I d

100 characterize the cleavage of heterotrimeric collagen I by both the human collagenase matrix metallop

101 We quantified production of fibronectin and collagen I by HEF and HEMC in response to eosinophil pro

102 s the deposition of matrix proteins, such as collagen I, by hepatic stellate cells (HSCs) that culmin

103 ned by using flow cytometric coexpression of collagen I, CD45, and CD34 or EGFR or a disintegrin and

104 A3 provides direct structural constraints on collagen I chain registry.

105 AIR-1, a novel immunoinhibitory receptor for collagen, is closely associated with some autoimmune dis

106 n umbilical vein endothelial cells plated on collagen I-coated plates and cultured in the confluent s

107 Here, we show that stromal collagen I (Col-I) fibers in the mammary fat pad are axi

108 Using a three-dimensional collagen-I (Col-1) gel assay that simulates epithelial i

109 interacted with three different substrates: collagen-I (Col-I), bovine serum albumin, and a monolaye

110 Collagen I (COL1A1), collagen III (COL3A1), hyaluronan s

111 of pancreatic adenocarcinoma cells through a collagen I (COLI) matrix.

112 ment of alpha2beta1 integrin with its ligand collagen I (ColI), reduces doxorubicin-induced apoptosis

113 lular matrix by decreasing the expression of collagen I, collagen III, and fibronectin mRNA and prote

114 ys consisting of 32 distinct combinations of collagen I, collagen III, collagen IV, fibronectin, and

115 ific extracellular matrix proteins-including collagen I, collagen IV, and laminin V-to modulate inter

116 We found that in vivo ITF2357 decreased collagen I, collagen IV, fibronectin, integrin alphaVbet

117 b(-/-) mice revealed lower amounts of mature collagen I compared with WT mice and exhibited significa

118 The ectodomain of this collagen is constitutively shed from the cell surface by

119 ionally towards blood vessels on fibronectin-collagen I-containing extracellular matrix (ECM) fibers

120 the tumor interstitial matrix by decreasing collagen I content.

121 etermination of amino-terminal propeptide of collagen I content.

122 erefore, the ability to monitor the state of collagen is crucial for determining the presence and pro

123 re isolated, and fibrocytes expressing CD45, collagen I, CTGF, ETAR, or alpha-SMA were identified by

124 loxP-mediated vinculin gene disruption in 3D collagen I cultures.

125 45(+) CD4(+) IL-17(+) cells, CD45(+) CD34(+) collagen I(+) CXCR4(+) fibrocytes, and HSP47(+) activate

126 n of HE4-neutralizing antibodies accelerated collagen I degradation and inhibited fibrosis in three d

127 collagen I, but the binding did not prevent collagen I degradation by matrix metalloproteinase 13.

128 ckdown of cathepsin B in tumor cells reduced collagen I degradation in vitro and bone metastasis in v

129 vs 2.45 [0.36], p<0.0001) indicating greater collagen I degradation.

130 thermore, TIMP3 modulates sDLK1 shedding and collagen I degradation.

131 down-regulation of ACTN4 by shRNA induces a collagen I-dependent amoeboidal-to-mesenchymal transitio

132 uding glomerulosclerosis, where it increases collagen I deposition in vivo and promotes mesangial cel

133 e healing tendon tissues by promoting better collagen I deposition, decreased cellularity, less vascu

134 tic fibromodulin activates HSCs and promotes collagen I deposition, which leads to liver fibrosis in

135 ctin expression, and a 2.4-fold reduction in collagen I deposition.

136 pathogenesis of liver fibrosis is fibrillar Collagen-I deposition; yet, mediators that could be key

137 However, their implementation into synthetic collagen is difficult and requires the replacement of th

138 ot demonstrate increased collagen I binding, collagen I-driven motility, or alpha2beta1-integrin expr

139 dentified five glycosylation sites in type I collagen (i.e. alpha1,2-87, alpha1,2-174, and alpha2-219

140 e of markers of fibroblast-like cells (e.g., collagen I, ecto-5'-nucleotidase, and PDGF receptor-beta

141 The medial collagen is engaged throughout the stretching process, a

142 cell-matrix adhesion by showing that type IV collagen is essential for inter-adipocyte adhesion in th

143 erance toward autologous intact alpha345(IV) collagen is established in hosts expressing this Ag, eve

144 sults demonstrate that the A1 site in type I collagen is exclusively 3-hydroxylated by P3H1, and pres

145 th a conditional knockout (CKO) of Notch1 in collagen I-expressing (mesenchymal) cells on treatment w

146 reased myofibroblast activation (P=0.01) and collagen I expression (P=0.04), compared with wild type

147 ent to collagen I, associated with increased collagen I expression and increased susceptibility to ap

148 r transforming growth factor beta(1)-induced collagen I expression but inhibited expression of alpha-

149 way was identified as an important driver of collagen I expression in Fib-MCs in experiments utilizin

150 trongly inhibited 4E-BP1 phosphorylation and collagen I expression in Fib-MCs.

