ライフサイエンスコーパス: megakaryocyte

1 (MM), lead to aromatase degradation in human megakaryocytes.

2 the functional defects observed in patients' megakaryocytes.

3 therefore differentiation of stem cells into megakaryocytes.

4 s are physically proximal to Nbeal2 in human megakaryocytes.

5 ed by large polyploid precursor cells called megakaryocytes.

6 take/storage of Fg in platelets and cultured megakaryocytes.

7 spleen, resulting in a four-fold increase in megakaryocytes.

8 lar features of adult-type cells on neonatal megakaryocytes.

9 ion also elicited adult features in neonatal megakaryocytes.

10 and progenitor cells (HSPCs) into functional megakaryocytes.

11 GATA1 effectively rescued maturation of PMF megakaryocytes.

12 timately lead to the production of polyploid megakaryocytes.

13 of the DMS from the surface membrane in rat megakaryocytes.

14 pon differentiation of HEL cells to adherent megakaryocytes.

15 pathway that has a low activity in polyploid megakaryocytes.

16 sive DNA methylation differences in maturing megakaryocytes.

17 , consistent with previous mRNA analysis, in megakaryocytes.

18 rmation of multiple poles typically found in megakaryocytes.

19 to Cxcl12 stroma and farther from sinusoids/megakaryocytes.

20 fold overexpression of PLAU, specifically in megakaryocytes.

21 of, as well as internalized to, bone marrow megakaryocytes.

22 ich is expressed abundantly in platelets and megakaryocytes.

23 enotype of mice lacking 1 or both factors in megakaryocytes.

24 restores the proximal association of HSCs to megakaryocytes.

25 confocal fluorescence imaging of primary rat megakaryocytes.

26 ting from the expression of JAK2V617F in the megakaryocytes.

27 s total cells 99-fold, erythrocytes 70-fold, megakaryocytes 0.5-fold, and CD34(+) stem/progenitor cel

28 plicated a platelet-independent role for the megakaryocyte, a Kit-dependent lineage that is selective

29 reshold level leading to erythrocytosis with megakaryocyte abnormalities.

30 , we explored the functional implications of megakaryocyte accumulation in the femurs of mice after i

31 dentified populations of mature and immature megakaryocytes along with haematopoietic progenitors in

32 as normal, whereas we observed deficiency of megakaryocyte alpha-granule proteins and emperipolesis.

33 A decreased percentage of megakaryocytes also predicted patient death in the ICU.

34 sability of proper chromosome segregation in megakaryocytes, an endomitotic SAC is activated in these

35 al to normal hematopoiesis, in particular to megakaryocyte and platelet development, as reflected in

36 normal glycosylation and thereby may impair megakaryocyte and platelet development.

37 onal characterization including iPSC-derived megakaryocyte and platelet experiments.

38 system, thereby transferring membrane to the megakaryocyte and to daughter platelets.

39 interacts with its cognate receptor c-MPL on megakaryocytes and bone marrow progenitor cells to promo

40 functional in sepsis due to trafficking from megakaryocytes and de novo synthesis in platelets and is

41 erythroid progenitors differentiated to both megakaryocytes and erythroblasts.

42 In human hematopoiesis, megakaryocytes and erythroid cells differentiate from a

43 or GATA-1 generated mast cells, eosinophils, megakaryocytes and erythroid cells, and a pathway lackin

44 that have a higher basal RhoA activity than megakaryocytes and express both NMIIA and NMIIB at the c

45 with increased and morphologically abnormal megakaryocytes and increased numbers of phenotypically d

46 hrombocytopenia, characterized by dysplastic megakaryocytes and intracranial bleeding, was diagnosed

47 nflammatory cytokines generated by malignant megakaryocytes and monocytes.

48 nally, iHPs generate acetylcholinesterase(+) megakaryocytes and phagocytic myeloid cells in vitro and

49 will focus on our understanding of committed megakaryocytes and platelet release in vivo and in vitro

50 rated mice selectively lacking Galpha(i2) in megakaryocytes and platelets (Gna(i2)(fl/fl)/PF4-Cre mic

51 transgenic mice expressing LOX in wild-type megakaryocytes and platelets (Pf4-Lox(tg/tg)) were gener

52 nt cellular composition, size, and function, megakaryocytes and platelets both depend on restraint of

53 Taken together, these results suggest that megakaryocytes and platelets may be a source of circulat

54 e to our understanding of the interaction of megakaryocytes and platelets with glycans.

