PMID- 9808151
OWN - NLM
STAT- MEDLINE
DCOM- 19981125
LR  - 20091119
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 177
IP  - 3
DP  - 1998 Dec
TI  - Receptor tyrosine kinase expression in human bone marrow stromal cells.
PG  - 426-38
AB  - Bone marrow stromal cells (BMSCs) are a heterogeneous population of cells derived 
      from colony-forming units-fibroblastic (CFU-Fs). These cells reside in the bone 
      marrow cavity and are capable of differentiating into several cell phenotypes 
      including osteoblasts, chondroblasts, hematopoiesis-supporting stromal cells, and 
      adipocytes. However, the factors that regulate the proliferation and 
      differentiation of the BMSC population are for the most part unknown. Since many 
      members of the receptor tyrosine kinase (RTK) family have been shown to 
      participate in growth control of various mesenchymal cell populations, in this 
      study we examined the expression and function of RTKs in the BMSC population. 
      Degenerate oligonucleotides corresponding to two conserved catalytic domains of 
      the RTK family and RT-PCR were used initially to determine which RTKs are 
      expressed in the human BMSC (hBMSC) system. After subcloning the amplification 
      product generated from mRNA of a multicolony-derived hBMSC strain, PDGF receptor 
      (beta), EGF receptor, FGF receptor 1, and Axl were identified by DNA sequencing 
      of 26 bacterial colonies. Furthermore, PDGF and EGF were found to enhance BMSC 
      growth in a dose-dependent manner and to induce tyrosine phosphorylation of 
      intracellular molecules, including the PDGF and EGF receptors themselves, 
      demonstrating the functionality of these receptors. On the other hand, bFGF was 
      found to have little effect on proliferation or tyrosine phosphorylation. Since 
      single colony-derived hBMSC strains are known to vary from one colony to another 
      in colony habit (growth rate and colony structure) and the ability to form bone 
      in vivo, the expression levels of these RTKs were determined in 18 hBMSC clonal 
      strains by semiquantitative RT-PCR and were found to vary from one clonal strain 
      to another. While not absolutely predictive of the osteogenic capacity of 
      individual clonal strains, on average, relatively high levels of PDGF-receptor 
      were found in bone-forming strains, while on average, nonbone-forming strains had 
      relatively high levels of EGF-receptor. Taken together, these results indicate 
      that RTKs play a role in the control of hBMSC proliferation, and that the 
      differential pattern of RTK expression may be useful in correlating the 
      biochemical properties of individual clonal strains with their ability to produce 
      bone in vivo.
FAU - Satomura, K
AU  - Satomura K
AD  - Craniofacial and Skeletal Diseases Branch, National Institute of Dental Research, 
      National Institutes of Health, Bethesda, Maryland 20892, USA.
FAU - Derubeis, A R
AU  - Derubeis AR
FAU - Fedarko, N S
AU  - Fedarko NS
FAU - Ibaraki-O'Connor, K
AU  - Ibaraki-O'Connor K
FAU - Kuznetsov, S A
AU  - Kuznetsov SA
FAU - Rowe, D W
AU  - Rowe DW
FAU - Young, M F
AU  - Young MF
FAU - Gehron Robey, P
AU  - Gehron Robey P
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Growth Substances)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
SB  - IM
MH  - Bone Marrow Cells/cytology/*metabolism
MH  - Bone Marrow Transplantation
MH  - Cell Division/drug effects
MH  - Cell Line
MH  - Cells, Cultured
MH  - Growth Substances/pharmacology
MH  - Humans
MH  - Osteogenesis/physiology
MH  - Phosphorylation
MH  - RNA, Messenger/metabolism
MH  - Receptor Protein-Tyrosine Kinases/genetics/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Stromal Cells/cytology/*metabolism
OTO - NASA
OT  - Non-programmatic
EDAT- 1998/11/10 03:02
MHDA- 2000/06/20 09:00
CRDT- 1998/11/10 03:02
PHST- 1998/11/10 03:02 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1998/11/10 03:02 [entrez]
AID - 10.1002/(SICI)1097-4652(199812)177:3<426::AID-JCP6>3.0.CO;2-F [pii]
AID - 10.1002/(SICI)1097-4652(199812)177:3<426::AID-JCP6>3.0.CO;2-F [doi]
PST - ppublish
SO  - J Cell Physiol. 1998 Dec;177(3):426-38. doi: 
      10.1002/(SICI)1097-4652(199812)177:3<426::AID-JCP6>3.0.CO;2-F.