Erratum to “Mitochondrial Rieske iron-sulfur protein in pulmonary artery smooth muscle: A key primary signaling molecule in pulmonary hypertension. [Archives of Biochemistry and Biophysics 664 (2019) 68–75]”

2020 ◽  
Vol 683 ◽  
pp. 108232
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Signaling Molecule ◽  
Iron Sulfur ◽  
Sulfur Protein ◽  
Iron Sulfur Protein ◽  
Pulmonary Artery Smooth Muscle ◽  
Rieske Iron Sulfur Protein

scholarly journals Endoplasmic reticulum Ca2+ release causes Rieske iron–sulfur protein-mediated mitochondrial ROS generation in pulmonary artery smooth muscle cells

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Dapeng Dong ◽  
Qiongyu Hao ◽  
Ping Zhang ◽  
Tao Wang ◽  
Fei Han ◽  
...  
Keyword(s):  
Cellular Responses ◽  
Ros Generation ◽  
Ros Production ◽  
Induced Responses ◽  
Iron Sulfur ◽  
Mitochondrial Ros ◽  
Sulfur Protein ◽  
Iron Sulfur Protein ◽  
Pulmonary Artery Smooth Muscle ◽  
Rieske Iron Sulfur Protein

Abstract Mitochondrial reactive oxygen species (ROS) cause Ca2+ release from the endoplasmic reticulum (ER) via ryanodine receptors (RyRs) in pulmonary artery smooth muscle cells (PASMCs), playing an essential role in hypoxic pulmonary vasoconstriction (HPV). Here we tested a novel hypothesis that hypoxia-induced RyR-mediated Ca2+ release may, in turn, promote mitochondrial ROS generation contributing to hypoxic cellular responses in PASMCs. Our data reveal that application of caffeine to elevate intracellular Ca2+ concentration ([Ca2+]i) by activating RyRs results in a significant increase in ROS production in cytosol and mitochondria of PASMCs. Norepinephrine to increase [Ca2+]i due to the opening of inositol 1,4,5-triphosphate receptors (IP3Rs) produces similar effects. Exogenous Ca2+ significantly increases mitochondrial-derived ROS generation as well. Ru360 also inhibits the hypoxic ROS production. The RyR antagonist tetracaine or RyR2 gene knockout (KO) suppresses hypoxia-induced responses as well. Inhibition of mitochondrial Ca2+ uptake with Ru360 eliminates N- and Ca2+-induced responses. RISP KD abolishes the hypoxia-induced ROS production in mitochondria of PASMCs. Rieske iron–sulfur protein (RISP) gene knockdown (KD) blocks caffeine- or NE-induced ROS production. Taken together, these findings have further demonstrated that ER Ca2+ release causes mitochondrial Ca2+ uptake and RISP-mediated ROS production; this novel local ER/mitochondrion communication-elicited, Ca2+-mediated, RISP-dependent ROS production may play a significant role in hypoxic cellular responses in PASMCs.

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