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Fig. 7 | BMC Biology

Fig. 7

From: Mesodermal ALK5 controls lung myofibroblast versus lipofibroblast cell fate

Fig. 7

Mesodermal progenitor-specific deletion of Pdgfra. (a and b) Immunohistochemistry showed PDGFRα (red) is lost in the lung mesenchyme and αSMA (green) is decreased in E18.5 Pdgfra Dermo1 lungs. Arrows indicate gaps in αSMA in mutant lungs. “aw” indicates airway. (c) Quantitative PCR (Q-PCR) showed a decrease in mRNA for PDGF signaling target genes, indicating an overall functional repression of the signaling pathway in E18.5 Pdgfra Dermo1 lungs. n = 2 pairs of separate lungs, repeated once for each. (d) Q-PCR showed myofibroblast-related genes are decreased in E18.5 Pdgfra Dermo1 lungs. n = 2 pairs of separate lungs, repeated once. (e) Q-PCR showing only Pparγ is robustly increased among lipofibroblast-related genes in E18.5 Pdgfra Dermo1 lungs. n = 2 pairs of separate lungs, repeated once. (f) Schematic model for ALK5 binary switch function in mesodermal progenitor cell fate determination. TGFβ via ALK5 is a direct activator of Prrx1 (Fig. 5f) a key transcriptional regulator of the αSMApos cell pathway. TGFβ via ALK5 also directly stimulates Pdgfrα mRNA (Fig. 6a), which further promotes αSMApos cell commitment [22]. PRRX1 and PDGFRα are reciprocal activators. In the absence of Alk5, Zfp423, which is normally repressed by TGFβ (Fig. 5l) is de-repressed, leading to activation of Pparγ [28], a transcriptional activator of lipogenic cell commitment. PRRX1 and PDGFRα inhibit adipogenesis by directly repressing PPARγ [44]. Error bars show standard error of the mean. Scale bar: b = 20 μm

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