ライフサイエンスコーパス: BMSC

1 BMSC CM contained a heat-labile factor that increased BM

2 BMSC co-transplantation doubles the number of functional

3 BMSCs from six of the eight centers were tested for thei

4 BMSCs inoculated alone induced osteoblast suppression, a

5 BMSCs isolated from femur and tibia of Sprague-Dawley ra

6 BMSCs may reduce pathogen burden by inhibiting growth th

7 BMSCs secreted TGF-beta1 into the cerebrospinal fluid, a

8 BMSCs that migrated from the injection site survived at

9 antly lower levels in cultures of Bag-1(+/-) BMSCs supplemented with BMP-2, while genes with roles in

10 vel genetically engineered Tet-Off-SDF-1beta BMSCs, which over-express SDF-1beta under tight doxycycl

11 mir which can mimic the effects of pri-miR-9-BMSCs and protect injured pancreas.

12 microRNA-9 (miR-9) modified BMSCs (pri-miR-9-BMSCs) can significantly reduce the pancreatic edema, in

13 Coinoculation of myeloma cells and a BMSC line, isolated from myeloma-permissive mice, into o

14 m both micro- and nanoscale surface-adherent BMSCs increased the osteoclast number (P < 0.01).

15 Difference in surface topography altered BMSC phenotype and influenced BMM osteoclastogenesis.

16 of the efficacy and specificity of AMSC and BMSC tropism towards glioma.

17 y, our results show novel roles of BMSCs and BMSC-derived Dkk1 in the pathogenesis of multiple myelom

18 increased expression of sFRP-1 in bones and BMSC.

19 roles in bone-immune cell communication and BMSC immune suppressive functions.

20 ses abnormalities in osteoblast function and BMSC differentiation and identify a previously unrecogni

21 ively interferes with CLL cell migration and BMSC-mediated drug resistance, and establishes a rationa

22 th the monocytes/macrophages population, and BMSC-induced monocyte CXCL1.

23 liferation rate of both commercial AMSCs and BMSCs as compared to primary culture AMSCs, suggesting p

24 osteoblastogenesis of MC3T3-E1 cultures and BMSCs induced towards the bone lineage by multi-layered

25 d demonstrates the requirement for NOTCH and BMSCs in fracture repair, irrespective of fracture stabi

26 the quantity formed was highly variable and BMSCs from only three centers supported hematopoiesis.

27 oreover, increased chondrogenesis of ank/ank BMSCs and increased chondrogenic transdifferentiation an

28 ctivity and decreased glutathione in ank/ank BMSCs.

29 colony-stimulating factor (M-CSF) as well as BMSC CM from each of the 4 surfaces.

30 Because BMSCs have been successfully given to humans and can eas

31 s amplifies multiorgan complications because BMSCs promote vascular repair.

32 ritical role mediating the crosstalk between BMSCs and T(reg) in the bone marrow microenvironment.

33 Both mandible and long-bone BMSCs differentiated into osteoblasts.

34 ore mineralized bone compared with long-bone BMSCs.

35 ence with the CXCL12 gradient established by BMSCs.

36 osis factor alpha and M-CSF was increased by BMSCs cultured on both micro- and nanoscale titanium top

37 or activated lymphocytes were each killed by BMSCs after 72 h of co-incubation.

38 ch can translate into protection mediated by BMSCs.

39 We found that GDF15 is produced by BMSCs after direct contact with plasma cells and enhance

40 at long-lasting antihyperalgesia produced by BMSCs required their chemotactic factors such as CCL4 an

41 d a preconditioned group with PVE and CD133+ BMSC cotreatment (PVE+SC group, n = 11) and a group pret

42 CD133 bone marrow-derived stem cell (CD133+ BMSC) application before extended right hepatectomy.

43 lysis suggest that PVE, together with CD133+ BMSC pretreatment, could positively impact overall outco

44 shown that portal venous infusion of CD133+ BMSCs substantially increases hepatic proliferation, whe

45 demonstrated that bone marrow stromal cell (BMSC) and CB-BF pellet cultures make cartilage in vitro

46 alizing nodules in bone marrow stromal cell (BMSC) cultures.

