Anti-fibrotic effects of different sources of MSC in bleomycin-induced lung fibrosis in C57BL6 male mice.

Periera-Simon, Simone; Xia, Xiaomei; Catanuto, Paola; Coronado, Ramon; Kurtzberg, Joanne; Bellio, Michael; Lee, Yee-Shuan; Khan, Aisha; Smith, Robin; Elliot, Sharon J; Glassberg, Marilyn K

Anti-fibrotic effects of different sources of MSC in bleomycin-induced lung fibrosis in C57BL6 male mice.

dc.contributor.author	Periera-Simon, Simone
dc.contributor.author	Xia, Xiaomei
dc.contributor.author	Catanuto, Paola
dc.contributor.author	Coronado, Ramon
dc.contributor.author	Kurtzberg, Joanne
dc.contributor.author	Bellio, Michael
dc.contributor.author	Lee, Yee-Shuan
dc.contributor.author	Khan, Aisha
dc.contributor.author	Smith, Robin
dc.contributor.author	Elliot, Sharon J
dc.contributor.author	Glassberg, Marilyn K
dc.date.accessioned	2022-03-25T20:08:45Z
dc.date.available	2022-03-25T20:08:45Z
dc.date.issued	2021-02
dc.date.updated	2022-03-25T20:08:44Z
dc.description.abstract	Background and objective IPF is a fatal and debilitating lung disorder increasing in incidence worldwide. To date, two approved treatments only slow disease progression, have multiple side effects and do not provide a cure. MSC have promising therapeutic potential as a cell-based therapy for many lung disorders based on the anti-fibrotic properties of the MSC. Methods Critical questions remain surrounding the optimal source, timing and efficacy of cell-based therapies. The present study examines the most effective sources of MSC. Human MSC were derived from adipose, WJ, chorionic membrane (CSC) and chorionic villi (CVC). MSC were injected into the ageing mouse model of BLM-induced lung fibrosis. Results All sources decreased Aschroft and hydroxyproline levels when injected into BLM-treated mice at day 10 with the exception of CSC cells that did not change hydroxyproline levels. There were also decreases in mRNA expression of α_v -integrin and TNFα in all sources except CSC. Only ASC- and WJ-derived cells reduced AKT and MMP-2 activation, while Cav-1 was increased by ASC treatment as previously reported. BLM-induced miR dysregulation of miR-29 and miR-199 was restored only by ASC treatment. Conclusion Our data suggest that sources of MSC may differ in the pathway(s) involved in repair.
dc.identifier.issn	1323-7799
dc.identifier.issn	1440-1843
dc.identifier.uri	https://hdl.handle.net/10161/24724
dc.language	eng
dc.publisher	Wiley
dc.relation.ispartof	Respirology (Carlton, Vic.)
dc.relation.isversionof	10.1111/resp.13928
dc.subject	Mesenchymal Stem Cells
dc.subject	Animals
dc.subject	Mice, Inbred C57BL
dc.subject	Humans
dc.subject	Pulmonary Fibrosis
dc.subject	Disease Models, Animal
dc.subject	Inflammation
dc.subject	Bleomycin
dc.subject	MicroRNAs
dc.subject	RNA, Messenger
dc.subject	Mesenchymal Stem Cell Transplantation
dc.subject	Transplantation, Homologous
dc.subject	Gene Expression Regulation
dc.subject	Adult
dc.subject	Male
dc.subject	Proto-Oncogene Proteins c-akt
dc.subject	Caveolin 1
dc.subject	Matrix Metalloproteinase 2
dc.subject	Biomarkers
dc.title	Anti-fibrotic effects of different sources of MSC in bleomycin-induced lung fibrosis in C57BL6 male mice.
dc.type	Journal article
duke.contributor.orcid	Kurtzberg, Joanne\|0000-0002-3370-0703
pubs.begin-page	161
pubs.end-page	170
pubs.issue	2
pubs.organisational-group	Duke
pubs.organisational-group	School of Medicine
pubs.organisational-group	Clinical Science Departments
pubs.organisational-group	Institutes and Centers
pubs.organisational-group	Pathology
pubs.organisational-group	Pediatrics
pubs.organisational-group	Duke Cancer Institute
pubs.organisational-group	Institutes and Provost's Academic Units
pubs.organisational-group	Initiatives
pubs.organisational-group	Duke Innovation & Entrepreneurship
pubs.organisational-group	Pediatrics, Transplant and Cellular Therapy
pubs.publication-status	Published
pubs.volume	26