Skip to main content
. 2013 Jan-Mar;3(1):31–49. doi: 10.4103/2045-8932.109912

Figure 7.

Figure 7

The canonical WNT pathway regulates lung MSC phenotype and function in response to oxidative stress, driving myofibroblast transdifferentiation. WT and EC-SOD KO lung MSCs and lung FB were isolated from mouse lungs by flow cytometry and expanded in culture. cDNA from each sample was hybridized to Affymetrix mouse whole genome microarrays. (A) Principal component analysis of array data showing clustering of cell populations WT lung MSCs (SP1, 2) and EC SOD KO lung MSCs (SOD KO 1, 2) separate from lung FB (FB1, 2). Supervised hierarchical cluster analysis of genes involved in WNT or TGFb signaling and stemness, following normalization of all data sets. Two independently isolated pooled cultures of WT and KO lung MSCs (n = 2) or lung FB (n = 2) were used for these analyses. (B-D) Quantitative PCR was performed to validate gene expression patterns in isolated lung MSCs identified by microarray analysis. (E) Quantitative PCR was performed to analyze changes in WT versus EC-SOD KO lung MSC gene expression in response to standard conditions (21%; black) or relative hypoxia (6% oxygen; blue) exposure over a period of 72 h; n = 3, 3, 3. (F) Quantitative PCR was performed to detect differences in gene expression in murine lung tissue following room air (black) or hypobaric hypoxia (blue) exposure; n = 3, 3, 3. **Indicates a difference between room air and hypoxia exposed in the same group.