55 e may primarily reflect changes occurring in megakaryocytes and platelets, including the ability of t

56 lenomegaly, and paucity of alpha-granules in megakaryocytes and platelets.

57 orm efforts to create alternative sources of megakaryocytes and platelets.

58 l line MEG-01 as an in vitro model for human megakaryocytes and platelets.

59 expression reversed the WDR1 KD phenotype of megakaryocytes and PLPs.

60 nce mitochondrial biogenesis and activity in megakaryocytes and preserve mitochondrial functions in p

61 iving cells, and JAK/STAT activation in both megakaryocytes and stromal cells in 3 murine PMF models.

62 pha5beta1 integrin, the major FN receptor in megakaryocytes, and augmented adhesion to FN compared wi

63 e that circRNAs are not enriched in cultured megakaryocytes, and demonstrate that linear RNAs decay m

64 e HSCs proximal to sinusoids, Cxcl12 stroma, megakaryocytes, and different combinations of those popu

65 evels by c-kit(+) hematopoietic progenitors, megakaryocytes, and Leptin Receptor(+) (LepR(+)) stromal

66 iptomes of naive progenitors and erythroid-, megakaryocyte-, and leukocyte-committed progenitors, and

67 ncreased basal and thrombopoietin-stimulated megakaryocyte antigen expression, as well as basal level

68 Megakaryocytes appear to be implicated in this process,

69 rrelates with decreased endosteal niches and megakaryocyte apposition to sinusoids.

70 gakaryocytes is defective, even while marrow megakaryocytes are greatly increased in number.

71 Megakaryocytes are produced via a shared pathway with th

72 ant-clone HSPCs have increased expression of megakaryocyte-associated genes compared to wild-type HSP

73 rogenitor differentiation into erythrocytes, megakaryocytes, basophils, and granulocytes, but not mac

74 owever, the specific role for Pak kinases in megakaryocyte biology remains elusive.

75 nvolving these TFs affect diverse aspects of megakaryocyte biology, and platelet production and funct

76 ased differentiation and polyploidization of megakaryocytes both in vivo and in vitro.

77 DKO megakaryocytes, but not single-knockout megakaryocytes,

78 Transit through megakaryocytes can be completed as rapidly as minutes, a

79 Recent studies have suggested that megakaryocytes can be generated from multiple pathways a

80 th GLP-1 receptor (GLP-1R) mRNA from a human megakaryocyte cell line (MEG-01), and found expression l

81 asses of assayable HPCs (colony-forming unit-megakaryocyte [CFU-MK], CFU-granulocyte/macrophage, burs

82 tion in mice, we show that a large number of megakaryocytes circulate through the lungs, where they d

83 Using induced pluripotent stem cell-derived megakaryocyte clones that produce functional platelets,

84 s with putatively causal platelet effects in megakaryocyte clones to examine effects on platelet prod

85 ts significantly promoted MkP generation and megakaryocyte colonies.

86 Indeed, a skewing of megakaryocyte commitment and differentiation may entail

87 roliferation, and biasing of the MEPs toward megakaryocyte commitment, which ultimately results in th

88 topoiesis in old mice reflected by increased megakaryocyte-committed progenitor cells, megakaryocyte

89 by synchronized expansion and maturation of megakaryocytes consistent with CPI203-mediated reprogram

90 and impaired differentiation were limited to megakaryocytes, consistent with a proproliferative effec

91 In this paper, we show that megakaryocytes contain extranuclear histones and transfe

92 , recent advances in genetic manipulation of megakaryocytes could lead to new and improved therapies

93 Megakaryocytes cultured from peripheral blood or bone ma

94 ession observed in standard 2D erythroid and megakaryocyte cultures.

95 potentially other cells passing through the megakaryocyte cytoplasm to modulate the production and m

96 ely from the protrusion and fragmentation of megakaryocyte cytoplasm.

97 e-bound vesicles before penetrating into the megakaryocyte cytoplasm.

98 For example, the megakaryocyte demarcation membrane system (DMS) provides

99 underlie inefficient platelet production by megakaryocytes derived from pluripotent stem cells.

100 crovessels close to these cells, and because megakaryocyte-derived supernatant fluid can reproduce th

101 human ontogenic master switch that restricts megakaryocyte development by modulating a lineage-specif

102 its requirement in normal hematopoiesis and megakaryocyte development has not been extensively chara

103 a GFI1B isoform that preferentially promotes megakaryocyte differentiation and platelet production.

