PMID- 15797995
OWN - NLM
STAT- MEDLINE
DCOM- 20050818
LR  - 20210206
IS  - 0006-4971 (Print)
IS  - 1528-0020 (Electronic)
IS  - 0006-4971 (Linking)
VI  - 106
IP  - 2
DP  - 2005 Jul 15
TI  - Transforming growth factor-beta1 modulates responses of CD34+ cord blood cells 
      to stromal cell-derived factor-1/CXCL12.
PG  - 485-93
AB  - Disruption of stromal cell-derived factor-1 (SDF-1/CXCL12 [CXC chemokine ligand 
      12]) interaction leads to mobilization of stem/progenitor cells from bone marrow 
      to circulation. However, prolonged exposure of CD34+ cells to SDF-1 desensitizes 
      them to SDF-1. So how do cells remain responsive to SDF-1 in vivo when they are 
      continuously exposed to SDF-1? We hypothesized that one or more mechanisms 
      mediated by cytokines exist that could modulate SDF-1 responsiveness of CD34+ 
      cells and the desensitization process. We considered transforming growth 
      factor-beta1 (TGF-beta1) a possible candidate, since TGF-beta1 has effects on 
      CD34+ cells and is produced by stromal cells, which provide niches for 
      maintenance and proliferation of stem/progenitor cells. TGF-beta1 significantly 
      restored SDF-1-induced chemotaxis and sustained adhesion responses in cord blood 
      CD34+ cells preexposed to SDF-1. Effects of TGF-beta1 were dependent on the dose 
      and duration of TGF-beta1 pretreatment. Phosphorylation of extracellular 
      signal-regulated kinase 1 (Erk1)/Erk2 was implicated in TGF-beta1 modulation of 
      migratory and adhesion responses to SDF-1. Our results indicate that low levels 
      of TGF-beta1 can modulate SDF-1 responsiveness of CD34+ cells and thus may 
      facilitate SDF-1-mediated retention and nurturing of stem/progenitor cells in 
      bone marrow.
FAU - Basu, Sunanda
AU  - Basu S
AD  - Department of Microbiology and Immunology, Walther Oncology Center, Indiana 
      University School of Medicine, Research Institute No. 2 Bldg, Rm 302, 950 W 
      Walnut St, Indianapolis, IN 46202-5181, USA. sunbasu@iupui.edu
FAU - Broxmeyer, Hal E
AU  - Broxmeyer HE
LA  - eng
GR  - R01 DK 53674/DK/NIDDK NIH HHS/United States
GR  - R01 HL 56416/HL/NHLBI NIH HHS/United States
GR  - R01 HL 67384/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20050329
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Actins)
RN  - 0 (Antigens, CD34)
RN  - 0 (CXCL12 protein, human)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Receptors, CXCR4)
RN  - 0 (TGFB1 protein, human)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Actins/metabolism
MH  - Antigens, CD34/metabolism
MH  - Calcium/metabolism
MH  - Cell Adhesion/drug effects
MH  - Chemokine CXCL12
MH  - Chemokines, CXC/*pharmacology
MH  - Chemotaxis/drug effects
MH  - Colony-Forming Units Assay
MH  - Fetal Blood/*cytology/*drug effects/immunology/physiology
MH  - Hematopoiesis/drug effects
MH  - Humans
MH  - In Vitro Techniques
MH  - Infant, Newborn
MH  - MAP Kinase Signaling System/drug effects
MH  - Receptors, CXCR4/metabolism
MH  - Transforming Growth Factor beta/*pharmacology
MH  - Transforming Growth Factor beta1
PMC - PMC1895172
EDAT- 2005/03/31 09:00
MHDA- 2005/08/19 09:00
PMCR- 2006/07/15
CRDT- 2005/03/31 09:00
PHST- 2005/03/31 09:00 [pubmed]
PHST- 2005/08/19 09:00 [medline]
PHST- 2005/03/31 09:00 [entrez]
PHST- 2006/07/15 00:00 [pmc-release]
AID - S0006-4971(20)53270-9 [pii]
AID - 01060485 [pii]
AID - 10.1182/blood-2004-10-4145 [doi]
PST - ppublish
SO  - Blood. 2005 Jul 15;106(2):485-93. doi: 10.1182/blood-2004-10-4145. Epub 2005 Mar 
      29.