PXD021376

PXD021376 is an original dataset announced via ProteomeXchange.

Title	Mitochondrial respiration is necessary to combat oxidative stress in quiescent cells
Description	Mitochondrial oxidative phosphorylation (OXPHOS) makes ATP and supports biosynthesis during proliferation, but its role in non-proliferating cells, beyond ATP production, is less understood. Here we show that OXPHOS protects quiescent (but not proliferating) cells from oxidative stress. Using in vivo models of OXPHOS deficiency (whole body and endothelium-specific) we show that OXPHOS mediated resistance to ROS (i) maintains selectivity of ROS-based anticancer therapy by protecting normal tissues during treatment, and in quiescent endothelium (ii) ameliorates systemic LPS-induced inflammation and (iii) attenuates symptoms of the inflammatory bowel disease. ROS-resistance provided by OXPHOS is independent of its role in biosynthesis or NADH recycling. Instead, in quiescent cells OXPHOS constitutively generates low levels of endogenous ROS that support basal autophagic flux and protect from exogenous ROS challenge. Hence, during evolution cells acquired mitochondria to profit from oxidative metabolism, but also built in an OXPHOS-dependent mechanism to guard against the resulting oxidative stress.
HostingRepository	PRIDE
AnnounceDate	2023-11-14
AnnouncementXML	Submission_2023-11-14_08:30:56.095.xml
DigitalObjectIdentifier	https://dx.doi.org/10.6019/PXD021376
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Supported dataset by repository
PrimarySubmitter	Karel Harant
SpeciesList	scientific name: Homo sapiens (Human); NCBI TaxID: 9606;
ModificationList	iodoacetamide derivatized residue
Instrument	Orbitrap Fusion

Revision	Datetime	Status	ChangeLog Entry
0	2020-09-09 06:58:18	ID requested
1	2022-10-13 12:05:33	announced
⏵ 2	2023-11-14 08:30:57	announced	2023-11-14: Updated project metadata.

10.6019/PXD021376;

Magalhaes-Novais S, Blecha J, Naraine R, Mikesova J, Abaffy P, Pecinova A, Milosevic M, Bohuslavova R, Prochazka J, Khan S, Novotna E, Sindelka R, Machan R, Dewerchin M, Vlcak E, Kalucka J, Stemberkova Hubackova S, Benda A, Goveia J, Mracek T, Barinka C, Carmeliet P, Neuzil J, Rohlenova K, Rohlena J, Mitochondrial respiration supports autophagy to provide stress resistance during quiescence. Autophagy, 18(10):2409-2426(2022) [pubmed]

submitter keyword: oxidative phosphorylation, autophagy, ATG4,Mitochondria, electron transport chain, reactive oxygen species, endothelial cells, cell death

Jakub Rohlena
contact affiliation	Institute of Biotechnology, Czech Academy of Sciences, 252 50 Vestec, Prague-West, Czech Republic
contact email	jakub.rohlena@ibt.cas.cz
lab head
Karel Harant
contact affiliation	Charles University
contact email	harant@natur.cuni.cz
dataset submitter

Dataset FTP location NOTE: Most web browsers have now discontinued native support for FTP access within the browser window. But you can usually install another FTP app (we recommend FileZilla) and configure your browser to launch the external application when you click on this FTP link. Or otherwise, launch an app that supports FTP (like FileZilla) and use this address: ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2022/10/PXD021376

PRIDE project URI

• PRIDE
  1. PXD021376
     1. Label: PRIDE project
     2. Name: Mitochondrial respiration is necessary to combat oxidative stress in quiescent cells