104 We identified a bias toward megakaryocyte differentiation apparent from early multip

105 The anti-platelet antibody hindered megakaryocyte differentiation from the progenitors, impa

106 of miR-1300 as a regulator of endomitosis in megakaryocyte differentiation where blockade of cytokine

107 a critical transcription factor (TF) during megakaryocyte differentiation, is among genes hemizygous

108 To clarify the cellular pathway in erythro-megakaryocyte differentiation, we correlate the surface

109 ell cultures, silencing of TRIB3 facilitated megakaryocyte differentiation.

110 onsive gene that is required for LEN-induced megakaryocyte differentiation.

111 rric chloride injury and are attenuated with megakaryocyte-directed deletion of the cyclophilin D gen

112 ls with biased megakaryocyte potential, with megakaryocytes directly arising from HSCs under steady-s

113 esulted in age-dependent progressive anemia, megakaryocyte dysplasia and loss of hematopoietic stem c

114 ncluding macrothrombocytopenia, BM fibrosis, megakaryocyte emperipolesis of neutrophils, splenomegaly

115 supports a growing body of evidence that the megakaryocyte endomitotic cell cycle differs significant

116 asts, LepR+ cells, Nes-cre-expressing cells, megakaryocytes, endothelial cells or hematopoietic cells

117 Nuclear protein extracts from megakaryocytes, endothelial cells, vs control HEK-293 ce

118 Bone marrow megakaryocytes engulf neutrophils in a phenomenon termed

119 ic interactions between PLAU and a conserved megakaryocyte enhancer found within the same topological

120 The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific e

121 uently, within the myeloid lineage, bipotent megakaryocyte-erythrocyte and granulocyte-macrophage pro

122 through a requisite multipotent or bipotent megakaryocyte-erythrocyte progenitor stage.

123 sulting from an arrest in development at the megakaryocyte-erythrocyte progenitor stage.

124 , granulocyte-macrophage progenitors (GMPs), megakaryocyte-erythrocyte progenitors (MEPs), pre-megaka

125 aryocyte-erythrocyte progenitors (MEPs), pre-megakaryocyte-erythrocyte progenitors (PreMegEs), and co

126 cell types, focusing on trajectories toward megakaryocyte-erythrocyte progenitors and lymphoid-prime

127 ly preleukemic expansion of a phenotypic pre-megakaryocyte/erythrocyte (Pre-Meg/E) progenitor populat

128 itor (CLP), common myeloid progenitor (CMP), megakaryocyte-erythroid progenitor (MEP), and granulocyt

129 s differentiate from a shared precursor, the megakaryocyte-erythroid progenitor (MEP), which remains

130 s(G12D/+) to promote increased quiescence in megakaryocyte-erythroid progenitors (MEPs).

131 t in the bone marrow environment affects the megakaryocyte-erythroid progenitors (MEPs).

132 elopmentally arrested GATA1-deficient murine megakaryocyte-erythroid progenitors derived from murine

133 me granulocyte-macrophage progenitors and as megakaryocyte-erythroid progenitors differentiated to bo

134 dy clarifies the cellular hierarchy in human megakaryocyte/erythroid lineage commitment and highlight

135 aberrant NLK activation is initiated at the Megakaryocyte/Erythroid Progenitor (MEP) stage of differ

136 Bipotent megakaryocyte/erythroid progenitors (MEPs) give rise to

137 Although immature megakaryocytes express 2 nonmuscle myosin II isoforms (M

138 f platelets, and we found that human and rat megakaryocytes express the BDNF gene.

139 the pathway contributes to the clearance of megakaryocytes following platelet shedding and constrain

140 Proplatelet formation was reduced in megakaryocytes from 7 cases relative to 6 controls.

141 resampled the transcriptomes of rare, single megakaryocytes from a complex mixture of lymphocytes and

142 These results demonstrate that cultured megakaryocytes from GPS patients provide a valuable mode

143 We report the first analysis of cultured megakaryocytes from GPS patients with NBEAL2 mutations.

144 Further, megakaryocytes from JAK2V617F+ mice have increased cell

145 roaches to study PLAU regulation in cultured megakaryocytes from participants with QPD and unaffected

146 rroborating our findings in mice, JAK2V617F+ megakaryocytes from patients showed elevated expression

147 Using stem/progenitor cells, megakaryocyte function and platelet generation were reco

148 nd multivalent heparin inhibits platelet and megakaryocyte function by inducing downstream signaling

149 tegies to increase the safety and benefit of megakaryocyte gene therapy will be discussed.

