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Published Erratum
. 2022 Mar 8;119(10):e2200781119.
doi: 10.1073/pnas.2200781119. Epub 2022 Mar 4.

Correction for Tang et al., Neural transcription factor Pou4f1 promotes renal fibrosis via macrophage-myofibroblast transition

No authors listed
Published Erratum

Correction for Tang et al., Neural transcription factor Pou4f1 promotes renal fibrosis via macrophage-myofibroblast transition

No authors listed. Proc Natl Acad Sci U S A. .
No abstract available

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Figures

Fig. 6.
Fig. 6.
Silencing of Pou4f1 in BMDM inhibits MMT in an adoptive transfer version of the UUO model. A day 5 UUO model was performed in LysM-Cre/DTR mice. Mice were treated with diptheria toxin (DT) for 3 d before UUO surgery to deplete macrophages. At 6 h after UUO surgery, mice were injected with either Pou4f1-knockdown (siPou4f1) or nonsense siRNA-treated (NC) BMDMs (2 × 106 cells/mouse) which had a 24-h stimulation with TGF-β1 (5 ng/mL) in culture prior to injection. (A) Immunostaining for Pou4f1 (Upper) and confocal microscopy for α-SMA (green) and F4/80 (red) (power panel), show that compared to the UUO control, DT treatment depleted both F4/80+ macrophages and Pou4f1+ interstitial cells. Both populations were restored by adoptive transfer with NC-BMDMs, while transfer of siPou4f1-BMDMs restored the F4/80+ macrophage population but not the interstitial Pou4f1+ cells on day 5 UUO. (B) Flow cytometry analysis shows that DT-induced macrophage depletion reduced both the total α-SMA+ myofibroblast population and SMA+CD68+ MMT cells. While NC-BMDM transfer restored both of these populations, the transfer of siPou4f1-BMDMs failed to achieve this. Data represent results from six mice/group. **P < 0.01, ***P < 0.001 vs. sham control; ##P < 0.01, ###P < 0.001 vs. UUO; @@P < 0.01, @@@P < 0.001 vs. adoptive transfer of NC-BMDMs under macrophage depletion (NC-BMDM). (Scale bars, 50 μm.)
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