47 mandible and long-bone marrow stromal cell (BMSC) isolation and culture.

48 To identify human bone marrow stromal cell (BMSC) subsets with enhanced ability to engraft/contribut

49 s (MSC) derived from bone marrow stem cells (BMSC) and adipose tissue stem cells (ASC) of humans and

50 c potential of human bone marrow stem cells (BMSC) with stem cells derived from human dental pulp (DP

51 dies suggest that bone marrow stromal cells (BMSC) can promote myeloma growth and survival and osteol

52 ells with patient bone marrow stromal cells (BMSC) showed similar beta1 integrin-specific enhancement

53 which stimulates bone marrow stromal cells (BMSC) to AML blast transfer of mitochondria through AML-

54 In bone marrow stromal cells (BMSC), GJIC and osteogenic differentiation were compromi

55 bone, while bone marrow stromal/stem cells (BMSCs) and other skeletal progenitors may also contribut

56 bone marrow-derived mesenchymal stem cells (BMSCs) are not known.

57 Bone marrow mesenchymal stem cells (BMSCs) exhibit an age-dependent reduction in osteogenesi

58 Bone marrow-derived mesenchymal stem cells (BMSCs) have the potential of repairing SAP, but the deta

59 bone marrow-derived mesenchymal stem cells (BMSCs) increases the production of T(reg) cells via a me

60 ntiation of cultured bone marrow stem cells (BMSCs) into the adipocyte lineage was suppressed by 17-b

61 d senescence of bone mesenchymal stem cells (BMSCs) isolated from a TDO patient, providing a molecula

62 of local bone marrow mesenchymal stem cells (BMSCs) on osteoarthritis (OA) of the temporomandibular j

63 bone marrow-derived mesenchymal stem cells (BMSCs) showed great potential in controlling T1DM.

64 s study, rat bone marrow stromal stem cells (BMSCs) were tracked after IV administration to rats with

65 bone marrow-derived mesenchymal stem cells (BMSCs), remains challenging.

66 d we now find that bone marrow stroma cells (BMSCs) are severely and permanently damaged by the pre-c

67 of primary mouse bone marrow stromal cells (BMSCs) and 3T3-L1 pre-adipocytes via interaction with Pp

68 iminished in both bone marrow stromal cells (BMSCs) and calvarial cells of mutant mice.

69 eloma adhesion to bone marrow stromal cells (BMSCs) and enhancing myeloma colony formation in semisol

70 BM stromal cells (BMSCs) are key players in the microenvironmental support

71 clear that human bone marrow stromal cells (BMSCs) can be immunosuppressive and escape cytotoxic lym

72 e metabolomics of bone marrow stromal cells (BMSCs) derived from hyperglycaemic (type 2 diabetes mell

73 enic potential of bone marrow stromal cells (BMSCs) differs between MB versus long bones (LB).

74 neath a confluent layer of BM stromal cells (BMSCs) due to interference with the CXCL12 gradient esta

75 imary FBLP-1 null bone marrow stromal cells (BMSCs) exhibited significantly reduced extracellular mat

76 .t.) injection of bone marrow stromal cells (BMSCs) following lumbar puncture alleviates early- and l

77 undifferentiated bone marrow stromal cells (BMSCs) from KO mice express higher levels of PPAR-gamma

78 rrow-derived mesenchymal stem/stromal cells (BMSCs) hold great potential for cell-based therapy, yet

79 -1(+) multipotent bone marrow stromal cells (BMSCs) in mice, as well as on well-characterized, clinic

80 antly secreted by bone marrow stromal cells (BMSCs) in MM.

81 implant-adherent bone marrow stromal cells (BMSCs) in osteoclastogenesis is influenced by surface to

82 n the presence of bone marrow stromal cells (BMSCs) in vitro.

