ライフサイエンスコーパス: cell proliferation

1 to determine the effects exerted by NETs on cell proliferation.

2 program whilst limiting lipid production and cell proliferation.

3 r greatest effect by targeting regulators of cell proliferation.

4 to downregulate MET and inhibit human tumor cell proliferation.

5 ression, was responsible for inhibition of T-cell proliferation.

6 that SCD is required for MITF(High) melanoma cell proliferation.

7 /-) MEFs failed to induce ROS and to inhibit cell proliferation.

8 tors led to synergistic inhibition of cancer cell proliferation.

9 t ELK-1 transcriptional activity and promote cell proliferation.

10 endent regulation of glucose consumption and cell proliferation.

11 viable tumor cells, thereby promoting glioma cell proliferation.

12 ther in regulating KSHV-infected endothelial cell proliferation.

13 mmed cell death 1 expression and increased T-cell proliferation.

14 enhanced Akt activity and increased rate of cell proliferation.

15 ly, fisetin also activates genes involved in cell proliferation.

16 d cytokine production and monocyte-induced T-cell proliferation.

17 AKT activation, but there was no increase in cell proliferation.

18 o showed that MBNL3 and KANSL2 do not affect cell proliferation.

19 Dosages of Si above 100 mug/ml decreased cell proliferation.

20 er of WUSCHEL, repressing the maintenance of cell proliferation.

21 sing food intake and promoting adaptive beta-cell proliferation.

22 ition, both of which are linked to increased cell proliferation.

23 arrest, whereas its overexpression promoted cell proliferation.

24 tabolism to meet the demands of uncontrolled cell proliferation.

25 Nav3 demonstrates heightened EGFRvIII-glioma cell proliferation.

26 ations in a cell and play differing roles in cell proliferation.

27 an lymphatic endothelial (HLEC) and melanoma cell proliferation.

28 cs, buffering ROS production, and supporting cell proliferation.

29 and were potentially favored by progressive cell proliferation.

30 lting in inhibition of proline synthesis and cell proliferation.

31 5 mug/ml of Si significantly stimulated hDFC cell proliferation.

32 ins, which then inhibit EBV-associated tumor cell proliferation.

33 in both human and mouse cells, and inhibited cell proliferation.

34 dentified critical nodes that restrict tumor cell proliferation.

35 ural rosette formation and neural progenitor cell proliferation.

36 ap-dependent translation and abrogated tumor cell proliferation.

37 l lymphopenia with impaired T-cell but not B-cell proliferation.

38 R-independent function of PLK1 in regulating cell proliferation.

39 without MAX suggest a major role for MNT in cell proliferation.

40 wed reduction in CD4(+) OVA-specific OT-II T cell proliferation.

41 rease in Akt activity and mammary epithelial cell proliferation.

42 of the chemokine CXCL-11, which suppressed T cell proliferation.

43 s, and knockdowns of PYCR1 lead to decreased cell proliferation.

44 iferation, and SMAD7 overexpression enhanced cell proliferation.

45 retion of extracellular matrix proteins, and cell proliferation.

46 , reduced glycolysis, and ultimately reduced cell proliferation.

47 cal regulators of insulin secretion and beta cell proliferation.

48 ing biosynthetic intermediates necessary for cell proliferation.

49 tion blocks glucose-induced fibrogenesis and cell proliferation.

50 cial role in pregnancy-induced maternal beta-cell proliferation.

51 to their ability to reduce inflammation and cell proliferation.

52 ne transport and a reduction in meristematic cell proliferation.

53 g MMP3 significantly reduced S100A9-mediated cell proliferation.

54 , impacts on either ERalpha binding or MCF-7 cell proliferation.

55 ported to regulate inflammatory response and cell proliferation.

56 tes alternative splicing and controls cancer cell proliferation.

57 and thereby couples protein production with cell proliferation.

58 by 2.8-fold and significantly inhibited U251 cell proliferation.

59 pendent factor(s) which regulate the myeloid cells proliferation.