150 In this study we examined the megakaryocyte genome in 12 patients with MPNs to determi

151 stromal cells in the bone marrow: promoting megakaryocyte growth and proplatelet formation by intera

152 Megakaryocytes had a higher actin turnover compared with

153 DKO megakaryocytes, but not single-knockout megakaryocytes, had reduced expression of Gata1, Fli1, N

154 In summary, genetic manipulation of megakaryocytes has progressed to the point where clinica

155 Nonetheless, whether megakaryocyte-HSC interactions change during pathologica

156 induced-pluripotent stem cell (iPSC)-derived megakaryocytes (iMegs) to better understand these clinic

157 s almost specifically expressed in platelets/megakaryocytes in humans.

158 proposed defective platelet production from megakaryocytes in ITP in 1915.

159 ow that genomic abnormalities are present in megakaryocytes in MPNs and that these appear to be assoc

160 Here, we have revealed that megakaryocytes in PMF show impaired maturation that is a

161 of long membrane extensions from bone marrow megakaryocytes in the blood flow.

162 l(-/-) hematopoiesis increased the number of megakaryocytes in the BM.

163 inical specimens, we observed an increase in megakaryocytes in the bone marrow of 6/8 patients with m

164 is, challenging present views on the role of megakaryocytes in this setting.

165 y reduces the percentage of CD41+ JAK2V617F+ megakaryocytes in vitro and in vivo.

166 How platelets are produced by megakaryocytes in vivo remains controversial despite mor

167 By contrast, BDNF is undetectable in mouse megakaryocytes, in line with the absence of BDNF in mous

168 ed myeloid:erythroid ratio of 5:1, increased megakaryocytes including micromegakaryocytes in the abse

169 es the activation of profibrotic pathways in megakaryocytes, inflammation in fibrosis-driving cells,

170 We showed that ex vivo-generated murine megakaryocytes infused into mice release platelets withi

171 purpura (ITP), production of platelets from megakaryocytes is defective, even while marrow megakaryo

172 m localization; thus, cytokinesis failure in megakaryocytes is the consequence of both the absence of

173 d been considered specific for platelets and megakaryocytes, is also prominently expressed in the mai

174 0 genes associated with myeloid neoplasms on megakaryocytes isolated from aspirated bone marrow.

175 nt proplatelet formation in murine and human megakaryocytes lacking Hyal-2.

176 re restricted, being highly expressed in the megakaryocyte lineage but downregulated during erythropo

177 In the megakaryocyte lineage, human fetal progenitors do not ex

178 ad comparison, we demonstrate more stringent megakaryocyte lineage-specific expression of the Gp1ba-C

179 dependent but required IL-1 and the platelet/megakaryocyte markers NF-E2 and glycoprotein VI.

180 Megakaryocyte maturation and polyploidization are critic

181 Megakaryocyte maturation signals through cascades that i

182 eased transcriptional repression and altered megakaryocyte maturation.

183 Little is known about how megakaryocytes may affect metastasis beyond serving as a

184 In support of the hypothesis that reducing megakaryocytes may reduce metastasis, we found that thro

185 nx1 KO mice, with a prominent skewing toward megakaryocyte (Meg) progenitors.

186 actor alpha (TNF-alpha), which functions via megakaryocyte metabolic reprogramming that leads to plat

187 s such as the bone marrow; we observed large megakaryocytes migrating out of the bone marrow space.

188 ade by this model, in particular relating to megakaryocyte (Mk) and erythroid (E) development.

189 s (MEPs) give rise to progeny limited to the megakaryocyte (Mk) and erythroid (E) lineages.

190 Glycosylation is critical to megakaryocyte (MK) and thrombopoiesis in the context of

191 for platelet activation and also involved in megakaryocyte (MK) development and platelet production.

192 Megakaryocyte (MK) differentiation occurs within the bon

193 s5 (type II) induced thrombocytosis due to a megakaryocyte (MK) hyperplasia.

194 in primary maturing mammalian erythroid and megakaryocyte (MK) lineages as well as their common prog

195 iption factors' (TFs) activities in terminal megakaryocyte (MK) maturation.

196 ing important changes in the distribution of megakaryocyte (MK) organelles.

197 pled to late EPO-dependent erythropoiesis by megakaryocyte (Mk) signals.

198 Platelets, anucleated megakaryocyte (MK)-derived cells, play a major role in h

199 Here, we show that murine megakaryocyte (MK)-specific knockdown of Dicer1, the rib

200 tory small RNAs inherited from the precursor megakaryocyte (MK).