83 Adherence to bone marrow stromal cells (BMSCs) increased the percentage, viability, and prolifer

84 and modulate CLL bone marrow stromal cells (BMSCs) known to provide a "homing and nurturing" environ

85 ifferentiation of bone marrow stromal cells (BMSCs) of Bag-1(+/-) (heterozygous) female mice was decr

86 hypothesized that bone marrow stromal cells (BMSCs) participate in this process, and that osterix (Os

87 Bone marrow-derived stromal cells (BMSCs) protect against acute lung injury (ALI).

88 odel in which the bone marrow stromal cells (BMSCs) remained unresponsive to OB differentiation signa

89 e, but can induce bone marrow stromal cells (BMSCs) to form bone in a mouse muscle pouch model, exhib

90 ne marrow derived mesenchymal stromal cells (BMSCs) were used to CBTs for ConA-induced ALF and Fah-de

91 ulations of mouse bone marrow stromal cells (BMSCs), a common problem being contamination with hemato

92 temic infusion of bone marrow stromal cells (BMSCs), a major type of multipotent stromal cells, produ

93 ghly expressed in bone-marrow stromal cells (BMSCs), hepatocytes, and adipocytes.

94 ing human primary bone marrow stromal cells (BMSCs), lymphoblasts, and skin fibroblasts, we show that

95 h can derive from bone marrow stromal cells (BMSCs), takes a role in modulating osteoblast and osteoc

96 iency using human bone marrow stromal cells (BMSCs).

97 co-cultured with bone marrow stromal cells (BMSCs).

98 o transfect human bone marrow stromal cells (BMSCs).

99 on of MM cells to bone marrow stromal cells (BMSCs).

100 cultured ank/ank bone marrow stromal cells (BMSCs).

101 Human bone marrow stromal cells (BMSCs, also known as bone marrow-derived mesenchymal ste

102 tipotent, bone marrow-derived stromal cells (BMSCs, also known as mesenchymal stem cells [MSCs]), are

103 Bone marrow stromal cells [BMSCs; also known as mesenchymal stem cells (MSCs)] effe

104 Once in the circulation, BMSCs also produced rapid alterations in host blood cell

105 /hypoxia-inducible factor-1alpha axis in CLL-BMSCs with production of vascular endothelial growth fac

106 ial and primary culture AMSCs and commercial BMSCs demonstrated no statistically significant differen

107 BMSC-supported osteoclastogenesis, confluent BMSCs were cultured with parathyroid hormone (PTH), 1,25

108 ression in freshly isolated BMSCs or control BMSCs cultured in parallel but in nondifferentiating med

109 necrosis factor alpha, and M-CSF in cultured BMSCs at different time points were measured by real-tim

110 ransplantation of primary, but not cultured, BMSCs quantitatively reconstitutes stroma function in vi

111 Bone marrow cultures (BMSC) from 18-kDa TgFGF2 mice produced more mineralized

112 lular pool, we transplanted clonally derived BMSCs into fetal sheep.

113 rast, triglyceride content in differentiated BMSCs or 3T3-L1 cells was suppressed as a result of memb

114 versely, deficiency of XBP1 in healthy donor BMSCs displayed a range of effects on BMSCs that were op

115 the intrinsic properties of OB/BMSCs (i.e., BMSC-extracellular matrix adhesion and migration, cell g

116 gnificantly protected genetically engineered BMSCs from H2O2-induced cell death through increasing au

117 vator of NF-kappaB ligand (RANKL), enhancing BMSC support of MM cell growth and osteoclast formation

118 SDF-1 in the therapeutic effect of exogenous BMSCs was examined by both in vitro and in vivo studies.

119 We concluded that exogenous BMSCs participate in the osseointegration after implanta

120 -Fas antibody did not result in the expected BMSC apoptosis, regardless of concentration, suggesting

121 We also show that GILZ-expressing BMSCs present antigen in a way that favors T(reg) cells.

122 pathway is a critical maintenance factor for BMSCs during skeletal development, although the precise

123 Two to four BMSC lots from each center were compared using global ge

124 Among the twenty-four BMSC lots from the eight centers intra-center transcript

125 Although mitochondrial transfer from BMSC to nonmalignant CD34(+) cells occurs in response to

126 OA cartilage and the rescuing effect of GFP-BMSC injections were impaired by the inhibitors of C-X-C

127 green fluorescent protein-labeled BMSCs (GFP-BMSCs) were weekly injected into the TMJ region for 4, 8

128 The reparative effects of exogenous GFP-BMSCs were investigated by morphological observation and

129 The implanted GFP-BMSCs differentiated into type II collagen-positive cell

130 The differentiation of GFP-BMSCs in the cartilage was examined by double immunofluo

131 on synergistically in the recruitment of GFP-BMSCs towards degraded cartilage in mice OA of the TMJ.

