ライフサイエンスコーパス: SAA

1 SAA added to POBs inhibited PTH-stimulated cAMP response

2 SAA has been detected within atherosclerotic lesions and

3 SAA increased IOP by approximately 40% (P < 0.05) in the

4 SAA instillation into the lungs elicits robust TLR2-, My

5 SAA intake was lower in RTRs compared with controls and

6 SAA is a protein precursor of reactive AA amyloidosis, t

7 SAA is normally associated with the high-density lipopro

8 SAA mRNA expression was positively associated with tissu

9 SAA predominately promoted expression of the TH17 polari

10 SAA promotes expression of IL-17A in gammadelta T cells

11 SAA proteins stimulated the transcription of RANTES (reg

12 SAA stimulation led to increased phosphorylation of MAPK

13 SAA supplementation, mTORC1 activation, or chemical/gene

14 SAA was rapidly incorporated into amyloid, acutely reduc

15 SAA, but not CRP, increased proteoglycan sulfate incorpo

16 SAA-1 not only induced anti-inflammatory interleukin 10

17 SAA-enriched HDL colocalized with cell surface-associate

18 SAA-induced cell activation was inhibited by a CD36 pept

19 SAA-induced inflammation was markedly reduced by a neutr

20 SAA-mediated effects were thermolabile, inhibitable by a

21 We now show that systemic serum amyloid A 1 (SAA-1) controls the plasticity of neutrophil differentia

22 Elevated levels of IL-1beta, SAA, and IL-17 are present in subjects with severe aller

23 The uptake of Alexa Fluor 488 SAA as well as of other well established CD36 ligands wa

24 Median serum concentrations of IL-6, SAA, ICAM-1, E-selectin, TNFalpha, and MPO and periphera

25 Here, we report long-term follow-up on 67 SAA patients (44 treatment-naive and 23 refractory) trea

26 The atomic ratio Pt:Cu = 1:125 yielded a SAA which exhibited excellent CO tolerance in H2 activat

27 The fibrillation of Serum Amyloid A (SAA) - a major acute phase protein - is believed to play

28 Serum amyloid A (SAA) 1 and 2 are produced predominantly by the liver and

29 ute-phase response proteins serum amyloid A (SAA) 1 and SAA3 are transcriptional targets of S100A4 vi

30 of the acute phase protein serum amyloid A (SAA) 1.

31 Inflammatory markers serum amyloid A (SAA) and C-reactive protein (CRP) are predictive of card

32 y C-reactive protein (CRP), serum amyloid A (SAA) and haptoglobin (Hpt) were analysed as inflammatory

33 -reactive protein (CRP) and serum amyloid A (SAA) are measures of low-grade chronic inflammation and

34 -associated genes Fizz1 and serum amyloid A (SAA) are significantly up-regulated in M2 macrophages st

35 Here, we identify serum amyloid A (SAA) as a candidate mediator of GC refractory inflammati

36 leads to overproduction of serum amyloid A (SAA) by the liver.

37 Since serum amyloid A (SAA) concentrations in HDL increase with inflammation, w

38 use AngII increases hepatic serum amyloid A (SAA) expression in an IL-6-dependent manner, we treated

39 The fibrillar deposition of serum amyloid A (SAA) has been linked to the disease amyloid A (AA) amylo

40 The acute phase protein serum amyloid A (SAA) has been well characterized as an indicator of infl

41 Serum amyloid A (SAA) is a family of acute-phase proteins which are shown

42 Serum amyloid A (SAA) is a major acute phase protein involved in multiple

43 Serum amyloid A (SAA) is an acute-phase plasma protein that functions in

44 Serum amyloid A (SAA) is best known for being the main component of amylo

45 The acute-phase protein serum amyloid A (SAA) is commonly considered a marker for inflammatory di

46 Serum amyloid A (SAA) is expressed locally in chronic inflammatory condit

47 The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wh

48 Serum amyloid A (SAA) is one such marker but its function remains unclear

49 ced histological damage and serum amyloid A (SAA) levels in IL-10(-/-) colitis mice, was efficacious

50 Serum amyloid A (SAA) promotes neutrophilic inflammation by its interacti

51 Serum amyloid A (SAA) proteins are strongly induced in the liver by syste

52 Serum amyloid A (SAA) represents an evolutionarily conserved family of in

53 SP-B), apolipoprotein C-II, serum amyloid A (SAA), and alpha-1-microglobulin/bikunin precursor.

54 g C-reactive protein (CRP), serum amyloid A (SAA), and S100 calcium-binding protein A12 (S100A12).

