Cigarette Smoke Exposure Alters mSin3a and Mi-2α/β Expression; implications in the control of pro-inflammatory gene transcription and glucocorticoid function

Table 1 Lung HDAC2 activity and KC expression in smoke-exposed mice [21]

	wt			PI3Kγ^-/-			PI3Kδ^D910/A910
	Sham	Smoke	Smoke + Budesonide	Sham	Smoke	Smoke + Budesonide	Sham	Smoke	Smoke + Budesonide
Lung HDAC-2 activity (% sham)	100	53.4 ± 6.5***	53.6 ± 8.2	100	61.1 ± 6.9***	39.9 ± 3.5##	100	104.6 ± 7.3	124.7 ± 10.5
Lung KC expression (pg/mg protein)	180.1 ± 12.7	1357.2 ± 162.8***	1346.1 ± 98.1	183.5 ± 5.7	1947.1 ± 215.3***	1777.5 ± 192.6	298.2 ± 91.6	2017.5 ± 246.6***	1030.8 ± 49.6###

This table summarises key published data from the cigarette smoke-mediated glucocorticoid insensitive model (20). This data demonstrates that reduction in budensonide-mediated repression of KC is impaired the smoke-exposed animals. Abolition of PI3Kδ, but not γ signalling, restored budesonide function. This coincided with the protection of the activity of the key co-repressor HDAC-2. **p > 0.01, ***p > 0.001 (versus sham control) ##p > 0.01, ###p > 0.001 (versus smoke-exposed without budesonide).

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