PMID- 12575918
OWN - NLM
STAT- Publisher
LR  - 20191120
IS  - 2058-7384 (Electronic)
IS  - 0394-6320 (Linking)
VI  - 15
IP  - 3
DP  - 2002 Sep-Dec
TI  - Effect of monocyte chemoattractant protein-1 on murine bone marrow cells: 
      proliferation, colony-forming ability and signal transduction pathway involved.
PG  - 183-194
AB  - Monocyte chemoattractant protein-1 (MCP-1) plays a crucial role in the migration 
      and activation of leukocytes in both physiological and pathological contexts. In 
      this paper, we report the in vitro effect of MCP-1 on myeloid haematopoiesis. 
      MCP-1-treated murine nonadherent bone marrow cells (NABMCs) were assayed for in 
      vitro proliferation and colony forming ability. It is observed that MCP-1 
      treatment in vitro caused an enhancement in the proliferation and colony forming 
      ability of the murine NABMCs as compared to the untreated cells. This response 
      was concentration-dependent and most effective at a dose of 100ng/ml MCP-1. In 
      the presence of MCSF (200U/ml), GCSF (200U/ml), GMCSF (200U/ml) or IL-3 
      (200U/ml), the MCP-1-induced colony forming ability of the NABMCs was 
      significantly augmented, indicating a synergistic effect of MCP-1 with these 
      CSFs. However, irrespective of the CSFs used, MCP-1 stimulated the 
      lineage-restricted differentiation of the murine BMCs into predominantly the 
      granulocytic lineage. NABMCs cultured in medium alone formed minimal colonies. 
      The probable signal transduction mechanism responsible for the MCP-1-induced 
      NABMC proliferation/differentiation was also investigated. The results of the 
      colony forming assay indicate that the protein kinase inhibitors, genistein 
      (10&mgr;g/ml), chelenthryin chloride (10&mgr;M), wortmannin (200nM) and PD98059 
      (10&mgr;M) significantly blocked the in vitro colony forming ability of the 
      MCP-1-treated NABMCs, while the phosphatase inhibitors, okadaic acid (10nM) and 
      sodium orthovanadate (10&mgr;M) caused an increase in the BMC colony forming 
      ability in response to MCP-1. These data suggests the involvement of the 
      respective protein kinases and phosphatases in the above process. Correlating 
      with this, the role of several signaling molecules likes Lyn, p42/44MAPK, PI3K 
      and STAT5 has also been implicated in the signal cascade of murine NABMC 
      proliferation/differentiation following MCP-1 treatment.
FAU - Biswas, S K
AU  - Biswas SK
AD  - School of Biotechnology, Banaras Hindu University, Varanasi, India.
FAU - Sodhi, A
AU  - Sodhi A
LA  - eng
PT  - Journal Article
PL  - England
TA  - Int J Immunopathol Pharmacol
JT  - International journal of immunopathology and pharmacology
JID - 8911335
EDAT- 2003/02/11 04:00
MHDA- 2003/02/11 04:00
CRDT- 2003/02/11 04:00
PHST- 2003/02/11 04:00 [pubmed]
PHST- 2003/02/11 04:00 [medline]
PHST- 2003/02/11 04:00 [entrez]
AID - 4 [pii]
AID - 10.1177/039463200201500304 [doi]
PST - ppublish
SO  - Int J Immunopathol Pharmacol. 2002 Sep-Dec;15(3):183-194. doi: 
      10.1177/039463200201500304.