We analyzed the MSC proteome of a group of 12 individuals (six AIS patients and six non-AIS controls) by 2D-DIGE.
Globally, 1658±37 spots (mean ± SD; n = 6, AIS; n = 6, non-AIS controls) were detected on each analytical gel loaded with 50 µg of total protein lysate per sample type (AIS or control).
Therefore, to investigate the molecular mechanism of decreased osteogenic differentiation ability of MSCs and gain an insight into the pathogenesis of AIS, we employed 2D-DIGE and MS-based proteomic approaches to explore the differential protein expression patterns in MSCs of AIS and non-AIS controls.
Treatment groups were as follows: 1) AIS experiment: control, AIS, MS, MS + AIS (n = 3 5 per group); and 2) CIS experiment: control, CIS, MS, MS + CIS (n = 3 5 per group).
These cells from both the AIS and control groups were persistently negative for CD31, CD34, and CD45, but expressed high levels of CD29, CD44, CD73, and CD105 (Figure 1).
The comparison between MSCs from AIS and control groups resulted in the identification of 41 significantly different spots, the locations of which on the 2D gels were labeled with spot ID (Figure 3).
No significant deviation of genotype frequencies from the Hardy-Weinberg equilibrium was noted in the AIS and control groups.
This genetic association study enrolled 192 patients with AIS and 134 controls.
The genotype and allele frequencies of SNP rs708567 in the AIS patients and controls are shown in Table 2.
The differences in genotype distributions and allelic frequencies between AIS patients and controls were examined using the χ2 test.
Immunofluorescent examination of Nav1.1 colocalization with PV and ankyrin-G, a marker for AISs, in P21.5 Scontrolsl confirmed confirmarkedrked Nav1.1 immunopositivity in AISs of neocortical PV cells (Fig. 9O), reported previously at P14 16 (15).