55 , C-reactive protein (CRP), serum amyloid A (SAA), intercellular adhesion molecule-1 (sICAM-1) and va

56 -reactive protein (hs-CRP), serum amyloid A (SAA), interleukin-6 (IL-6), leukocyte, and neutrophil le

57 Concentrations of HDL-bound serum amyloid A (SAA), lipopolysaccharide binding protein (LBP), apolipop

58 production by adipocytes of serum amyloid A (SAA), monocyte chemoattractant protein (MCP)-1, and hyal

59 SFB cause an increase in serum amyloid A (SAA), suggesting that SAA might mediate SFB's effects on

60 -reactive protein (CRP) and serum amyloid A (SAA), the prototype acute-phase response proteins, in th

61 of the acute-phase reactant serum amyloid A (SAA).

62 of the acute-phase protein, serum amyloid A (SAA).

63 ury score (HIS), and plasma serum amyloid A (SAA).

64 and C-reactive protein and serum amyloid A [SAA] levels).

65 C-reactive protein [hsCRP], serum amyloid A [SAA], and IL-6) were determined at 3, 6, 9, 12, and 24 m

66 is factor alpha [TNFalpha], serum amyloid A [SAA], vascular endothelial growth factor, neutrophil cou

67 ], haptoglobin, and serum amyloid protein A [SAA]), inflammatory markers (matrix metalloproteinase 1

68 A-SAA in blood correlated with total leukocytes, macrophag

69 A-SAA mRNA and protein were increased in the liver.

70 The acute-phase protein serum amyloid A (A-SAA) was significantly increased by 24 h, whereas C-reac

71 Serum amyloid A (A-SAA/Saa3) was shown before to affect osteoblastic metabo

72 Finally, A-SAA protein, but not mRNA, was increased in the CNS 24 h

73 We found that both isoforms of A-SAA completely crossed the intact blood-brain barrier, a

74 ammation in our O3 exposure model and that A-SAA could be an important systemic signal of O3 exposure

75 Our findings suggest that A-SAA is functionally linked to pulmonary inflammation in

76 on and distal systemic acquired acclimation (SAA).

77 tress (termed systemic acquired acclimation [SAA]).

78 ncreased cellular triglyceride accumulation, SAA, and MCP-1 expression; generated reactive oxygen spe

79 resistance, we found that sulfur amino acid (SAA) restriction increased expression of the transsulfur

80 mounts of acid-producing sulfur amino acids (SAA) and examined how this adaption requires the RhCG am

81 nd product of sulfur-containing amino acids (SAAs), contributes to metabolic acid load and may advers

82 To determine its direct actions, SAA was administered into murine lung, leading to induct

83 nosensitive single-unit afferent activities (SAAs) in rats with a bladder outlet obstruction (BOO) an

84 In addition, SAA-induced secretion of G-CSF was sensitive to heat and

85 d protein were significantly increased after SAA stimulation.

86 tients with COPD and in vivo using an airway SAA challenge model in BALB/c mice.

87 entity among different SAA isoforms, not all SAA proteins are pathogenic.

88 e we demonstrate that the single-atom alloy (SAA) strategy applied to Pt reduces the binding strength

89 Although SAA is thought to play a key role in plant survival duri

90 inus of SAA, which is highly conserved among SAA sequences in all vertebrates, might play important s

91 s rarely involves the heart, but amyloidotic SAA transgenic mice consistently had minor cardiac amylo

92 lantation (HSCT) in severe aplastic anaemia (SAA) have improved steadily over the past decades, large

93 Targeting the high levels of IL-6 and SAA in catabolic disorders might be a therapeutic approa

94 els of AngII: Hepatic production of IL-6 and SAA increases, and these mediators act synergistically t

95 Both IL-6 and SAA levels rose significantly in ApoE(-/-) BL/6 mice com

96 CD36 is a receptor mediating SAA binding and SAA-induced pro-inflammatory cytokine secretion predomin

97 Circulating concentrations of CRP and SAA in patients with a range of early to late objective

98 e findings indicate that circulating CRP and SAA levels are highest when the concentration of spiroch

99 CRP and SAA levels were significantly elevated in early localize

100 At the end of part 2, median CRP and SAA values were normal (<10 mg per liter for both measur

101 Elevated CRP and SAA were also associated with reduced disease-free survi

102 Circulating concentrations of CRP and SAA were measured approximately 31 months after diagnosi

103 ch were accompanied by reductions in CRP and SAA, continued over the treatment duration.

