PXD041281

PXD041281 is an original dataset announced via ProteomeXchange.

Title	SARS-CoV-2 infection causes periodontal fibrotic pathogenesis through deregulating mitochondrial beta-oxidation
Description	The global high prevalence of COVID-19 is a major challenge for health professionals and patients. SARS-CoV-2 virus has four kinds of structural protein components: the spike protein, envelope protein, membrane protein, and nucleocapsid protein. SARS-CoV-2 virus mutate predominantly in the spike proteins, whilst the other key viral components remain stable. Essentially the pathological functions of the SARS-CoV-2 virus on different cell types are still largely unknown. Previous studies have shown that the human oral cavity can potentially act as reservoir of the SARS-CoV-2 virus. However, the consequence of SARS-CoV-2 viral infection on human oral health has not been systematically examined. COVID-19 can cause severe oral mucosa lesions and is likely to be connected with poor periodontal conditions. Fibroblasts are the key component of periodontal ligament (PDL) and express the SARS-CoV-2 receptor: Angiotensin-converting enzyme 2 (ACE2), whose expression level can increase upon bacterial infection hence potentially provide a direct route of SARS-CoV-2 infection to PDL fibroblasts. In this research, we aimed to study the pathogenicity of SARS-CoV-2 viral components on human fibroblasts. We found that by exposing to SARS-CoV-2, especially to the viral envelope and membrane proteins, the human periodontal fibroblasts could develop fibrotic pathogenic phenotypes, including hyperproliferation that was concomitant induced together with increased apoptosis and senescence. The fibrotic degeneration was mediated by a down-regulation of mitochondrial -oxidation in the fibroblasts. Fatty acid -oxidation inhibitor, etomoxir treatment could mirror the same pathological consequence on the cells, similar to SARS-CoV-2 infection. Our results therefore provide novel mechanistic insights into how SARS-CoV-2 infection can affect human periodontal health at the cell and molecular level with potential new therapeutic targets for COVID-19 induced fibrosis.
HostingRepository	PRIDE
AnnounceDate	2023-11-14
AnnouncementXML	Submission_2023-11-14_09:03:44.299.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Vikram Sharma
SpeciesList	scientific name: Homo sapiens (Human); NCBI TaxID: 9606;
ModificationList	No PTMs are included in the dataset
Instrument	LTQ Orbitrap Velos

Revision	Datetime	Status	ChangeLog Entry
0	2023-04-02 11:53:39	ID requested
1	2023-07-20 12:01:44	announced
⏵ 2	2023-11-14 09:03:49	announced	2023-11-14: Updated project metadata.

Gao Y, Kok WL, Sharma V, Illsley CS, Hanks S, Tredwin C, Hu B, SARS-CoV-2 infection causes periodontal fibrotic pathogenesis through deregulating mitochondrial beta-oxidation. Cell Death Discov, 9(1):175(2023) [pubmed]

submitter keyword: COVID19, Periodontal, infection

Vikram Sharma
contact affiliation	School of Biomedical Sciences, University of Plymouth, UK
contact email	vikram.sharma@plymouth.ac.uk
lab head
Vikram Sharma
contact affiliation	Plymouth University Peninsula Schools of Medicine and Dentistry
contact email	vikram.sharma@plymouth.ac.uk
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/2023/07/PXD041281

PRIDE project URI

• PRIDE
  1. PXD041281
     1. Label: PRIDE project
     2. Name: SARS-CoV-2 infection causes periodontal fibrotic pathogenesis through deregulating mitochondrial beta-oxidation