Primary glia expressing the G93A-SOD1 mutation present a neuroinflammatory phenotype and provide a cellular system for studies of glial inflammation

Table 1 Cytokine and apoptosis-associated message levels in nontransgenic and G93A-SOD1 astrocyte cultures in the basal (unstimulated) condition and 4 hours following stimulation with 50 U/mL IFNγ, 20 ng/mL TNFα or a combination of both cytokines. Data represent pooled samples from 6 wells in a typical experiment (see Fig. 1). Band intensities were normalized to the sum of GAPDH + L32 message levels prior to comparison between genotypes.

mRNA	Unstimulated G93A-SOD1 as % of unstimulated nonTg	Stimulated message level as % of unstimulated level, within genotypes
		NonTg stimulated with:			G93A-SOD1 stimulated with:
		IFNγ	TNFα	IFNγ + TNFα	IFNγ	TNFα	IFNγ + TNFα
Caspase 8	237	108	98	108	181	177	233
FADD	168	90	114	126	106	114	100
FAF	94	94	87	70	101	100	92
FAP	129	136	103	151	149	128	220
FAS	145	186	622	757	868	777	1392
IL1α	329	136	252	103	100	203	110
IL1β	644	152	1740	1101	161	724	223
IL1-RA	147	157	114	159	180	163	373
IL6	34	148	768	991	1461	1228	2755
IL18	307	221	104	92	199	205	194
IL12p35	341	141	239	263	108	71	103
IL12p40	325	121	137	165	197	94	1402
IFNγ	158	121	480	798	534	605	1792
MIF	70	83	129	133	95	110	108
RIP	159	130	152	225	230	161	258
TNFα	428	700	512	1511	2302	1669	3352
TNF-RI	166	132	99	131	180	112	176
TGFβ1	353	99	122	145	94	116	115
TGFβ3	155	90	96	87	94	132	148
TRADD	182	111	101	125	125	105	115
TRAIL	284	300	458	749	1307	734	1644

ISSN: 1742-2094