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Biswas SK, Sodhi A. Effect of monocyte chemoattractant protein-1 on murine bone marrow cells: proliferation, colony-forming ability and signal transduction pathway involved. Int J Immunopathol Pharmacol. 2002;15(3):183-194doi: 10.1177/039463200201500304.
Biswas, S. K., & Sodhi, A. (2002). Effect of monocyte chemoattractant protein-1 on murine bone marrow cells: proliferation, colony-forming ability and signal transduction pathway involved. International journal of immunopathology and pharmacology, 15(3), 183-194. https://doi.org/10.1177/039463200201500304
Biswas, S. K., and Sodhi, A.. "Effect of monocyte chemoattractant protein-1 on murine bone marrow cells: proliferation, colony-forming ability and signal transduction pathway involved." International journal of immunopathology and pharmacology vol. 15,3 (2002): 183-194. doi: https://doi.org/10.1177/039463200201500304
Biswas SK, Sodhi A. Effect of monocyte chemoattractant protein-1 on murine bone marrow cells: proliferation, colony-forming ability and signal transduction pathway involved. Int J Immunopathol Pharmacol. 2002 Sep-Dec;15(3):183-194. doi: 10.1177/039463200201500304. PMID: 12575918.
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Int J Immunopathol Pharmacol. 2002 Sep-Dec;15(3):183-194. doi: 10.1177/039463200201500304.

Effect of monocyte chemoattractant protein-1 on murine bone marrow cells: proliferation, colony-forming ability and signal transduction pathway involved.

International journal of immunopathology and pharmacology

S. K. Biswas, A. Sodhi

Affiliations

  1. School of Biotechnology, Banaras Hindu University, Varanasi, India.

PMID: 12575918 DOI: 10.1177/039463200201500304

Abstract

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.

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