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Dear Colleagues,

Thijsj G. Rttema described “Mitochondria in the second act”, citing Pittis and Gabaldón (page 101), who provide evidence that the host cell from which eukaryotes evolved was already genetically chimaeric before the mitochondrial symbiosis, suggesting that mitochondria evolved later in eukaryotic evolution than was previously presumed (https://www.nature.com/articles/nature16876; Nature volume 531, pages 39–40 (03 March 2016)). This means that when mitochondria are established, it is possible to commence cross-talk between mitochondria and other organelles. This is one of the newest topics to reconsider intracellular organelle cross-talk. Majima et al. were the first to report that reactive oxygen species (ROS) generated from mitochondria promote apoptosis (Majima et al., J Biol. Chem. 1998), while Itoh et al. described the function of the Nrf2-Keap1 intercellular signal for the first time (Itoh et al., Biochem. Biophys. Res. Commun. 1997, Itoh et al., Genes Dev. 1999). A recent study has described that ROS generated from mitochondria initiate cellular transduction in cytosol (Indo et al. Handb Exp Pharmacol. 2017). In this Special Issue, the further roles of mitochondria-generated ROS and the subsequent intraorganellar cross-talks, signal exchange, and protein import will be important to retain cellular networks and homeostasis. We aim to establish a new world of cellular functions.

Prof. Dr. Hideyuki J. Majima
Prof. Dr. Ken Itoh
Guest Editors

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Published Papers (2 papers)

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Research

12 pages, 3446 KiB

Open AccessArticle

Differences in the Intracellular Localization of Methylated β-Cyclodextrins-Threaded Polyrotaxanes Lead to Different Cellular States

by Yuma Yamada, Shinnosuke Daikuhara, Atsushi Tamura, Kei Nishida, Nobuhiko Yui and Hideyoshi Harashima

Biomolecules 2023, 13(6), 903; https://doi.org/10.3390/biom13060903 - 29 May 2023

Cited by 1 | Viewed by 1554

Abstract

Activation of autophagy represents a potential therapeutic strategy for the treatment of diseases that are caused by the accumulation of defective proteins and the formation of abnormal organelles. Methylated β-cyclodextrins-threaded polyrotaxane (Me-PRX), a supramolecular structured polymer, induces autophagy by interacting with the endoplasmic reticulum. We previously reported on the successful activation of mitochondria-targeted autophagy by delivering Me-RRX to mitochondria using a MITO-Porter, a mitochondria-targeted nanocarrier. The same level of autophagy induction was achieved at one-twentieth the dosage for the MITO-Porter (Me-PRX) compared to the naked Me-PRX. We report herein on the quantitative evaluation of the intracellular organelle localization of both naked Me-PRX and the MITO-Porter (Me-PRX). Mitochondria, endoplasmic reticulum and lysosomes were selected as target organelles because they would be involved in autophagy induction. In addition, organelle injury and cell viability assays were performed. The results showed that the naked Me-PRX and the MITO-Porter (Me-PRX) were localized in different intracellular organelles, and organelle injury was different, depending on the route of administration, indicating that different organelles contribute to autophagy induction. These findings indicate that the organelle to which the autophagy-inducing molecules are delivered plays an important role in the level of induction of autophagy. Full article

(This article belongs to the Special Issue The Physiological and Pathological New Function of Mitochondrial ROS and Intraorganellar Cross-Talks)

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0 pages, 2470 KiB

Open AccessArticle

Evidence of Nrf2/Keap1 Signaling Regulation by Mitochondria-Generated Reactive Oxygen Species in RGK1 Cells

by Hiroko P. Indo, Daisuke Masuda, Sompong Sriburee, Hiromu Ito, Ikuo Nakanishi, Ken-ichiro Matsumoto, Samlee Mankhetkorn, Moragot Chatatikun, Sirirat Surinkaew, Lunla Udomwech, Fumitaka Kawakami, Takafumi Ichikawa, Hirofumi Matsui, Jitbanjong Tangpong and Hideyuki J. Majima

Biomolecules 2023, 13(3), 445; https://doi.org/10.3390/biom13030445 - 27 Feb 2023

Cited by 4 | Viewed by 1643

Abstract

It has been known that reactive oxygen species (ROS) are generated from the mitochondrial electron transport chain (ETC). Majima et al. proved that mitochondrial ROS (mtROS) caused apoptosis for the first time in 1998 (Majima et al. J Biol Chem, 1998). It is speculated that mtROS can move out of the mitochondria and initiate cellular signals in the nucleus. This paper aims to prove this phenomenon by assessing the change in the amount of manganese superoxide dismutase (MnSOD) by MnSOD transfection. Two cell lines of the same genetic background, of which generation of mtROS are different, i.e., the mtROS are more produced in RGK1, than in that of RGM1, were compared to analyze the cellular signals. The results of immunocytochemistry staining showed increase of Nrf2, Keap1, HO-1 and 2, MnSOD, GCL, GST, NQO1, GATA1, GATA3, GATA4, and GATA5 in RGK1 compared to those in RGM1. Transfection of human MnSOD in RGK1 cells showed a decrease of those signal proteins, suggesting mtROS play a role in cellular signals in nucleus. Full article

(This article belongs to the Special Issue The Physiological and Pathological New Function of Mitochondrial ROS and Intraorganellar Cross-Talks)

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