Tumor necrosis factor-alpha promotes survival in methotrexate-exposed macrophages by an NF-kappaB-dependent pathway

Table 1 Cell cycle analysis of BMDM treated with TNF-α or its control, followed by MTX exposure for 24 hr or M-CSF withdrawal for 48 hr*.

	Cell cycle distribution (% of cells)
	sub G0	G0/G1	S	G2/M
Control	3.5 ± 0.5	78.6 ± 2.9	6.0 ± 1.0	10.7 ± 2.7
MTX (10 μM)	7.5 ± 1.0^a	62.7 ± 2.2^a	16.0 ± 1.2^a	12.0 ± 1.2
TNF-α (10 ng/mL)	3.6 ± 0.4	77.0 ± 2.2	7.5 ± 1.7	10.7 ± 2.0
TNF-α + MTX	5.8 ± 0.8^b	65.7 ± 4.8	13.8 ± 3.2	13.1 ± 2.6
M-CSF (30 ng/mL)	1.5 ± 0.4	74.2 ± 2.6	8.4 ± 1.9	13.9 ± 2.2
- M-CSF	15.4 ± 4.1^a	74.7 ± 5.1	2.8 ± 0.7^a	5.5 ± 0.9^a
M-CSF + TNF-α	1.5 ± 0.2	71.8 ± 1.9	9.3 ± 1.3	15.3 ± 2.7
- M-CSF + TNF-α	4.4 ± 2.3^b	82.3 ± 3.7^b	1.9 ± 0.4	9.7 ± 2.7

* Results are mean ± SEM of at least three independent experiments in each case. ^a P < 0.05 compared to controls. ^b P < 0.05 compared to MTX alone or no M-CSF.
BMDM, bone marrow-derived macrophages; M-CSF, macrophage colony stimulating factor; MTX, methotrexate; TNF-α, tumor necrosis factor-alpha.

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