201 hanced the production of proplatelet-bearing megakaryocytes (MKs) and platelet-like elements.

202 ion, the mechanisms controlling [Mg(2+)]i in megakaryocytes (MKs) and platelets are largely unknown.

203 ass III phosphoinositide 3-kinase (PI3K), in megakaryocytes (MKs) and platelets, we created a mouse m

204 receptor kinases (Trk) in the development of megakaryocytes (MKs) and their progeny cells, platelets.

205 Megakaryocytes (MKs) are exposed to shear flow as they m

206 e gene expression in health and disease, and megakaryocytes (MKs) deficient in miRs have lower platel

207 During thrombopoiesis, megakaryocytes (MKs) form proplatelets within the bone m

208 ted calcium (Ca2+) entry (SOCE) machinery in megakaryocytes (Mks) from healthy individuals and from p

209 Megakaryocytes (MKs) generate platelets by extending lon

210 olving evidence indicates that platelets and megakaryocytes (MKs) have unexpected activities in infla

211 Increasing the number of megakaryocytes (MKs) in the bone marrow results in a hig

212 where low MPL levels on platelets and mature megakaryocytes (MKs) lead to high serum THPO levels, whe

213 show that the absence of the FLNa protein in megakaryocytes (MKs) leads to their incomplete maturatio

214 Intriguingly, we found that treating megakaryocytes (MKs) with the releasate from activated p

215 Defining the platelet-producing megakaryocytes (MKs) within the heterogeneous MK culture

216 Megakaryocytes (MKs), the precursor cells for platelets,

217 upon differentiation into CD41+/CD42b+ human megakaryocytes (MKs), to flow cytometric detection of su

218 d by large bone marrow (BM) precursor cells, megakaryocytes (MKs), which extend cytoplasmic protrusio

219 The production of megakaryocytes (MKs)--the precursors of blood platelets-

220 oietic stem cell differentiation into mature megakaryocytes (Mks).

221 ltered regulation of platelet formation from megakaryocytes (MKs).

222 ation mechanism that is known to drive adult megakaryocyte morphogenesis.

223 s were used to investigate megakaryopoiesis, megakaryocyte morphology and platelet formation.

224 ) had severe macrothrombocytopenia, abnormal megakaryocyte morphology, defective pro-platelet formati

225 understanding of the complex processes that megakaryocytes must undergo to generate platelets both i

226 d not yet fully understood interaction among megakaryocytes, myeloid cells, fibroblasts, and endothel

227 Megakaryocyte number and ploidy are normal in all 3 mous

228 to alpha5 subunit reduced adhesion to FN and megakaryocyte number derived from CD34+ cells.

229 olony forming units, sternal cellularity and megakaryocyte numbers in drug treated mice compared to f

230 Megakaryocyte numbers were significantly increased in bo

231 r, our results suggested that an increase in megakaryocytes occurring in response to metastatic cells

232 Moreover, megakaryocytes of our patients showed impaired maturatio

233 ythroid colony-forming ability and decreased megakaryocyte output.

234 1(+/-) iMegs replicate many of the described megakaryocyte/platelet features, including a decrease in

235 o induce expression of the Syk mutant in the megakaryocyte/platelet lineage.

236 , including the existence of multipotent but megakaryocyte/platelet-biased HSCs.

237 s the current model of choice for generating megakaryocyte/platelet-specific KO mice.

238 In humans and mice, megakaryocytes/platelets and endothelial cells constitut

239 ed megakaryocyte-committed progenitor cells, megakaryocyte ploidy status, and thrombocytosis.

240 Megakaryocyte polyploidy is characterized by cytokinesis

241 t HSCs contain a subset of cells with biased megakaryocyte potential, with megakaryocytes directly ar

242 anuclear cells that inherit their mRNA from megakaryocyte precursors and maintain it unchanged durin

243 heme has been challenged, with the origin of megakaryocyte precursors being one of the most debated s

244 Every day, megakaryocytes produce billions of platelets that circul

245 Here, megakaryocyte progenitor cells are genetically engineere

246 ntegrity and stability of mRNAs derived from megakaryocyte progenitor cells remain poorly quantified

247 counting for the increased cell death in the megakaryocyte progenitor compartment.

248 A sub-fraction of myelofibrosis megakaryocyte progenitors (MkPs) are transcriptionally s

249 nd mouse hematopoietic stem cells (HSCs) and megakaryocyte progenitors (MkPs).