60 Here, we explored sex differences in (a) cell proliferation (5'-bromo-2'-deoxyuridine [BrdU]), (b

61 Assessment of cell proliferation across zebrafish embryo segmentation,

62 Methods: Inhibition of cell proliferation after incubation of the RPMI8226 cell

63 r localization of mitochondria and decreased cell proliferation, altered expression levels of pyruvat

64 on showed that Pten mutants have increased B-cell proliferation and a proclivity towards increased T-

65 Cell proliferation and actomyosin contractility dominate

66 After knocking down RSK1 or MSK2, cell proliferation and anchorage-independent cell growth

67 we investigated the effects of IL2RA on AML cell proliferation and apoptosis, and on pertinent signa

68 here enzymatic inactivation of IKBKE reduced cell proliferation and AR expression.

69 Indeed, to support cell proliferation and biomass production, the clock may

70 ailability in vitro severely inhibited CD4 T cell proliferation and cell cycle progression.

71 e features and "M1" high tumors enriched the cell proliferation and cell cycle related gene sets in G

72 number is determined by the balance between cell proliferation and cell death.

73 d with an increase in vascular smooth muscle cell proliferation and changes in vessel morphology and

74 ogical inhibition of CSNK1A1 attenuates PDAC cell proliferation and clonogenic growth.

75 cinoma cells and counteracts the decrease in cell proliferation and colony formation caused by UV-ind

76 elial invagination, and decreases progenitor cell proliferation and dental epithelium cell differenti

77 tance, NCoR1 and SMRT regulate neuronal stem cell proliferation and differentiation during brain deve

78 , including the Hippo pathway which controls cell proliferation and differentiation in eukaryotes.

79 cience that type III IFNs disrupt epithelial cell proliferation and differentiation in the lung.

80 Prostate development depends on balanced cell proliferation and differentiation, and acetylated K

81 cytoskeletal organization and cell polarity, cell proliferation and differentiation, intracellular me

82 s an important epigenetic reader involved in cell proliferation and differentiation.

83 HDL-associated increases in prostate cancer cell proliferation and disease progression.

84 iR-133b targets as well as genes involved in cell proliferation and fibrosis.

85 gamma (IFNgamma), two factors critical for T cell proliferation and function.

86 t checkpoint inhibitor treatment increased T cell proliferation and functionality, but its influence

87 several cell lines, GLS2 knockdown decreased cell proliferation and glutamine-linked metabolic phenot

88 tion of monounsaturated PC with hallmarks of cell proliferation and hepatic carcinogenesis.

89 Cell proliferation and immune activity pathways were enr

90 ciency of ATG5-dependent autophagy reduced T-cell proliferation and increased apoptosis following in

91 ses markers of inflammation, DNA damage, and cell proliferation and increases colorectal tumorigenesi

92 factors in cuSCC cell lines suppressed tumor cell proliferation and induced apoptosis.

93 ronic T cell stimulation allowed sustained T cell proliferation and induced genes associated with ste

94 sults demonstrate that RBM10 inhibits cancer cell proliferation and induces apoptosis in part by bloc

95 ss of RIalpha LLPS in normal cells increases cell proliferation and induces cell transformation.

96 PFBS exposure interrupted cell proliferation and invasion in a dose-dependent mann

97 for PHF19 in controlling the balance between cell proliferation and invasiveness in prostate cancer.

98 The coordination of cell proliferation and migration in growing tissues is c

99 naling plays a key role in alphaSMA-positive cell proliferation and migration in PH.

100 mbrane protein angiomotin (AMOT130) controls cell proliferation and migration of many cell types.

101 opment, ciliogenesis, and various aspects of cell proliferation and migration.

102 wth factors and cytokines that enhance tumor cell proliferation and migration.

103 RGS12 in OSCC cells significantly increased cell proliferation and migration.

104 ll cycle pathways and inhibiting lung cancer cell proliferation and migration.

105 in an HIF1alpha-dependent manner, leading to cell proliferation and migration.

106 ular zones provide a platform for progenitor cell proliferation and migration.

107 atenin perturbs adherens junctions, enhances cell proliferation and motility, and decreases dependenc

108 trates a role for the satellite RNA in tumor cell proliferation and movement.

109 ng that these genes reduce neural progenitor cell proliferation and neurite growth.

110 on preferentially expresses genes related to cell proliferation and neuronal development, while Tcf21

111 The Hippo pathway regulates cell proliferation and organ size through control of the

112 estingly, Smoothened agonist-SAG rescued OAF cell proliferation and osteogenic differentiation.

113 (platelet-derived growth factor BB)-induced cell proliferation and particularly migration.

