Abstract
Objectives: Murine macrophages were playing a key role against microbes and foreign particles as well as help in solid tumorigenesis in the host body. In this experiment we were trying to evaluate the protein tyrosine kinase (PTK) activity in macrophages from experimentally induced leukemic animal model.Methods: Balb/C mice were divided into four groups, two groups were challenged with N-N ethyl nitrosourea (ENU) and two groups remained without ENU challenged condition. After confirmation of leukemia induction, one normal and one ENU challenged groups were received rmIL-3 for 4 days followed by rmGM-CSF for 4 days. Disease was confirmed by histological studies of peripheral blood and bone marrow smear. PTK activity assay were done using universal protein tyrosine assay kit.Results: Protein tyrosine kinase (PTK) activity of macrophages was increased in leukemic animal significantly which were reduced after combination of IL-3 and GM-CSF treatment. IFN- ? level in blood serum were increased in leukemic mice and reduced after treatment as normal level. Conclusion: Results suggest that, in leukemia reduced macrophage number can be increased by IL-3 and GM-CSF administration in combination but PTK activity is not involved to increase the number of macrophages. PTK activity may be involved in macrophage activation process in Leukemic animal.
Highlights
Protein tyrosine kinase is the key protein for cell signaling pathway including receptor tyrosine kinase (RTK) and non-receptor tyrosine kinase (NRTK)
The total leukocyte count was much higher (Fig: 2) compared to control group after 5 months of ethyl nitrosourea (ENU) injection which was the other evidence of leukemia induction by conventional method of diagnosis
This may suggest that macrophage activation followed through induction of IFN-γ which up-regulate the protein tyrosine kinase (PTK) activity [22]
Summary
Protein tyrosine kinase is the key protein for cell signaling pathway including receptor tyrosine kinase (RTK) and non-receptor tyrosine kinase (NRTK). NRTKs are either attached with cytoplasmic portion of receptors or in the cytoplasm which mediate signals upon stimulation from membrane receptor. Activation of this enzyme leads to proliferation, differentiation, metabolism, vasculogenesis, T-cell and B-cell activation, apoptosis etc. In general this enzyme prevents the deregulating proliferation signal, but in cancer cells altered signals are dominated to establish proliferation resulting defective signaling network[1]
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