132 The migration of GFP-BMSCs towards OA cartilage and the rescuing effect of GF

133 apability of attracting the migration of GFP-BMSCs.

134 hat, at 7 d post-transplant, the EphB2(high) BMSCs engrafted in the ISC region at levels of 2.1 +/- 0

135 In the host, BMSCs may attenuate pro-inflammatory cytokine and chemok

136 hing, we suggest that cultured, banked human BMSCs may be effective in treating sepsis in high-risk p

137 XBP1s overexpression in healthy human BMSCs enhanced gene and/or protein expression of VCAM-1,

138 racterized, clinical-grade multipotent human BMSCs.

139 en with either mouse BMSCs (mBMSCs) or human BMSCs (hBMSCs).

140 y more total population doublings than human BMSCs (hBMSC) and rhesus ASCs (rASC).

141 e (GFP group) - were incorporated with human BMSCs into a solution of photocrosslinkable gelatin, whi

142 ed induced mouse asthma model, we studied if BMSCs could be beneficial in an allergic, Th2-dominant e

143 Importantly, BMSCs isolated from Gfi1(-/-) mice were significantly re

144 Moreover, silencing of sFRP-1 in BMSC from FGF2(lmw)(-/-) mice reversed the decrease in b

145 sed and decreased TCF-luciferase activity in BMSC from 18-kDa TgFGF2 and FGF2(lmw)(-/-) mice, respect

146 uclear factor-kappaB (NF-kappaB) activity in BMSC.

147 ationship between apoptosis and autophagy in BMSC homeostasis is complex and not well understood.

148 Such exquisite balance in BMSC function appears intrinsically linked to Toll-like

149 cells toward bendamustine and fludarabine in BMSC cocultures.

150 cell death and reduced clonogenic growth in BMSC-adherent myeloma cell lines, aldehyde dehydrogenase

151 ount of blood vessels in DPSC-MG, but not in BMSC-MG.

152 1-CXCR2 signaling plays an important role in BMSC-produced antihyperalgesia.

153 In BMSCs exposed to the PPAR-gamma (peroxisome proliferator

154 hermore, increased expression of miR-146a in BMSCs correlated with inhibition of PGE synthase-2 and i

155 Overexpression of Cdo1 in BMSCs inversely suppressed the osteogenesis.

156 adipocyte precursor population decreased in BMSCs harvested from the KO animals.

157 Dkk1 was highly expressed in BMSCs and in myeloma-permissive bone marrow.

158 Knockdown of Dkk1 expression in BMSCs decreased their ability to promote myeloma and the

159 e detected a high level of Fas expression in BMSCs, stimulation of Fas with anti-Fas antibody did not

160 in the TCA cycle, is increased by 24-fold in BMSCs from T2D mice.

161 Strikingly, siRNA knockdown of Gfi1 in BMSCs from MM patients significantly restored expression

162 ious findings that overexpression of GILZ in BMSCs antagonizes TNF-alpha-elicited inflammatory respon

163 microRNA-188 (miR-188) is markedly higher in BMSCs from aged compared with young mice and humans.

164 creased expression of cyclin D1 and c-myc in BMSCs.

165 d adipogenesis and decreased osteogenesis in BMSCs from these mice.