114 y epithelial cells is sufficient to increase cell proliferation and produce an invasive phenotype.

115 ses basal stem cell and crypt injury-induced cell proliferation and promotes colon tumorigenesis in a

116 Cell proliferation and quiescence are intimately coordin

117 ly, its genetic silencing increases melanoma cell proliferation and reduces cell death.

118 (PLD), which promotes both mTORC1-dependent cell proliferation and sphingosine-1-phosphate (S1P)-dep

119 that VEGF A and FGF 2 induced angiogenesis, cell proliferation and steroidogenesis in wild type lute

120 ed both mTORC1 and mTORC2 signals to promote cell proliferation and survival, but also induced an AKT

121 on of a subset of breast cancers by inducing cell proliferation and survival.

122 anscriptional activator of genes involved in cell proliferation and survival.

123 get of rapamycin (mTOR), a critical node for cell proliferation and survival.

124 that regulate cellular processes, including cell proliferation and survival.

125 source by activating endocytosis to sustain cell proliferation and survival.

126 hallmarks and enablers of cancer, including cell proliferation and the response to DNA damage.

127 zymes ODC1 or GOT2 selectively inhibited AML cell proliferation and their downstream products partial

128 inhibition of caspase-3 activation, promotes cell proliferation and Tipe deficiency is associated wit

129 are activated, leading to increased rates of cell proliferation and tissue growth.

130 rposes, the effect of these nanoparticles on cell proliferation and toxicity was evaluated, which cle

131 erexpression also required ABCE1 to maintain cell proliferation and translation.

132 abolic processes that contribute to aberrant cell proliferation and tumorigenesis.

133 nce hedgehog (Hh) signaling regulates cancer cell proliferation and tumorigenicity, Hh inhibitors hav

134 oduced under these conditions promote tumour cell proliferation and turnover and modulate blood vesse

135 substituents, through in vitro assays: MCF-7 cell proliferation and VM7Luc4E2 transactivation.

136 efective amino acid anabolism, reduced T reg cell proliferation, and a rampant autoimmune disorder si

137 pharmacologically and genetically activated cell proliferation, and HCC.

138 ssion enhanced overall MCM2 levels, promoted cell proliferation, and improved the synergistic cytotox

139 action for markers of autophagy, DNA damage, cell proliferation, and inflammation.

140 of E2F signaling for Theileria-induced host cell proliferation, and its potential direct manipulatio

141 se inflammatory genes, as well as EMT, tumor cell proliferation, and migration in vitro and tumor gro

142 onizes cell cycle progression, hematopoietic cell proliferation, and oncogene-induced transformation

143 in response to protein misfolding, oncogenic cell proliferation, and other environmental stresses.

144 ivity is required for PLP production and AML cell proliferation, and pharmacological blockade of the

145 CH-1 KO cells restores proline synthesis and cell proliferation, and suppresses DRP1 expression and m

146 in the body(1), and regulates inflammation, cell proliferation, and tissue regeneration(2-4).

147 ells, including suppression of inflammation, cell proliferation, and wound healing.

148 2 and TMZ alone, and combined experiments of cell proliferation, apoptosis, wound healing assay, as w

149 ed suppressive effects of CB-LDG on CD4(+) T cell proliferation are exclusively due to phagocytosis o

150 on and upregulation of genes associated with cell proliferation as compared to liposomes alone.

151 The RNASeq data identified cell proliferation as the most dysregulated pathway, wit

152 mbinant peptides of Gly-m-Bd-30K by SPOT and cell proliferation assays.

153 lopment of glomerular lesions and glomerular cell proliferation at day 4.

154 dherin and EdU revealed decreased epithelial cell proliferation at the cervical region of the molar i

155 antileishmanial drugs inhibit CD4 and CD8 T cell proliferation at the doses that are not related to

156 the same CD25 Ab permitted CD8(+) effector T cell proliferation before progressing to more widespread

157 e and long-term imaging, we monitored single-cell proliferation before, at the time of, and after tre

158 production of eicosanoids, acting to promote cell proliferation beyond a cell-autonomous manner.