151 TGFbeta3-microS yielded significantly higher collagen I expression in the AP bands compared with the

152 myofibroblasts and significantly diminished collagen I expression relative to those from control mic

153 and mTORC2 signaling and leads to increased collagen I expression via the mTORC1-dependent 4E-BP1/eI

154 on systemic sclerosis and is known to induce collagen I expression, but the mechanism(s) behind this

155 actin (alpha-SMA), desmin, fibronectin, and collagen I expression, suggesting that Shh signaling pro

156 HSCs and their alpha-smooth muscle actin and collagen I expression, thus increasing tumor fibrosis.

157 H cellular signaling pathway and mouse/human collagen I expression.

158 reased mTORC1 signaling was shown to augment collagen I expression.

159 ulating the HSC pro-fibrogenic phenotype and Collagen-I expression.

160 chanical strain sensors and demonstrate that collagen I fibres preferentially co-localize with more-r

161 nct tissue-specific effect of collagen VI on collagen I fibrillogenesis.

162 In the skin, collagen I fibrils are the major structural component of

163 We previously found that collagen I fibrils induced the formation of peculiar lin

164 its function in cartilage ECM, by organizing collagen I fibrils into a suprastructure, mainly in the

165 lass transition temperature, we propose that collagen I fibrils may be in a glassy state while hydrat

166 ed and characterized the function of CD45(+)/collagen I(+) fibrocytes in acutely injured skeletal mus

167 enafil substantially blocked the increase in collagen I, fibronectin 1, TGFbeta, and CTGF mRNA in Ctr

168 l remodeling, including vimentin, TGF-beta1, collagen I, fibronectin, and matrix metalloproteases, an

169 to RELM-beta increased TGF-beta1, TGF-beta2, collagen I, fibronectin, smooth muscle alpha-actin, lami

170 unostaining of tumor-xenograft sections with collagen-I, fibronectin (major extracellular-matrix prot

171 A 5-fold increase in collagen I fibrosis is detected in the remote surviving

172 emonstrate a step-by-step process to isolate collagen I from commercially available animal byproducts

173 the ones expressing the scrambled shRNA on a collagen I gel (two-dimensional) although these two cell

174 estores the amoeboidal morphology and limits collagen I gel compaction.

175 n of WM1158 cells into the three-dimensional collagen I gel, a representative of the dermis.

176 n and growth/survival in a three-dimensional collagen I gel.

177 cue the amoeboidal morphology and to compact collagen I gel.

178 we validate the utility of DS-OCT using pure collagen I gels and 3D mammary fibroblast cultures seede

179 l, 1.0 mg/ml, and 2.0 mg/ml acid-solubilized collagen I gels forming at 27 degrees C, 32 degrees C, a

180 al ovarian cancer cells on three-dimensional collagen I gels led to a dramatic down-regulation of the

181 Interestingly, in three-dimensional collagen I gels, ACTN4 KD cells are more polarized compa

182 an alignment of these fossil sequences with collagen (I) gene transcripts from available mammalian g

183 st often caused by dominant mutations in the collagen I genes COL1A1/COL1A2, whereas rarer recessive

184 This is the first time that crosslinking of collagen I has been shown to enhance metastatic growth.

185 Although type IV collagen is heavily glycosylated, the influence of this

186 Collagen is highly valued both as a food additive and a

187 The mechanical strength of fibrillar collagens is highly dependent on the formation of covale

188 Here, we combine the usefulness of a collagen I hydrogel membrane with entrapped ribonuclease

189 isting of cancer cells cultured within dense collagen I hydrogels, which have been shown to acquire p

190 Positive staining of elastin, collagen I, III and IV, decorin, versican, fibronectin,

191 Expression of collagen I, III, and IV (COL1A1, COL3A1, COL4A1) transcr

192 was more severe with increased deposition of collagen I, III, and IV.

193 A messenger ribonucleic acid transcripts for collagen I, III, transforming growth factor, and angiote

194 rity of RV dysfunction, whereas the ratio of collagen I/III expression was only elevated in severe RV

195 Therefore, aggravation of the collagen I/III ratio and cardiac stiffening by excess n-

196 Excess dietary LA increased the collagen I/III ratio in the mouse myocardium, leading to

197 a, metalloproteinase-2, metalloproteinase-9, collagen I/III, and reduced connexin 43 phosphorylation

198 and Fast Green and analyzed to determine the collagen I:III ratio.