104 of the acute-phase reactants ESR, hsCRP, and SAA were lower at the higher doses; the difference was s

105 Markers of inflammation (ESR, hsCRP, and SAA) showed statistically significant reductions (P < 0.

106 hermore, coordinate expression of S100A4 and SAA in tumor samples from colorectal carcinoma patients

107 transplantation for severe aplastic anemia (SAA) has improved, with survival rates now approximately

108 Survival in severe aplastic anemia (SAA) has markedly improved in the past 4 decades because

109 Severe aplastic anemia (SAA) is a life-threatening bone marrow failure disorder

110 Acquired severe aplastic anemia (SAA) is a rare hematologic disease associated with signi

111 irst-line therapy of severe aplastic anemia (SAA) with high-dose cyclophosphamide causes toxicity and

112 ing hematopoiesis in severe aplastic anemia (SAA).

113 in HSCT for acquired severe aplastic anemia (SAA).

114 Although splenic artery aneurysms (SAAs) are common, their giant forms (more than 10 cm in

115 fects were thermolabile, inhibitable by anti-SAA antibody, and also neutralized by association with h

116 proved small-angle scattering approximation (SAA) to radiative transfer for sub-diffusive light refle

117 ieu (IL-6) and acute phase reactants such as SAA may reflect alterations in the Th1/Th2 balance.

118 "Surface-associated astrocytes" (SAAs) in posterior piriform cortex (PPC) are unique by v

119 hese data suggest that during atherogenesis, SAA can amplify the involvement of smooth muscle cells i

120 Because SAA-1-producing melanomas promoted differentiation of IL

121 The relationship between SAA and neutrophils was investigated in lung sections fr

122 alizing antibody to IL-17A was used to block SAA responses in vivo, and a cell-sorting strategy was u

123 During acute exacerbation, peripheral blood SAA levels increased dramatically and were disproportion

124 e SAAs of Adelta-fibers were attenuated, but SAAs of both Adelta- and C-fibers were intermittently en

125 Cellular sources of IL-17A induced by SAA include CD4(+) T cells, gammadelta T cells, and an E

126 CONCLUSION Circulating SAA and CRP may be important prognostic markers for long

127 Most circulating SAA is protected from proteolysis and misfolding by bind

128 d into amyloid, acutely reducing circulating SAA concentrations by up to 90%.

129 deposition is determined by the circulating SAA concentration.

130 In contrast, SAAs of C-fibers were not significantly different betwee

131 peared-because the stressors heightened CRP, SAA, sICAM-1 and sVCAM-1 responses to the sunflower oil

132 oss reduced inflammatory biomarkers (hs-CRP, SAA, and IL-6) compared with controls.

133 ion and NFkappaB translocation and decreased SAA and MCP-1 expression and monocyte chemotaxis.

134 Immunohistochemistry detected SAA was in close proximity to airway epithelium, and in

135 e the high sequence identity among different SAA isoforms, not all SAA proteins are pathogenic.

136 This study reports that HS dissociates SAA from HDLs isolated from inflamed mouse plasma.

137 n of Jmjd3 H3K27 demethylase activity during SAA treatment or blockade of granulocyte-macrophage colo

138 oth muscle cells were stimulated with either SAA or CRP (1 to 100 mg/L) and proteoglycans were then i

139 Results Elevated SAA and CRP were associated with reduced overall surviva

140 flammation, we investigated whether elevated SAA is a causal factor in HDL dysfunction.

141 which secreted IL-22 that induced epithelial SAA production in a Stat3-dependent manner.

142 Mice that received adenovirus expressing SAA had increased TGF-beta concentrations in plasma and

143 Extrahepatic SAA was detected locally in COPD bronchoalveolar lavage

144 Diet was assessed for SAA content and various risk factors were measured.

145 The HRs for SAA and CRP tertiles suggested a threshold effect on sur

146 29 microg/ml LDL versus 90 microg/ml LDL for SAA versus control proteoglycans; P < 0.005).

147 show that TLR2 is a functional receptor for SAA.

