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Published Erratum
. 2021 Jan:63:103073.
doi: 10.1016/j.ebiom.2020.103073. Epub 2021 Jan 6.

Corrigendum to "Endoplasmic reticulum stress is activated in post-ischemic kidneys to promote chronic kidney disease" [EBioMedicine 37 (2018) 269-280]

Shaoqun Shu  1 , Jiefu Zhu  2 , Zhiwen Liu  1 , Chengyuan Tang  1 , Juan Cai  1 , Zheng Dong  3
Affiliations
Published Erratum

Corrigendum to "Endoplasmic reticulum stress is activated in post-ischemic kidneys to promote chronic kidney disease" [EBioMedicine 37 (2018) 269-280]

Shaoqun Shu et al. EBioMedicine. 2021 Jan.
No abstract available

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Figures

Fig 3
Fig. 3
4-PBA and TUDCA suppress post-IRI ER stress in kidney tubules. C57Bl/6 mice (male, 8–10 week old) were subjected to 30 min of unilateral ischemia of left kidney followed by reperfusion for 7 or 14 days. 4-PBA at 20 mg/kg/day, TUDCA at 250 mg/kg/day, or normal saline (NS) was given from day 3 after uIR. Then kidney tissues were collected for biochemical and histological analyses. (a) Representative images of immunohistochemical staining of BiP. Bar = 200 μm. (b) Quantitative analysis of BiP staining. (c) Representative immunoblots of p-PERK, PERK, BiP, CHOP, and GAPDH. GAPDH was used as a loading control. (d) Quantitative analysis of immunoblot signals of p-PERK, BiP and CHOP. For densitometric analysis, the protein level of sham group was arbitrarily set as 1, and the signals of other conditions were normalized with the sham control group to indicate their protein fold changes. (e) Representative images of immunohistochemical staining of CHOP. Arrows point to positive CHOP staining. Bar = 200 μm. (f) Quantitative analysis of CHOP staining. Data are expressed as mean ± SEM. n = 4. *p < 0.05;**p < 0.01;***p < 0.001; ns, not significant.
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