166 o metabolites are substantially regulated in BMSCs from T2D mice, with the tricarboxylic acid (TCA) c

167 etermined that removal of NOTCH signaling in BMSCs and subsequent depletion of this population result

168 hereby a nutrient-responsive gene influences BMSCs differentiation, adipogenesis, and ultimately body

169 Consistent with its role in influencing BMSCs allocation, Noc(-/-) mice have reduced bone marrow

170 Fas/Fc fusion protein strongly inhibited BMSC-induced lymphocyte apoptosis.

171 In contrast, few injected BMSCs traveled to the brain and almost none endured ther

172 regulation caused migration of i.t.-injected BMSCs to DRGs through the CXCL12 receptor CXCR4, which w

173 with miR-146a expression in freshly isolated BMSCs or control BMSCs cultured in parallel but in nondi

174 have shown previously that freshly isolated BMSCs when induced to express neuronal stem cell markers

175 tiation capabilities of the locally isolated BMSCs.

176 e this hypothesis, we tracked double-labeled BMSCs in implantation sites created in nude mice transpl

177 ity of radiolabeled or fluorescently labeled BMSCs traveled to and remained in peripheral organs (lun

178 Exogenous green fluorescent protein-labeled BMSCs (GFP-BMSCs) were weekly injected into the TMJ regi

179 To explore MB versus LB BMSC-supported osteoclastogenesis, confluent BMSCs were

180 1,25D3- or PTH+1,25D3-treated LB BMSCs expressed significantly higher RANKL and lower ost

181 ls of 2.1 +/- 0.2%, while control EphB2(low) BMSCs engrafted at 0.3 +/- 0.1% (P<0.01).

182 Mandible BMSC cultures formed more colonies, suggesting an increa

183 However, mandible BMSCs demonstrated augmented alkaline phosphatase activi

184 , upon implantation into nude mice, mandible BMSCs formed 70% larger bone nodules containing three-fo

185 potential and augmented capacity of mandible BMSCs to induce bone formation in vitro and in vivo.

186 ls (hMSC) may be harvested from bone marrow (BMSC) and adipose (AMSC) tissue.

187 MM-BMSC cell-cell contact was not required for MM cells to

188 strate here that microRNA-9 (miR-9) modified BMSCs (pri-miR-9-BMSCs) can significantly reduce the pan

189 ysaccharide (LPS) and then with either mouse BMSCs (mBMSCs) or human BMSCs (hBMSCs).

190 potential reason for the low yield of mouse BMSCs is the flushing of the marrow used to remove singl

191 reover, the expression of FAP by multipotent BMSCs may point toward the cellular origins of tumor str

192 ccordingly, both mouse and human multipotent BMSCs were recognized by FAP-reactive T cells.

193 Nonetheless, BMSC treatment produced dramatic changes in the number a

194 y of bone in vivo, relative to nontransduced BMSCs.

195 reduction (a TBD-associated gene) in normal BMSCs by small interfering TERC-RNA (siTERC-RNA) recapit

196 bone or support hematopoiesis, unlike normal BMSCs.

197 However, in the CLF model, not BMSCs but adult HCs transplantation lessened liver injur

198 Notably, BMSC-specific inhibition of miR-188 by intra-bone marrow

199 Notably, BMSCs appear to function as a critical fulcrum, providin

200 ation, was markedly increased in FBLP-1 null BMSCs.

201 rentiation) and the communication between OB/BMSCs and BMMs (i.e., RANKL expression) that controls os

202 dulating both the intrinsic properties of OB/BMSCs (i.e., BMSC-extracellular matrix adhesion and migr

203 In addition, the effects of BMSC treatment on blood cell composition, brain glia and

204 his effect was associated with inhibition of BMSC/MM cell adhesion and production of IL-6.

205 The presence of BMSC-derived mitochondria in the epithelia was evident o

206 To determine the role of BMSC mitochondria in this protection, we airway-instille

207 rutinib reverses the cyto-protective role of BMSC on FLT3-ITD AML survival.

208 Herein, we tested the role of BMSC-derived Wnt5a/Ror2 signaling in regulating osteocla

209 tch between osteogenesis and adipogenesis of BMSCs and may represent a potential therapeutic target f

210 on observed after systemic administration of BMSCs to MCAO rats is likely due to the cellular changes

211 an in vitro system, and the contributions of BMSCs to myeloma pathogenesis in an intact, immune compe

212 vated during osteoblastic differentiation of BMSCs in vitro.

