K63 Ubiquitination of P21 Can Facilitate Pellino-1 in the Context of Chronic Obstructive Pulmonary Disease and Lung Cellular Senescence

Chronic obstructive pulmonary diseases (COPD) is a kind of age-related, airflow-obstruction disease mostly caused by cigarette smoke. However, the relationship between COPD and lung cellular senescence is still not fully understood. Here, we found silencing Pellino-1 could inhibit the protein level...

Full description

Saved in:
Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2022-10, Vol.11 (19), p.3115
Main Authors: Ma, Jia-Hui, Zhang, Yi-Ting, Wang, Lu-Ping, Sun, Qing-Yu, Zhang, Hao, Li, Jian-Jiang, Han, Ning-Ning, Zhu, Yao-Yao, Xie, Xiao-Yu, Li, Xia
Format: Article
Language:English
Subjects:
Adenoviruses
Age
Aging
Airway management
Analysis
Bronchodilator agents
Care and treatment
Cell cycle
Cell lines
Cells
Chronic illnesses
Chronic obstructive pulmonary disease
Cigarette smoke
COPD
Cyclin-dependent kinase inhibitor p21
D-Galactose
Development and progression
Dosage and administration
Galactose
GTP-binding protein
Laboratory animals
Lung cancer
Lung diseases
Lung diseases, Obstructive
lung senescence
Medical research
Mortality
Obstructive lung disease
Oxidative stress
P21
Pellino-1
Proteins
Senescence
Ubiquitin
Ubiquitin-proteasome system
Ubiquitin-protein ligase
Ubiquitination
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Chronic obstructive pulmonary diseases (COPD) is a kind of age-related, airflow-obstruction disease mostly caused by cigarette smoke. However, the relationship between COPD and lung cellular senescence is still not fully understood. Here, we found silencing Pellino-1 could inhibit the protein level of P21. Then, through constructing cell lines expressed ubiquitin-HA, we found that the E3 ubiquitin ligase Pellino-1 could bind to senescence marker p21 and modify p21 by K63-site ubiquitination by co-IP assays. Furthermore, we found that p21-mediated lung cellular senescence could be inhibited by silencing Pellino-1 in a D-galactose senescence mice model. Moreover, by constructing a COPD mouse model with shPellino-1 adenovirus, we found that silencing Pellino-1 could inhibit COPD and inflammation via reduction of SASPs regulated by p21. Taken together, our study findings elucidated that silencing E3 ligase Pellino-1 exhibits therapeutic potential for treatment to attenuate the progression of lung cellular senescence and COPD.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells11193115