Intra-arterial Stem Cell Therapy Diminishes Inflammasome Activation After Ischemic Stroke: a Possible Role of Acid Sensing Ion Channel 1a (vol 71, pg 419, 2021)

It has come to our notice that there was an inadvertent misupload of Fig. 2 (c, d) in the loading control (GAPDH) for ASIC1a and NLRP1 blots. We would like to replace the same with the correct image. This change anyhow does not affect the conclusion of the study. However, the use of GAPDH as a loading control for stroke studies sometimes is debatable (Zhai et al. 2014; Kang et al. 2018). Hence, we repeated our experiments to check the expression of ASIC1a and NLRP1 at different time points following stroke, using beta actin as a loading control. We found that at 24 h post stroke, maximal and significant expression of both ASIC1a and NLRP1 was observed (Fig. 2 e, f). The expression at 48 and 72 h post stroke were not significantly different as compared to that of sham. The expression results obtained using beta actin as a loading control were concurrent with the previous results published with GAPDH as a loading control.

Automated summary

The inadvertent misupload of loading control images for ASIC1a and NLRP1 blots was corrected without affecting the study conclusions. Despite the debate over using GAPDH as a loading control, the results obtained with beta-actin as the loading control were consistent with previous findings.