213 do1 suppresses osteogenic differentiation of BMSCs, through a potential mechanism which involves in W

214 P-2-stimulated osteogenic differentiation of BMSCs.

215 BMP-2-directed osteogenic differentiation of BMSCs.

216 idomide abrogated this stimulatory effect of BMSCs and significantly decreased the percentage of SP c

217 In comparison, the cytotoxic effect of BMSCs on non-activated lymphocytes and on caspase-8(-/-)

218 The beneficial effect of BMSCs was eliminated by macrophage depletion or pretreat

219 not IL-10, reversed the analgesic effect of BMSCs.

220 une regulation without actual engraftment of BMSCs.

221 show that miR-9 is a key paracrine factor of BMSCs attenuating SAP targeting the NF-kappaB1/p50 gene

222 n vivo transplantation (defining features of BMSCs).

223 ver, studies have shown that the majority of BMSCs are trapped in the lungs immediately after intrave

224 e role for NOTCH and the requisite nature of BMSCs following fracture is unknown.

225 The nonadherent population of BMSCs harvested from the long bone diaphysis of KO anima

226 The osteogenic potential of BMSCs treated with these polyplexes was validated by det

227 ed investigation of hepatogenic potential of BMSCs v/s DMSCs (DPSC, SCAP & DFSC) along-with secretome

228 control of the immunoregulatory potential of BMSCs.

229 s a result of bortezomib, in the presence of BMSCs in coculture.

230 ture, which may adversely affect recovery of BMSCs physically associated with the abluminal surface o

231 ta-estradiol (E2) enhanced responsiveness of BMSCs of wild-type and Bag-1(+/-) mice to BMP-2, and pro

232 ollectively, our results show novel roles of BMSCs and BMSC-derived Dkk1 in the pathogenesis of multi

233 The delayed senescence of BMSCs leads to increased bone formation by compensating

234 and culturing an expandable subpopulation of BMSCs with enhanced intestinal homing and contribution t

235 ficantly impaired the growth and survival of BMSCs in vitro and decreased the number of osteoblast (O

236 that SDF-1beta can mediate cell survival of BMSCs in vitro through increasing autophagy.

237 on of connexin 43 (Cx43) via transduction of BMSCs with a lentivirus overcame this problem, enhancing

238 In the capacity of therapeutic use of BMSCs other than structural repair and replacement, more

239 Additional transplants based on BMSC EphB2 expression demonstrated that, at 7 d post-tra

240 We found that SDF-1beta had no effect on BMSC proliferation; however, SDF-1beta significantly pro

241 ufacturing methods used and their effects on BMSC characteristics and function.

242 donor BMSCs displayed a range of effects on BMSCs that were opposite to those cells with overexpress

243 XCL12 receptor CXCR4, which was expressed on BMSCs.

244 The results showed that only BMSCs remitted liver damage and rescued ALF in ConA-trea

245 Here, we evaluated whether NOTCH and/or BMSCs are required for fracture repair by performing non

246 giva (GMSCs), which has many advantages over BMSCs, can delay or prevent progress of T1DM.

247 Knock-down of XBP1 in MM patient BMSCs greatly compromised their increased VCAM-1 protein

248 SSCs) within the BM stromal cell population (BMSCs, also known as BM-derived mesenchymal stem cells),

249 find both Fas and FasL expression by primary BMSCs.

250 2 levels in MC-4 before OBs or naive primary BMSCs, and Gfi1 induction was blocked by anti-TNF-alpha

251 Treatment of primary BMSCs and lymphoblasts from SDS patients with nocodazole

252 We observed that primary BMSCs and lymphoblasts from SDS patients exhibited an in

253 In this process, BMSCs inhibited ConA-induced inflammatory response by de

254 J subchondral BMSCs enhanced by UAC promoted BMSCs to increase Cxcl12 and Rankl expression, in which

255 Purified BMSC populations devoid of hematopoietic contamination a

256 isoform, plays a critical role in regulating BMSC survival under oxidative stress through increasing

257 Human ASCs (hASC) and rhesus BMSCs (rBMSC) underwent significantly more total populat

258 CD73)(+) ENG(-) (CD105)(-) LY6A(+) (SCA1)(+) BMSC subpopulation.

259 Microarray profiles of control and siTERC-BMSCs showed decreased hematopoietic factors at the mess

260 findings are consistent with defects in SSCs/BMSCs contributing to BM failure in TBD.