199 agen IV in the basal lamina and of fibrillar collagen I in the adjacent interstitium in the dual infe

200 ene (PKCdelta KO) show a marked reduction of collagen I in the arterial wall.

201 y; indeed, apigenin dose-dependently reduced collagen I in the human HSC line, TWNT-4.

202 owed double the amino-terminal propeptide of collagen I in their blood, indicating increased collagen

203 xhibit enhanced secretion of fibronectin and collagen I, increased migratory/invasive abilities, and

204 Asn(260), Asn(371), and Asn(394)), result in collagen I-independent constitutive phosphorylation.

205 ion of primary HSCs with an Ad-OPN increased Collagen-I, indicating correlation between both proteins

206 Importantly, collagen I induced a similar initial response of protrus

207 We found that fibrillar collagen I induced linear F-actin structures, distribute

208 often caused by mutations in genes encoding collagen I-interacting proteins.

209 strate that upon miR-200 loss integrin beta1-collagen I interactions drive 3D in vitro migration/inva

210 Interestingly, deposition of collagen I is observed only under 5% O(2) tension.

211 the MMP-1 recognition site in heterotrimeric collagen I is partially unwound at equilibrium.

212 MMP-9, and MMP-13, whereas non-cross-linked collagen I, IV, and natively glycosylated SLRPs are susc

213 In this murine model, deficiency of collagen I leads to a myocardial wound-healing defect.

214 Mesangial cell attachment to collagen I led to increased Hic-5 expression within 2-4

215 expression in mesangial cells by adhesion to collagen I led to TGF-beta expression, which was abolish

216 observe that the cleavage of heterotrimeric collagen is less force sensitive than the proteolysis of

217 ated albumin-induced increases in TIMP-1 and collagen-I levels.

218 In vitro, collagen I limited the lipolytic flux between acinar cel

219 nal breast cancer cells in three-dimensional collagen I matrices in vitro.

220 e membranes by dedifferentiated RPE cells on collagen I matrices.

221 Collagen I matrix assembly in vivo requires active fibro

222 nd striking rearrangement of the surrounding collagen I matrix.

223 In an unnatural collagen I microenvironment, ARF6-depleted, inverted epi

224 Moreover, the unsecreted collagen I molecules accumulate in large perinuclear pun

225 ult, rounded-amoeboid melanoma cells degrade collagen I more efficiently than elongated-mesenchymal c

226 Less collagen I mRNA within the infarct area was found in OIM

227 including fibrotic disease states with high collagen, is now utilizing 'omics data sets and is revea

228 OPN induction of Collagen-I occurred via integrin alpha(v)beta(3) engagem

229 peptide analog of the cell-binding domain of collagen I, on the in vitro progression of osteogenic ce

230 igating the functional relationships between collagen I organization and invadosome induction.

231 magnification electron microscopy shows that collagen is organized into perimysial cables which incre

232 esis, the carboxyl terminal peptide from pro-collagen I (PICP) and the amino terminal peptide from pr

233 Collagen I-positive cells (89.43% +/- 6.53%) in day 28 a

234 Collagen is post-translationally modified by prolyl and

235 stress of the collagen fibrils, whereas the collagen is predominantly responsible for the material's

236 al-to-mesenchymal transition and intensified collagen I production and MUC5AC expression.

237 Increased TGF-beta1 and TGF-beta1-dependent Collagen I production in intestinal mesenchymal cells re

238 ous vacuoles in the cytoplasm, a decrease in collagen I production, and augmented LC3 II expression.

239 assay (LDH), electronic microscopy analysis, collagen I production, flow cytometry lysosome compartme

240 ECM protein network driving the increase in Collagen-I protein contributing to scarring and liver fi

241 Recombinant OPN (rOPN) up-regulated Collagen-I protein in primary HSCs in a transforming gro

242 tor is stimulated with collagenase-resistant collagen I (r/r) or with a triple-helical peptide harbor

243 fe for three different tryptic peptides from collagen (I) ranged from 2000 to 6000 s under high tempe

244 y, we show that mutant DDR1 that cannot bind collagen is recruited into DDR1 signalling clusters.

245 ies, where a polymer matrix of nanofibrillar collagen is reinforced by apatite mineral crystals.

246 on and secondary accumulation of MSC-derived collagen is responsible for hematopoietic failure in aut

247 Fibre stretch-assay studies reveal that collagen I's Fn-binding domain is responsible for the me

248 method to manufacture unidirectional laminar collagen I scaffolds.

