Ann: CYP MSC Data in Asthma Model Published in Sceintific Journal, page-65

Article published on iPSC-MSCs (not ours). It is very reassuring that scientists in other parts of the world come to the same conclusion.
The more of these articles getting published, especially when using iPSC-MSCs, the better for us. Free publicity. Besides, only one company out there that has access to a large superdonor iPSC database.

Mesenchymal stem cells alleviate oxidative stress-induced mitochondrial dysfunction in the airways

Xiang Li, PhD∗, Charalambos Michaeloudes, PhD∗, Yuelin Zhang, PhD∗, Coen H. Wiegman, PhD, Ian M. Adcock, PhD, Qizhou Lian, PhD, Judith C.W. Mak, PhD, Pankaj K. Bhavsar, PhD

Email the author PhD Pankaj K. Bhavsar, Kian Fan Chung, MD
∗These authors contributed equally to this study.
Published Online: September 11, 2017
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DOI: http://dx.doi.org/10.1016/j.jaci.2017.08.017

Publication stage: In Press Accepted Manuscript
Article Infoclick to expand contents

Background
Oxidative stress-induced mitochondrial dysfunction may contribute to inflammation and remodeling in chronic obstructive pulmonary disease (COPD). Mesenchymal stem cells (MSCs) protect against lung damage in animal models of COPD. It is unknown whether these effects occur through attenuating mitochondrial dysfunction in airway cells.

Objective
To examine the effect of induced-pluripotent stem cell-derived MSCs (iPSC-MSCs) on oxidative stress-induce mitochondrial dysfunction in human airway smooth muscle cells (ASMCs) in vitro and in mouse lungs in vivo.

Methods
ASMCs were co-cultured with iPSC-MSCs in the presence of cigarette smoke medium (CSM), and mitochondrial reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm) and apoptosis were measured. Conditioned media from iPSC-MSCs and trans-well co-cultures were used to detect any paracrine effects. The effect of systemic injection of iPSC-MSCs on airway inflammation and hyper-responsiveness in ozone-exposed mice was also investigated.

Results
Co-culture of iPSC-MSCs with ASMCs attenuated CSM-induced mitochondrial ROS, apoptosis and ΔΨm loss in ASMCs. iPSC-MSC-conditioned media or trans-well co-cultures with iPSC-MSCs reduced CSM-induced mitochondrial ROS but not ΔΨm or apoptosis in ASMCs. Mitochondrial transfer from iPSC-MSCs to ASMCs was observed after direct co-culture and was enhanced by CSM. iPSC-MSCs attenuated ozone-induced mitochondrial dysfunction, airway hyper-responsiveness and inflammation in mouse lungs.

Conclusion
iPSC-MSCs offered protection against oxidative stress-induced mitochondrial dysfunction in human ASMCs and in mouse lungs, whilst reducing airway inflammation and hyper-responsiveness. These effects are, at least partly, dependent on cell-cell contact that allows for mitochondrial transfer, and paracrine regulation. Therefore, iPSC-MSCs show promise as a therapy for oxidative stress-dependent lung diseases such as COPD.

iPSC-MSCs protect against oxidative stress-induced mitochondrial dysfunction, apoptosis, hyper-responsiveness and inflammation in the airways. These findings highlight the potential use of iPSC-MScs as a novel cell-based therapy for COPD.

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Co-Corresponding authors: Dr Qizhou Lian, Departments of Medicine, and Ophthalmology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong SAR, Email: [email protected] Dr Judith C.W. Mak, Departments of Medicine and Pharmacology and Pharmacy, and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong SAR. Email: [email protected]

This study was supported by project grants from Imperial College Trust, from National Natural Science Fund of China (NSFC No. 81370140 to JCW Mak; STFGD No.2015B020225001; RGC/GRF No. HKU17113816 and NSFC No. 31571407 to Q Lian) and by Respiratory Disease Biomedical Research Unit at the Royal Brompton NHS Foundation Trust and Imperial College London. KFC is a Senior Investigator of NIHR, UK.
http://www.jacionline.org/article/S0091-6749(17)31431-8/abstract