Imperial College London

ProfessorFanChung

Faculty of MedicineNational Heart & Lung Institute

Professor of Respiratory Medicine
 
 
 
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Contact

 

+44 (0)20 7594 7954f.chung Website

 
 
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Assistant

 

Miss Carolyn Green +44 (0)20 7594 7959

 
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Location

 

227BGuy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Frankenberg:2022:10.1165/rcmb.2022-0041OC,
author = {Frankenberg, Garcia J and Rogers, A and Mak, J and halayko, A and Hui, C and xu, B and Chung, KF and Rodriguez, T and Michaeloudes, C and Bhavsar, P},
doi = {10.1165/rcmb.2022-0041OC},
journal = {American Journal of Respiratory Cell and Molecular Biology},
pages = {471--481},
title = {Mitochondrial transfer regulates bioenergetics in healthy and COPD airway smooth muscle},
url = {http://dx.doi.org/10.1165/rcmb.2022-0041OC},
volume = {67},
year = {2022}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Mitochondrial dysfunction has been reported in chronic obstructive pulmonary disease (COPD). Transfer of mitochondria from mesenchymal stem cells to airway smooth muscle cells (ASMCs) can attenuate oxidative stress-induced mitochondrial damage. It is not known whether mitochondrial transfer can occur between structural cells in the lungs or what role this may have in modulating bioenergetics and cellular function in healthy and COPD airways. Here, we show that ASMCs from both healthy ex-smokers and subjects with COPD can exchange mitochondria, a process that happens, at least partly, via extracellular vesicles. Exposure to cigarette smoke induces mitochondrial dysfunction and leads to an increase in the donation of mitochondria by ASMCs, suggesting that the latter may be a stress response mechanism. Healthy ex-smoker ASMCs that receive mitochondria show increases in mitochondrial biogenesis and respiration and a reduction in cell proliferation, irrespective of whether the mitochondria are transferred from healthy ex-smoker or COPD ASMCs. Our data indicate that mitochondrial transfer between structural cells is a homeostatic mechanism for the regulation of bioenergetics and cellular function within the airways and may represent an endogenous mechanism for reversing the functional consequences of mitochondrial dysfunction in diseases such as COPD.
AU - Frankenberg,Garcia J
AU - Rogers,A
AU - Mak,J
AU - halayko,A
AU - Hui,C
AU - xu,B
AU - Chung,KF
AU - Rodriguez,T
AU - Michaeloudes,C
AU - Bhavsar,P
DO - 10.1165/rcmb.2022-0041OC
EP - 481
PY - 2022///
SN - 1044-1549
SP - 471
TI - Mitochondrial transfer regulates bioenergetics in healthy and COPD airway smooth muscle
T2 - American Journal of Respiratory Cell and Molecular Biology
UR - http://dx.doi.org/10.1165/rcmb.2022-0041OC
UR - http://hdl.handle.net/10044/1/100045
VL - 67
ER -