148 use of an alemtuzumab-based HSCT regimen for SAA results in durable engraftment with a low incidence

149 These results suggest a potential role for SAA in inflammatory diseases through activation of TLR2.

150 nor (MSD) HSCT remains the gold standard for SAA patients younger than 40-50 years, with HLA-matched

151 outcomes of PBPC and BM transplantation for SAA.

152 ed in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of poly

153 Furthermore, SAA can be found in association with apoB-containing lip

154 Furthermore, SAA drives production of IL-1alpha, IL-1beta, IL-6, IL-2

155 Furthermore, SAA levels in ESRD-HDL inversely correlated with its ant

156 Furthermore, SAA up-regulated biglycan via the induction of endogenou

157 Furthermore, SAA-differentiated macrophages stimulated with lipopolys

158 year-old male patient with symptomatic giant SAA (13 cm) was urgently admitted to our hospital for th

159 an be an efficient method to treat the giant SAA.

160 se of this method of treatment of true giant SAA.

161 neously binds to two apolipoproteins of HDL, SAA and ApoA-I, and thereby induce SAA dissociation.

162 injected with an adenovirus expressing human SAA-1, a null virus, or saline.

163 ion of a disease-associated isoform of human SAA - human SAA1.1 (hSAA1.1) - using techniques ranging

164 Here we show that mouse and human SAAs are retinol binding proteins.

165 Mouse and human SAAs bound retinol with nanomolar affinity, were associa

166 Taken together, these findings identify SAA as a therapeutic target for inhibition and implicate

167 Our results thus identify SAAs as a family of microbe-inducible retinol binding pr

168 TSP4, TIMP-2, SEPR, MRC-2, Antithrombin III, SAA, CRP, NPS-PLA2, LEAP-1, and LBP.

169 rapeutic target for inhibition and implicate SAA as a mediator of GC-resistant lung inflammation that

170 anti-CD52 mAb alemtuzumab might be active in SAA because of its lymphocytotoxic properties.

171 Although cyclophosphamide has activity in SAA, its toxicity is not justified when far less dangero

172 We conclude that alemtuzumab is effective in SAA, but best results are obtained in the relapsed and r

173 that HDL from HD+ patients were enriched in SAA but had lower levels of sialylation across glycoprot

174 HDL from HD patients were enriched in SAA, LBP, ApoC-III, di-sialylated ApoC-III (ApoC-III2) a

175 nd apex of the hexamer, that are involved in SAA association with heparin.

176 nderstanding of the role HSCT has to play in SAA with particular emphasis on alternative donor source

177 Diets rich in SAA stimulated expression of enzymes and transporters in

178 ource for unrelated donor transplantation in SAA.

179 ocalized with SAA and GCs markedly increased SAA in vitro (THP-1, pEC(50) 43 nM).

180 age, tumor stage, race, and body mass index (SAA P trend < .0001; CRP P trend = .002).

181 s of HDL, SAA and ApoA-I, and thereby induce SAA dissociation.

182 Of particular interest, SAAs lack the domain organization observed in neocortex

183 Interestingly, SAA activated smooth muscle cell IL-1beta mRNA expressio

184 wer Th17 and Treg proportions and intestinal SAA expression than in controls, suggesting key roles in

185 Intriguingly, SAA reverses T(reg) anergy via its interaction with mono

186 High level SAA expression induced amyloidosis in all mice after a s

187 imals receiving a high-protein diet with low SAA content, the kidney excreted alkaline urine, with lo

188 higher number of microcontractions and lower SAAs of Adelta-fibers compared with those of the Sham gr

189 ladder filling, the bladder mechanosensitive SAAs of Adelta-fibers were attenuated, but SAAs of both

190 s indicate that CD36 is a receptor mediating SAA binding and SAA-induced pro-inflammatory cytokine se

191 functions as a novel SAA receptor mediating SAA proinflammatory activity.

192 Prolonged modest SAA overexpression occasionally produced amyloidosis aft

193 Moreover, SAA activated the inhibitor of NF-kappaB kinase (IKK) in

194 -free survival was 58% in 44 treatment-naive SAA patients.

195 ucture of SAA1.1, suggesting that the native SAA is nonpathogenic.

196 slowly regressed with restoration of normal SAA production after doxycycline withdrawal.

197 Levels of CRP, but not SAA, were also found to be significantly increased in pa

198 s B scavenger receptor, functions as a novel SAA receptor mediating SAA proinflammatory activity.

