Imperial College London
Alternate

ProfessorNadiaRosenthal

Faculty of Medicine, National Heart & Lung Institute

Chair in Cardiovascular Science&ScientificDirector
 
 
 
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Contact

 

+44 (0)20 7594 2737n.rosenthal

 
 
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Location

 

424W2ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Bouvet:2020:10.1038/s41598-020-68223-8,
author = {Bouvet, M and Claude, O and Roux, M and Skelly, D and Masurkar, N and Mougenot, N and Nadaud, S and Blanc, C and Delacroix, C and Chardonnet, S and Pionneau, C and Perret, C and Yaniz-Galende, E and Rosenthal, N and Trégouët, D-A and Marazzi, G and Silvestre, J-S and Sassoon, D and Hulot, J-S},
doi = {10.1038/s41598-020-68223-8},
journal = {Scientific Reports},
pages = {11404--11404},
title = {Anti-integrin αv therapy improves cardiac fibrosis after myocardial infarction by blunting cardiac PW1+ stromal cells.},
url = {http://dx.doi.org/10.1038/s41598-020-68223-8},
volume = {10},
year = {2020}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - There is currently no therapy to limit the development of cardiac fibrosis and consequent heart failure. We have recently shown that cardiac fibrosis post-myocardial infarction (MI) can be regulated by resident cardiac cells with a fibrogenic signature and identified by the expression of PW1 (Peg3). Here we identify αV-integrin (CD51) as an essential regulator of cardiac PW1+ cells fibrogenic behavior. We used transcriptomic and proteomic approaches to identify specific cell-surface markers for cardiac PW1+ cells and found that αV-integrin (CD51) was expressed in almost all cardiac PW1+ cells (93% ± 1%), predominantly as the αVβ1 complex. αV-integrin is a subunit member of the integrin family of cell adhesion receptors and was found to activate complex of latent transforming growth factor beta (TGFβ at the surface of cardiac PW1+ cells. Pharmacological inhibition of αV-integrin reduced the profibrotic action of cardiac PW1+CD51+ cells and was associated with improved cardiac function and animal survival following MI coupled with a reduced infarct size and fibrotic lesion. These data identify a targetable pathway that regulates cardiac fibrosis in response to an ischemic injury and demonstrate that pharmacological inhibition of αV-integrin could reduce pathological outcomes following cardiac ischemia.
AU  - Bouvet,M
AU  - Claude,O
AU  - Roux,M
AU  - Skelly,D
AU  - Masurkar,N
AU  - Mougenot,N
AU  - Nadaud,S
AU  - Blanc,C
AU  - Delacroix,C
AU  - Chardonnet,S
AU  - Pionneau,C
AU  - Perret,C
AU  - Yaniz-Galende,E
AU  - Rosenthal,N
AU  - Trégouët,D-A
AU  - Marazzi,G
AU  - Silvestre,J-S
AU  - Sassoon,D
AU  - Hulot,J-S
DO  - 10.1038/s41598-020-68223-8
EP  - 11404
PY  - 2020///
SN  - 2045-2322
SP  - 11404
TI  - Anti-integrin αv therapy improves cardiac fibrosis after myocardial infarction by blunting cardiac PW1+ stromal cells.
T2  - Scientific Reports
UR  - http://dx.doi.org/10.1038/s41598-020-68223-8
UR  - https://www.ncbi.nlm.nih.gov/pubmed/32647159
UR  - http://hdl.handle.net/10044/1/81827
VL  - 10
ER  -
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