159 Since GH plays a key role in cell proliferation, body growth, and metabolism, our fin

160 affect TGF-beta signaling and modulates beta-cell proliferation but does not appear to alter beta-cel

161 SMI#9 treatment inhibited melanoma cell proliferation but not normal melanocytes.

162 d KLF6 in keratinocytes not only compromised cell proliferation, but also increased inflammation and

163 tivation as a protective response to inhibit cell proliferation, but how extra centrosomes activate t

164 icellular organisms use mitogens to regulate cell proliferation, but how fluctuating mitogenic signal

165 he expansion does not involve an increase in cell proliferation, but rather results from re-specifica

166 repair, chromatin remodeling, apoptosis, and cell proliferation; but it remains unclear whether varia

167 BM10 can induce apoptosis and inhibit cancer cell proliferation by activating p53.

168 y A member 1 (CYP24A1) increases lung cancer cell proliferation by activating RAS signaling and that

169 ) showed that knockdown of IL18RAP inhibited cell proliferation by cell cycle arrest in NKTCL cells.

170 essenger cGAMP, which suppressed endothelial cell proliferation by downregulating YAP1 signaling.

171 ed to control protein acetylation and tumour cell proliferation by inhibiting calcineurin and NFATc3

172 plays a vital role in pregnancy-induced beta-cell proliferation by promoting PL expression in trophob

173 a B and RepoMan independently promote cancer cell proliferation by reducing checkpoint--induced cell-

174 d excellent DYRK1A inhibition and human beta-cell proliferation capability.

175 line, palbociclib treatment had no effect on cell proliferation, cell cycle or apoptosis in the PDXC

176 ferentiation without significantly affecting cell proliferation, cell death, or UPR induction in muri

177 HGF stimulates cell proliferation, cell dispersion, neuronal survival,

178 tal for many physiological processes such as cell proliferation, cell migration, and morphogenesis.

179 Knockdown of GDH1 significantly reduced the cell proliferation, colony formation and tumorigenesis a

180 ed lung endothelial cell and alveolar type 2 cell proliferation.Conclusions: Postnatal rhIGF-1/BP3 tr

181 cluding expression of stalk-cell markers and cell proliferation, consistent with an integral role of

182 Thus, promoting beta-cell proliferation could be one approach toward diabetes

183 novo infection) and mitotic spread (infected cell proliferation), creating a population structure of

184 ltaneously inhibits the STAT3-induced cancer cell proliferation, demonstrating a novel approach in ca

185 via mechanotransduction pathways to control cell proliferation, differentiation and death.

186 cting tissue growth in adults and modulating cell proliferation, differentiation, and migration in de

187 that regulate signaling pathways controlling cell proliferation, differentiation, and survival.

188 developing human brain, likely arising from cell proliferation during mid-neurogenesis.

189 cell survival (e.g. Hipk4) intertwined with cell proliferation (e.g. Scn4b) and cellular senescence

190 e.g., IKZF1 and RUNX3), factors that enhance cell proliferation (e.g., HDGF), or factors that promote

191 Interestingly, MNT was required for cell proliferation even in the absence of MAX.

192 exhibited much stronger Ag-specific CD4(+) T cell proliferation ex vivo.

193 Cell proliferation exerts a high demand on protein synth

194 co analysis was validated ex vivo, through T cell proliferation experiments, proving that the fusion

195 alongside its established role in promoting cell proliferation FASN may also promote invasion.

196 enhanced GABAergic specification and reduced cell proliferation following diminished Wnt signaling in

197 but typical culture conditions only support cell proliferation for 30-40 population doublings (PD),

198 icrobial-derived products in promoting pTreg cell proliferation for re-establishing oral tolerance in

199 one candidate (miR-216a) implicated in beta cell proliferation for subsequent validation by RT-PCR.

200 te that ATG5-dependent autophagy uncouples T-cell proliferation from its effector functions and offer

201 y dynamic cytodifferentiation, body-axis and cell-proliferation gene sets that were further character

202 ypes and induces multiple effects, including cell proliferation, gene expression, protection from apo

203 g lifespan is associated with restriction of cell proliferation, genome instability and aging.

204 ht contribute to behavior later in life when cell proliferation has slowed.

205 ad increased expression of genes involved in cell proliferation, immune responses, and cholesterol bi

206 egulation of Cdk1 is an early driver of cyst cell proliferation in ADPKD due to Pkd1 inactivation.

207 DNA replication is fundamental for cell proliferation in all organisms.

208 tion appears to be needed for optimal cancer cell proliferation in an anchorage-independent manner.