199 A pronounced reduction (up to 60-75%) of SAA-induced pro-inflammatory cytokine secretion was obse

200 eoglycans in the ECM restored the ability of SAA-containing HDL to inhibit palmitate-induced inflamma

201 ergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize m

202 The association of SAA with high density lipoprotein abrogated the SAA-indu

203 A chronically high plasma concentration of SAA results in the aggregation of amyloid into cross-bet

204 This effect of SAA is dependent on Toll-like receptor 2 (TLR2).

205 The effect of SAA on gene expression of cultured human TM cells was te

206 iting transcription eliminated the effect of SAA on sPLA(2) mRNA suggested that the increase was tran

207 ing that the induction is a direct effect of SAA.

208 r 25 mmol/l (high) glucose for evaluation of SAA, MCP-1, and HA regulation in vitro.

209 xycycline-inducible transgenic expression of SAA in mice, we show that AA amyloid deposition can occu

210 njected S100A4 protein induced expression of SAA proteins and cytokines in an organ-specific manner.

211 s in the oligomerization and fibrillation of SAA, we truncated the proline-rich final 13 residues of

212 omerization, misfolding, and fibrillation of SAA.

213 The biological functions of SAA in inflammation have not been fully defined, althoug

214 Conversely, incorporation of SAA into HDL preparations reduced antiinflammatory prope

215 ceptors and lead to allosteric inhibition of SAA-initiated epithelial responses (pA(2) 13 nM).

216 Levels of SAA, sTNF-R1, and sTNF-R2 were measured with enzyme-link

217 However, management of SAA patients remains challenging, both acutely in addres

218 ients with COPD and a chronic mouse model of SAA exposure.

219 understand the amyloid formation pathway of SAA, we characterized the oligomerization, misfolding, a

220 arison between the biophysical properties of SAA isoforms with distinct pathogenicities, and the resu

221 ent structural and biophysical properties of SAA.

222 l stability and resistance to proteolysis of SAA oligomers at pH 3.5-4.5 help them escape lysosomal d

223 Selective reduction of SAA-induced gene expression was observed in tlr2-/- mous

224 lipoprotein involves only the apex region of SAA and can be inhibited by heparin.

225 Reinduction of SAA overproduction revealed that, following amyloid regr

226 In this study, the role of SAA in regulating macrophage differentiation was investi

227 es suggest a novel anti-inflammatory role of SAA in the induction of a micro-environment that support

228 To determine the role of SAA on aortic smooth muscle cell gene expression, a prel

229 imental evidence supporting a causal role of SAA with atherosclerosis.

230 ature suggesting that localized synthesis of SAA within the vasculature, or adipose tissue, may play

231 leavage or removal of the C-terminal tail of SAA resulted in formation of various-sized structural ag

232 reas the importance of the amino terminus of SAA for fibril formation has been well documented, the i

233 results suggest that the carboxy terminus of SAA, which is highly conserved among SAA sequences in al

234 in crucial steps for successful treatment of SAA.

235 that the spatially distributed character of SAAs in PPC reflects and supports the spatially distribu

236 unique and functionally relevant features of SAAs in PPC of the rat were identified by light and elec

237 er, blocking IL-1 receptors had no effect on SAA-mediated activation of sPLA(2) expression.

238 ther apolipoproteins that bind to CD36, only SAA induced a 10-50-fold increase of interleukin-8 secre

239 tion of these uremia-specific proteins, only SAA mimicked ESRD-HDL by promoting inflammatory cytokine

240 Transient gut colonization with SFB or SAA administration alone transiently increased the H3K27

241 matory conditions associated with persistent SAA expression.

242 re any differences in colon length or plasma SAA.

243 s separable events, each sensitive to plasma SAA concentration.

244 d that, in addition to descending processes, SAAs give rise to an extensive matrix of "superficial pr

245 p them escape lysosomal degradation, promote SAA accumulation in lysosomes, and ultimately damage cel

246 ta (MIP-1beta), and serum amyloid A protein (SAA) during acute SIVmac251 infection, but not during SI

247 e protein (CRP) and serum amyloid A protein (SAA).

248 Serum AA protein (SAA), an acute phase plasma protein, is deposited extrac

249 etween ROS and abscisic acid regulates rapid SAA to heat stress in plants.