249 role for TANGO1 and the UPR in facilitating collagen I secretion and fibrogenesis.

250 our data demonstrate that PKCdelta mediates collagen I secretion from SMCs, likely through a Cdc42-d

251 ssion partially rescues Cdc42 expression and collagen I secretion in PKCdelta KO SMCs.

252 Depletion of TANGO1 in HSCs blocked collagen I secretion without affecting other matrix prot

253 Associated with diminished collagen I secretion, PKCdelta KO SMCs exhibit a signifi

254 Cdc42 expression in PKCdelta KO SMCs enables collagen I secretion.

255 r secramine A in PKCdelta WT SMCs eliminates collagen I secretion.

256 ion 1 (TANGO1) as a potential participant in collagen I secretion.

257 Although both groups showed high collagen I staining, content of collagen I was significa

258 express DDR1 and that short-term exposure to collagen is sufficient to activate DDR1 in Hodgkin lymph

259 breast cancer cells readily transfer to new collagen I surfaces, and away from basement membrane pro

260 icate that calpain mediates cytokine-induced collagen-I synthesis and proliferation of ASMCs via the

261 ted cytokine-induced phosphorylation of Akt, collagen-I synthesis, and cell proliferation of ASMCs an

262 Collagen-I synthesis, cell proliferation, and phosphoryl

263 nd serum from patients with asthma increased collagen-I synthesis, cell proliferation, and phosphoryl

264 s occurs in Col-r/r mice that have a mutated collagen-I that is uncleavable by MMPs.

265 (ECM) is comprised of biopolymers, primarily collagen I, that are created and maintained by stromal f

266 Collagen is the fundamental structural component of a wi

267 Collagen is the main structural and load-bearing element

268 Fibrillar type I collagen is the major organic component in bone, providi

269 iculum (rER), and the triple-helical protein collagen is the most abundant extracellular matrix compo

270 Collagen is the most abundant protein family in mammals.

271 Collagen is the most abundant protein in animals and is

272 Collagen is the most abundant protein in the extracellul

273 Type I collagen is the most abundant protein in the human body

274 Type I fibrillar collagen is the most abundant protein in the human body,

275 Collagen is the most prevalent component of the extracel

276 Type I collagen is the predominant collagen in mature tendons a

277 alpha2beta1 integrin, the receptor of type I collagen, is the major collagen-binding integrin express

278 We tested the hypothesis that collagen I, the main constituent of the extracellular ma

279 In vivo, collagen I, the major structural protein in human body,

280 MCs to increase secretion of fibronectin and collagen I; this was inhibited by blocking transforming

281 ons of alpha smooth muscle actin (alphaSMA), collagen I, tissue inhibitor of metalloproteinase-1 (TIM

282 reduced collagen III levels and the ratio of Collagen I to Collagen III.

283 els to model the normal microenvironment and collagen I to model the stromal ECM.

284 the ubiquitous interstitial matrix component collagen I to undergo metastatic reactivation in multipl

285 into microfluidic devices and modified with collagen (I) to promote hepatocyte adhesion.

286 ncreased adhesion and aggregate formation on collagen I under flow, and accelerated clot retraction a

287 The amino acid composition of collagen is unique due to its high (33%) glycine content

288 conclude that in atherosclerosis, type VIII collagen is up-regulated in the absence of ApoE and func

289 Type VIII collagen, a short-chain collagen, is up-regulated in atherosclerosis; however, l

290 disassembly of fibrils formed from purified collagen I using turbimetry, probe the fibril morphology

291 A recombinant bacterial collagen is utilized to characterize the sequence requir

292 play cell surface alpha smooth muscle actin, collagen I/V, and mediate angiogenesis.

293 showed high collagen I staining, content of collagen I was significantly higher in PRP-treated tendo

294 The ratio of collagen III to collagen I was significantly lower in PRP samples (p=0.0

295 of alpha-smooth muscle actin (alpha-SMA) and Collagen I were reduced as was the activity of matrix me

296 In vivo, MMP-1 and GVSK degraded collagen I when perfused in Zucker rat ventral skin and

297 iorycteropus, obtained from the bone protein collagen (I), which places the 'Malagasy aardvark' as mo

298 inhibitor of metalloproteinase (TIMP)-1 and collagen-I, which were blocked by HIF-1alpha shRNA.

299 Here, we show that copolymerization of collagen I with polyacrylamide produces minimal matrix m

300 terial smooth muscle cells (SMCs) to secrete collagen I without significantly altering the intracellu