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. 2018 Feb 1;7(1):2–9. doi: 10.1089/biores.2017.0049

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© Zhi-Yang Xie et al. 2018; Published by Mary Ann Liebert, Inc.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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FIG. 2. — (A) Compared with the two control groups, expression of ASIC1a was notably downregulated in the siASIC1a group. (B) Ca²⁺ imaging demonstrated that intracellular Ca²⁺ concentration significantly increased in response to the acidic extracellular solution (acid) containing Ca²⁺. (C) Ca²⁺imaging indicated by Fura-2/AM at the indicated time. Acidic incubation (pH 6.5) failed to increase [Ca²⁺]_i in the siASIC1a cells. (D, E) NPCs were incubated with acidity of pH 7.2 or 6.5 for 24 h (flow cytometry). Apoptotic cells = early apoptotic cells (lower right)+late apoptotic cells (upper right). Acid exposure induced apoptosis of rat NPCs. The ER stress inhibitor 4-PBA significantly promoted the apoptosis rate of NPCs under acid stimulus. ASIC1a knockdown reduced acid-induced apoptosis of NPCs, even in the presence of 4-PBA. **p < 0.01. ER, endoplasmic reticulum. 4-PBA, 4-phenylbutyrate.