Fig. 5: ANO5 deficit causes [Ca2+]c overload in injured cells without affecting ER stress response. | Cell Death Discovery

Fig. 5: ANO5 deficit causes [Ca2+]c overload in injured cells without affecting ER stress response.

From: Dysregulated calcium homeostasis prevents plasma membrane repair in Anoctamin 5/TMEM16E-deficient patient muscle cells

Fig. 5

a Psuedocolor images showing measurement of [Ca2+]c by Fluo-4 following PM injury in healthy and patient myoblasts. b Time course of Fluo-4 fluorescence (ΔF/F0) in healthy and Ano5 myoblasts. Ano5 patient myoblasts took significantly longer time to clear the [Ca2+]c increases following cell injury than that of healthy myoblasts. Fluo4 fluorescence was calculated for different groups as mentioned and presented as mean ± SEM. N = 36 cells (healthy) and 46 cells (patient) (****p < 0.0001). c–g Analyses of ER stress response in the human myoblasts in basal and induced states. c Western blot image and d densitometric quantification of normalized band intensities (n = 3 independent blots) in untreated healthy and ANO5 patient myoblasts. e Western blot image and f, g kinetic plots of normalized band intensities (n = 3 independent blots; mean ± SEM) for f calnexin and g GRP78 following induction of ER stress for the indicated time periods by treatment with ER calcium modulator thapsigargin (TG)

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