Table 1.
Clinical features of patients with aplastic anemia.
Table 2.
Phenotype characteristics of BM-MSCs (n = 11).
Figure 1.
The representative morphology and multiple differentiation capacity of BM-MSCs from AA patients and healthy controls.
The morphology of BM-MSCs was shown after staining with β-tubulin (A). The adipogenic differentiation capacity of BM-MSCs detected by un-staining (B) and positive staining of Oil Red O (C). The osteogenic differentiation capacity of BM-MSCs detected by positive staining of Allizarin Red (D), von Kossa (E) and ALP (F).
Figure 2.
The proliferation and CFU-F capacity of BM-MSCs.
(A) The proliferation rate of BM-MSCs were detected using BrdU-ELISA method after different incubation times. *P<0.05, ***P<0.001. (B) The clonogenic capacity was assessed by colony-forming unit-fibroblast (CFU-F) assay. Data represented mean ± SD (n = 10).
Figure 3.
The apoptosis rate of BM-MSCs from AA patients and healthy controls.
The apoptotic rate of BM-MSCs was assessed with Annexin V Apoptosis Detection Kit (A). The representative dotplots of apoptotic rate of BM-MSCs from healthy controls (B) and AA patients (C). Data represented mean ± SD (n = 10).
Figure 4.
Global view of gene expression profile of BM-MSCs.
Gene expression profile of BM-MSCs was determined using Affymetrix oligoarrays. (A) The scatter plot for two biological replicates. (B) The comparison of cluster data between AA patients and healthy controls. (C) Validation of GeneChip results by quantitative real-time PCR. Data were relative to the amount of GAPDH.
Table 3.
The top 10 differential up-regulated genes expression.
Table 4.
The top 10 differential down-regulated genes expression.
Table 5.
Differential pathways of BM-MSCs between AA and healthy controls.
Table 6.
Differential biological process associated with BM-MSCs.
Figure 5.
Gene expression patterns of BM-MSCs from AA patients in key biological signal pathways.
Gene expression patterns were grouped and displayed in the following categories: cell cycle, cell division, cell proliferation, apoptosis, chemotaxis, immune response, adipogenesis, and hematopoietic cell lineage. Relative genes expression were analyzed and compared between AA patients and healthy controls. Genes differentially expressed in BM-MSCs from AA patients were identified with at least a 2.0-fold change with respect to healthy control pools. The up-regulated genes are shown in red while down-regulated genes are shown in green.