261 that Wnt5a/Ror2 signaling in TMJ subchondral BMSCs enhanced by UAC promoted BMSCs to increase Cxcl12

262 Moreover, i.t. BMSCs reduced CCI-induced spontaneous pain and axonal in

263 support a paracrine mechanism by which i.t. BMSCs target CXCL12-producing DRGs to elicit neuroprotec

264 TERC-RNA (siTERC-RNA) recapitulated the TBD-BMSC phenotype by reducing proliferation and secondary c

265 TBD-BMSCs exhibited reduced clonogenicity, spontaneous diffe

266 Upon in vivo transplantation into mice, TBD-BMSCs failed to form bone or support hematopoiesis, unli

267 (DPSC-MG) induced more vessel formation than BMSC-MG.

268 Many of the studies concluded that BMSC-driven immunomodulation is mediated by the suppress

269 ng an aptamer delivery system, we found that BMSC-specific overexpression of miR-188 in mice reduced

270 These results demonstrated that BMSCs and adult HCs are the optimal sources of CBTs for

271 mmunohistochemical results demonstrated that BMSCs can recruit from peripheral circulation and partic

272 We found that BMSCs from both MM-bearing mice and MM patients had incr

273 Here, we test the hypothesis that BMSCs suppress immune responses by Fas-mediated apoptosi

274 Furthermore, we investigate that BMSCs deliver miR-9 to the injured pancreas or periphera

275 s the first evidence, to our knowledge, that BMSCs protect against ALI by restituting alveolar bioene

276 Our results suggest that BMSCs (activated by LPS or TNF-alpha) reprogram macropha

277 Emerging preclinical studies suggest that BMSCs may protect against infectious challenge either by

278 Reducing Ror2 expression in the BMSC cell line by siRNA or blocking the downstream signa

279 strated a suppression of the capacity of the BMSC cell line to promote Wnt5a-dependent migration (inc

280 lls, some of which might be recruited by the BMSCs.

281 study, we found that XBP1s is induced in the BMSCs of the MM microenvironment.

282 d/or IL-13 activate the STAT6 pathway in the BMSCs resulting in an increase of their TGF-beta product

283 avage from ragweed challenged animals on the BMSCs in vitro.

284 receptor tyrosine kinase Axl directly to the BMSCs in association with AKT activation.

285 These BMSCs showed an increased CXCL12 protein expression leve

286 Thus BMSCs may have an endogenous mechanism to evade Fas-medi

287 in beta7/alphaE-mediated myeloma adhesion to BMSCs, and -vascular endothelial growth factor-induced b

288 o Furthermore, upon in vivo transplantation, BMSC pellets remodelled into miniature bone/marrow organ

289 Transplanted BMSCs often fail to engraft within the bone marrow (BM),

290 le for the impaired survival of transplanted BMSCs.

291 hesion and migration compared with wild type BMSCs.

292 that XBP1s is a pathogenic factor underlying BMSC support of MM cell growth and osteoclast formation

293 explore the mechanism of the effect we used BMSCs isolated from a variety of knockout mice, performe

294 y discovered cellular therapy approach using BMSCs.

295 But there exists much difficulty in using BMSCs as a clinical therapy.

296 rences in manufacturing resulted in variable BMSC characteristics including their ability to form bon

297 Vnn1(-/-) BMSCs demonstrated delayed chondrogenesis mediated by in

298 When BMSCs were injected i.v. at the time of the antigen chal

299 e IL-10 when prepared from mice treated with BMSCs versus untreated mice.

300 ion of prominent differentiation genes in WT BMSCs.