209 pression of TIMP-1, which in turn stimulates cell proliferation in an autocrine manner.

210 type (SASP), which is correlated with cancer cell proliferation in culture and xenograft models.

211 GZMB produced by B cells promoted GZMB(+) B cell proliferation in ERK1/2-dependent manner, facilitat

212 well tolerated and resulted in suppressed T-cell proliferation in in vitro MLR comparable to animals

213 rovide evidence that mutation of Dw2 reduces cell proliferation in internode intercalary meristems, i

214 upregulated Wnt target genes and stimulated cell proliferation in liver but not intestine (which is

215 ked the deleterious effect of cocaine on SVZ cell proliferation in males.

216 d retinal neovascularization and endothelial cell proliferation in OIR.

217 containing proteins that negatively regulate cell proliferation in plants.

218 ted in a significant reduction in epithelial cell proliferation in PSW compared to controls.

219 nitiates a centriole-derived signal to limit cell proliferation in response to centrosome amplificati

220 nockdown of HB-EGF in rat islets blocks beta-cell proliferation in response to glucose ex vivo and in

221 downregulation of PTEN and increase in beta cell proliferation in that group.

222 Grass pollen allergen induced cT(FH)-cell proliferation in the GPA group but not in the NAC g

223 ingly, we found increased pulpal mesenchymal cell proliferation in the presumptive root furcating reg

224 with osimertinib, potently suppressed tumor cell proliferation in vitro and caused tumor regression

225 ockdown of GULP1 in UCB cells promoted tumor cell proliferation in vitro and enhanced tumor growth in

226 Depletion of SFMBT1 abolished ccRCC cell proliferation in vitro and inhibited orthotopic tum

227 knockdown of NTN4 in breast cells increased cell proliferation in vitro and tumor growth in vivo.

228 Exposure to used MWF stimulated murine B-cell proliferation in vitro, a hallmark cell subtype fou

229 y, the addition of periostin enhanced cancer cell proliferation in vitro.

230 it is unclear how this relates to mammalian cell proliferation in vivo.

231 olecular pathway crucial for limiting cancer cell proliferation, in which ABHD5-mediated lipolysis cr

232 this protection is accompanied by decreased cell proliferation, inflammation, steroid biosynthesis,

233 stingly, IL-12 and anti-IL-10 Abs improved T cell proliferation inhibited by AmB.

234 PBFS exposure altered trophoblast cell proliferation/invasion which might be mediated by p

235 Selective targeting of cyst cell proliferation is an effective means of slowing ADPK

236 phosphorylated ERK-mediated KRT5(+)/KRT14(-) cell proliferation, leading to early urothelial regenera

237 Investigation of the mechanism for alpha-cell proliferation led to the description of a conserved

238 ormation, with deregulated cell death and/or cell proliferation, loss of apical-basal polarity, and a

239 miR-21 via miRzip extensively targets tumor cell proliferation, migration and invasion in vitro in a

240 Most interestingly, cell proliferation, migration and nuclear localization o

241 ase activated by collagens that can regulate cell proliferation, migration, adhesion, and remodeling

242 n, progression, and metastasis by regulating cell proliferation, migration, invasion, drug resistance

243 VEC and HMVEC-L), did not affect endothelial cell proliferation, migration, or tube formation.

244 ytotoxic T cells and capable of inhibiting T cell proliferation more than macrophages cultured in low

245 sis includes sequential stages of progenitor cell proliferation, myogenic commitment and differentiat

246 rity) and brain-specific risk genes disrupts cell proliferation, neurogenesis, migration, and cell fa

247 tegrative analyses revealing GNL3's roles in cell proliferation, neuronal functions, and brain phenot

248 ownregulate c-MYC and directly inhibit tumor cell proliferation, NHWD-870 blocks the proliferation of

249 ncreased the expression of CXCR2 ligands and cell proliferation of Cl66 cells.

250 lly, CRC factors contribute significantly to cell proliferation of Ewing sarcoma both in vitro and in

251 ckdown of SREBP1 significantly inhibited the cell proliferation of mutant KRAS-expressing cells.

252 MEOX1 knockdown abolished cell proliferation of p53- and PTEN-deficient TNBC in vi

253 c inhibitor) attenuated colony formation and cell proliferation of skin cancer cells.

