内质网
未折叠蛋白反应
线粒体
细胞生物学
氧化应激
莱菔硫烷
钙信号传导
化学
平衡
抗氧化剂
生物化学
生物
信号转导
作者
Alejandro Silva-Palacios,Arana-Hidalgo Dana,Colín-Val Zaira,Vicente Castrejón-Téllez,Castro-Soria Elizabeth,José Pedraza-Chaverri,López-Marure Rebeca,Cecilia Zazueta
标识
DOI:10.1016/j.cbi.2023.110616
摘要
Mitochondria-endoplasmic reticulum (ER) communication relies on platforms formed at the ER membrane with the mitochondrial outer membrane contact sites (MERCs). MERCs are involved in several processes including the unfolded protein response (UPR) and calcium (Ca2+) signaling. Therefore, as alterations in MERCs greatly impact cellular metabolism, pharmacological interventions to preserve productive mitochondrial-ER communication have been explored to maintain cellular homeostasis. In this regard, extensive information has documented the beneficial and potential effects of sulforaphane (SFN) in different pathological conditions; however, controversy has arisen regarding the effect of this compound on mitochondria-ER interaction. Therefore, in this study, we investigated whether SFN could induce changes in MERCs under normal culture conditions without damaging stimuli. Our results indicate that non-cytotoxic concentration of 2.5 μM SFN increased ER stress in cardiomyocytes in conjunction with a reductive stress environment, that diminishes ER-mitochondria association. Additionally, reductive stress promotes Ca2+ accumulation in the ER of cardiomyocytes. These data show an unexpected effect of SFN on cardiomyocytes grown under standard culture conditions, promoted by the cellular redox unbalance. Therefore, it is necessary to rationalize the use of compounds with antioxidant properties to avoid triggering cellular side effects.
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