250 pulations: "Pre-MEP," enriched for erythroid/megakaryocyte progenitors but with residual myeloid diff

251 CD41(+) megakaryocyte progenitors derived from these cells expre

252 P1 knock-in megakaryocyte progenitors have reduced proliferative cap

253 cripts and a maturation of SL-MkPs and other megakaryocyte progenitors.

254 TPO causes megakaryocyte proliferation and increased platelet produ

255 Megakaryocytes promote quiescence of neighboring HSCs.

256 tion, SL-MkPs become activated, resulting in megakaryocyte protein production from pre-existing trans

257 Megakaryocytes readily produce proplatelet structures in

258 epletion of GNB1 (encoding Gbeta1) in murine megakaryocytes reduced protease-activated receptor 4, ac

259 On average, megakaryocytes release 10(11) platelets per day into the

260 Thrombopoiesis is the process by which megakaryocytes release platelets that circulate as unifo

261 evidence that TNF-alpha critically regulates megakaryocytes resident in the bone marrow niche and agi

262 Transfer of WT but not IL-1-deficient megakaryocytes restored arthritis susceptibility to KitW

263 ufficient TPM4 expression in human and mouse megakaryocytes resulted in a defect in the terminal stag

264 Megakaryocytes secreted IL-1 directly and as a component

265 cell RNA-sequencing analysis of native mouse megakaryocytes showed significant reprogramming of infla

266 In vivo, megakaryocyte-specific Munc18-2 conditional knockout mic

267 How this duplication causes megakaryocyte-specific PLAU overexpression is unknown.

268 s similar to those noted with other critical megakaryocyte-specific TFs; however, unlike those TFs, F

269 erythroid-specific genes are upregulated and megakaryocyte-specific transcripts are downregulated.

270 RUNX1 is crucial for the regulation of megakaryocyte specification, maturation, and thrombopoie

271 Megakaryocytes store BDNF in alpha-granules, with more t

272 are anucleate cytoplasmic discs derived from megakaryocytes that circulate in the blood and have majo

273 by increased numbers of abnormal bone marrow megakaryocytes that induce fibrosis, destroying the hema

274 Megakaryocytes that release platelets in the lungs origi

275 en of the 12 patients had genomic defects in megakaryocytes that were not present in nonmegakaryocyti

276 aluronan within their bone marrow and within megakaryocytes, the cells responsible for platelet gener

277 haematopoietic progenitor cells give rise to megakaryocytes, the giant bone marrow cells that in turn

278 predicted to regulate granule trafficking in megakaryocytes, the platelet progenitors.

279 latelets, we established primary cultures of megakaryocytes, the progenitors of platelets, and we fou

280 s and establish an unanticipated capacity of megakaryocytes to mediate IL-1-driven systemic inflammat

281 ient to deviate cells from an erythroid to a megakaryocyte trajectory, showing that quantitative chan

282 Mitotic arrest in wild-type megakaryocytes treated with Plk1 inhibitors or Plk1-null

283 The megakaryocyte-unique mutations were predominantly in gen

284 ability to differentiate to erythrocytes and megakaryocytes upon geminin silencing.

285 Proplatelet formation by Hyal-2 knockout megakaryocytes was disrupted because of abnormal formati

286 In vitro differentiation of megakaryocytes was normal, whereas we observed deficienc

287 demonstrated that platelet formation by GPS megakaryocytes was severely affected, a defect which mig

288 chymal and osteoblastic populations, whereas megakaryocytes were decreased.

289 The fibrinogen and the percentage of megakaryocytes were significantly lower in nonsurvivors

290 aftment potential, but directly matures into megakaryocytes when placed in culture.

291 therapy because they can differentiate into megakaryocytes which are capable of forming several thou

292 re red blood cells; increased and persistent megakaryocytes which release high levels of platelets fo

293 nd BM of patients harbor atypical, clustered megakaryocytes, which contribute to the disease by secre

294 mbrane-localized stem cell factor (m-SCF) in megakaryocytes, which was regulated, in turn, by vascula

295 e platelet factor 4 (Pf4) promoter generated megakaryocytes with markedly reduced but not absent Scl

296 ve the capacity to differentiate into mature megakaryocytes with the ability to produce functional pl

297 tiated HEL cells and those differentiated to megakaryocytes, with a shift to more N-linked sialoglyco

298 creased ITGA2B was identified in bone marrow megakaryocytes within 24 hours of sepsis onset.

299 nt mice exhibited a 90% relative decrease in megakaryocytes, yet they developed more aggressive metas

300 ction from their bone marrow precursors, the megakaryocytes, yielding giant platelets in reduced numb