254 of CARM1 and PRMT6 inhibitors suppresses the cell proliferation of WT MEFs, suggesting a synergistic

255 idic acid (LPA) have been linked to aberrant cell proliferation, oncogenesis, and metastasis.

256 nesis and reduces oligodendrocyte progenitor cell proliferation (OPC) in the developing SVZ, thereby

257 ion of HuR does not impair neural progenitor cell proliferation or differentiation, but it disturbs t

258 However, T cell proliferation or IL-2 secretion were only triggered

259 these parameters, such as the rate of tumour cell proliferation or sensitivity to hypoxia, can produc

260 ntration there were no detectable effects on cell proliferation or viability.

261 telomeres (P <= 0.05), and reduced rates of cell proliferation (P <= 0.001), with no changes in the

262 No changes in tumor cell proliferation (primary endpoint) or other secondary

263 levels that can vastly change, depending on cell proliferation profiles.

264 of activated B cells (NF-kappaB) signaling, cell proliferation, programmed cell death, and survival

265 fforts to identify molecules to promote beta-cell proliferation, protection, and imaging.

266 tion between IVIG dose and toxin-triggered T-cell proliferation (r = -.67, P < .0001).

267 er, the mechanism of CYP24A1-mediated cancer cell proliferation remains unclear.

268 herapeutic effects of Tris DBA on glomerular cell proliferation, renal inflammation, and immune cells

269 Cytokines that stimulate T cell proliferation, such as interleukin (IL)-15, have be

270 otent antitumor effects, markedly inhibiting cell proliferation, survival, and tumor growth by suppre

271 Moreover, ectopic GLS2 expression rescued cell proliferation, TCA anaplerosis, redox balance, and

272 e short telomeres constitute a road block to cell proliferation, telomere shortening is currently vie

273 er a lincRNA, lincNMR, which regulates tumor cell proliferation through a YBX1-RRM2-TYMS-TK1 axis gov

274 biology, mediating organ size by controlling cell proliferation through the activity of a core kinase

275 ect on cell shape, cytoskeleton tension, and cell proliferation through the Hippo signaling effector

276 d cell proliferation, while SSTR1 KO induced cell proliferation, thus suggesting that HRH1 and SSTR1

277 plays a critical role in regulation of stem cell proliferation, tissue regeneration, and organ size

278 Addition of IL-12 restored T-cell proliferation to baseline levels.

279 om cell structural integrity, signaling, and cell proliferation to cell death.

280 n with RBR plays a role in the inhibition of cell proliferation to establish quiescence.

281 rparts, increasing polygenic drive for blood-cell proliferation traits.

282 The passenger domain of BafA induces cell proliferation, tube formation and sprouting of micr

283 Aberrant SHP2 activity leads to uncontrolled cell proliferation, tumorigenesis, and metastasis.

284 knockdown and NF2 reconstitution suppressed cell proliferation, tumour growth and invasion, both in

285 Remarkably, iron supplementation restores cell proliferation under both pharmacologic and genetic-

286 We show here that AX-024 reduces T cell proliferation upon weak TCR stimulation but does no

287 Blocking cell proliferation via a chemotherapeutic agent 5-fluoro

288 Ghr but not DG, decreased cell proliferation via AMPK activation in cholangiocytes

289 cell-permeable proteomimetic that activates cell proliferation via regulation of the Hippo pathway,

290 In vitro, cell proliferation was not affected by GM2/GD2 expressio

291 a h 2; P < .05), but its ability to induce T-cell proliferation was retained.

292 Kupffer cell proliferation was seen in all patients, and chronic

293 ated genes, indicating that tumor growth and cell proliferation were hormone dependent in addition to

294 multaneously, their ability to promote tumor cell proliferation, which appeared to be mediated via th

295 ears to augment the innate immune system and cell proliferation, which play an important role in the

296 s with the highest MDK levels promoted tumor cell proliferation, which was attenuated after the addit

297 How salamanders accomplish progenitor cell proliferation while faithfully maintaining genomic

298 onsistent with this, PHF19 silencing reduces cell proliferation, while promotes invasive growth and a

299 , HRH1 knockout (KO) significantly inhibited cell proliferation, while SSTR1 KO induced cell prolifer

300 P-induced CSF1R activation and Iba1-positive cell proliferation, without a reduction of the basal Iba