250 toll-like receptor-4 (TLR4) markedly reduced SAA and MCP-1 expression in response to palmitate but no

251 in treatment-naive, relapsed, and refractory SAA in 3 separate research protocols at the National Ins

252 Patients with refractory SAA fared less well after high-dose cyclophosphamide the

253 At 37 degrees C and inflammation-related SAA concentrations, SAA1.1 exhibits an oligomer-rich fib

254 In the acute-phase response SAA is synthesized by the liver and transported primaril

255 ults from a solid-phase binding assay showed SAA interaction with the ectodomain of TLR2.

256 ssociations were of borderline significance (SAA P trend = .04; CRP P trend = .07).

257 However, unbound soluble SAA is intrinsically disordered and is either rapidly de

258 connections have a role in spatial-temporal SAA induction.

259 component of both immediate and longer term SAA signaling responses.

260 onse relationship (highest v lowest tertile: SAA HR = 3.15; 95% CI, 1.73 to 5.65; CRP HR = 2.27; 95%

261 In this study, we demonstrate that SAA is a potent endogenous stimulator of granulocyte col

262 We further demonstrate that SAA is stress specific and that a temporal-spatial inter

263 Demonstrating that SAA increased expression of sPLA(2) heteronuclear RNA an

264 Here we provide unexpected evidences that SAA induces the proliferation of the tolerogenic subset

265 fined, although recent reports indicate that SAA induces proinflammatory cytokine expression.

266 Here, we report that SAA in plants requires at least two different signals: a

267 These data show that SAA proteins are effectors for the metastasis-promoting

268 In conclusion, our findings suggest that SAA can promote a distinct CD11c(high)CD11b(high) macrop

269 se in serum amyloid A (SAA), suggesting that SAA might mediate SFB's effects on BMDCs.

270 usly forms fibrils in vitro, suggesting that SAA proteins are inherently amyloidogenic.

271 We have also shown for the first time that SAA stimulate their own transcription as well as that of

272 We conclude that SAAs provide a potential substrate for bidirectional sig

273 The SAA mRNA levels were increased in glaucoma TM tissues by

274 The SAA-IL-17A axis represents an important innate defense n

275 The SAA-induced increase in sPLA(2) was validated by real ti

276 The SAA-rich diet increased diuresis paralleled by downregul

277 with high density lipoprotein abrogated the SAA-induced increase in sPLA(2) expression.

278 , which appears to partially result from the SAA component of HDL binding to cell-surface proteoglyca

279 However, the SAA fragments potently synergized with CCL3 to induce mo

280 Furthermore, dissociation of the SAA hexamer appears insufficient to initiate amyloidogen

281 e was performed under flow conditions on the SAA NPs supported on alumina without activity loss in th

282 We have used the SAA isoform, SAA2.2, from the CE/J mouse strain, as a mo

283 The SAAs of Adelta- or C-fibers from the L6 dorsal roots wer

284 In the BOO group at day 10, the SAAs of both Adelta- and C-fibers at the "ascending" pha

285 Unlike intact SAA1alpha, these SAA fragments failed to directly chemoattract neutrophil

286 ith cardiovascular disease, but whether this SAA contributes causally to atherosclerosis development

287 Thus, SAA alters vascular proteoglycans in a pro-atherogenic m

288 nd three MAPKs all appeared to contribute to SAA-induced cytokine release.

289 n of the microbiota and systemic exposure to SAA can influence myelopoiesis and susceptibility to ame

290 HeLa cells expressing TLR2 responded to SAA with potent activation of NF-kappaB, which was enhan

291 in sPLA(2) expression were not secondary to SAA-induced IL-1 receptor activation.

292 of the basic signaling mechanisms underlying SAA in plants and reveal that signaling events and trans

293 proximity to airway epithelium, and in vitro SAA triggered release of IL-8 and other proinflammatory

294 In vivo, SAA administration induced the development of a CD11c(hi

295 ns with the largest median fold changes were SAA (serum amyloid protein A), NPS-PLA2 (secreted phosph

296 med most mice for explosive amyloidosis when SAA production subsequently increased.

297 rpose of this study was to determine whether SAA and/or CRP alters vascular proteoglycan synthesis an

298 To determine whether SAA stimulated proteoglycan synthesis in vivo, ApoE(-/-)

299 lung macrophages (CD68(+)) colocalized with SAA and GCs markedly increased SAA in vitro (THP-1, pEC(

300 Differentiation of human monocytes with SAA stimulated the proinflammatory monokines IL-6 and IL