Correction to: J Transl Med (2018) 16:117 https://doi.org/10.1186/s12967-018-1493-8
Following publication of the original article [1], the authors reported errors in Fig. 5a, e. The GAPDH band in Fig. 5a was duplicated with Fig. 4b GAPDH band. In Fig. 5e, the sham picture (Cx32+/+, sham, GRP78) and the sham pictures (Cx32−/−, sham, GRP78, CHOP) were duplicated. The correct version of Fig. 5 is given below.
Cx32 gene deletion mitigated I/R-induced ROS generation and ERS activation. a, b Renal I/R induced the alteration of Cx32 protein expression was detected by western blotting analysis. n = 6, *p < 0.05 vs Sham group. c Cx32 gene deletion significantly alleviated ROS production and distribution (magnification ×200). d–f Cx32 gene deletion significantly alleviated I/R (24 h)-induced GRP78, XBP1and CHOP expression increase. Changes of GRP78, XBP1and CHOP expressions were determined by western blotting analysis. Immunofluorescence staining (magnification ×400; red: GRP78 and XBP1; green, CHOP; blue: the nuclear labeled by DAPI) and immunohistochemistry (magnification ×400)
Reference
Gu Y, Huang F, Wang Y, Chen C, Wu S, Zhou S, Hei Z, Yuan D. Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury. J Transl Med. 2018;16:117. https://doi.org/10.1186/s12967-018-1493-8.
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Gu, Y., Huang, F., Wang, Y. et al. Correction to: Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury. J Transl Med 18, 212 (2020). https://doi.org/10.1186/s12967-020-02375-z
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DOI: https://doi.org/10.1186/s12967-020-02375-z