Blumental-Perry A, Jobava R, Bederman I, Degar A J, Kenche H, Guan B J, Pandit K, Perry N A, Molyneaux N D, Wu J, Prendergas E, Ye Z-W, Zhang J, Nelson C E, Ahangari F, Krokowski D, Guttentag S H, Linden P A, Townsend D M, Miron A, Kang M-J, Kaminski N, Perry Y, Hatzoglou M
Department of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.
Department of Genetics and Genome Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Commun Biol. 2020 Oct 30;3(1):626. doi: 10.1038/s42003-020-01322-4.
Alveolar epithelial type II (AETII) cells are important for lung epithelium maintenance and function. We demonstrate that AETII cells from mouse lungs exposed to cigarette smoke (CS) increase the levels of the mitochondria-encoded non-coding RNA, mito-RNA-805, generated by the control region of the mitochondrial genome. The protective effects of mito-ncR-805 are associated with positive regulation of mitochondrial energy metabolism, and respiration. Levels of mito-ncR-805 do not relate to steady-state transcription or replication of the mitochondrial genome. Instead, CS-exposure causes the redistribution of mito-ncR-805 from mitochondria to the nucleus, which correlated with the increased expression of nuclear-encoded genes involved in mitochondrial function. These studies reveal an unrecognized mitochondria stress associated retrograde signaling, and put forward the idea that mito-ncRNA-805 represents a subtype of small non coding RNAs that are regulated in a tissue- or cell-type specific manner to protect cells under physiological stress.
肺泡II型上皮细胞（AETII）对肺上皮的维持和功能至关重要。我们证明，暴露于香烟烟雾（CS）的小鼠肺中的AETII细胞会增加由线粒体基因组控制区域产生的线粒体编码非编码RNA（mito-RNA-805）的水平。mito-ncR-805的保护作用与线粒体能量代谢和呼吸的正向调节有关。mito-ncR-805的水平与线粒体基因组的稳态转录或复制无关。相反，CS暴露导致mito-ncR-805从线粒体重新分布到细胞核，这与参与线粒体功能的核编码基因表达增加相关。这些研究揭示了一种未被认识的线粒体应激相关逆行信号，并提出mito-ncRNA-805代表一种小非编码RNA的亚型，其以组织或细胞类型特异性方式受到调节，以在生理应激下保护细胞。
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