Pioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance.
<h4>Background</h4>Evidence suggests that the PPARγ-agonist insulin sensitizer pioglitazone, may provide potential beneficial cardiovascular (CV) effects beyond its anti-hyperglycaemic function. A reduced endothelial progenitor cell (EPC) number is associated with impaired glucose tolera...
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2012
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oai:doaj.org-article:d0c2c141123543ff8cc35f48394d56ee2021-11-18T08:10:06ZPioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance.1932-620310.1371/journal.pone.0048283https://doaj.org/article/d0c2c141123543ff8cc35f48394d56ee2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23139771/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Evidence suggests that the PPARγ-agonist insulin sensitizer pioglitazone, may provide potential beneficial cardiovascular (CV) effects beyond its anti-hyperglycaemic function. A reduced endothelial progenitor cell (EPC) number is associated with impaired glucose tolerance (IGT) or diabetes, conditions characterised by increased CV risk.<h4>Aim</h4>To evaluate whether pioglitazone can provide benefit in vitro in EPCs obtained from IGT subjects.<h4>Materials and methods</h4>Early and late-outgrowth EPCs were obtained from peripheral blood mononuclear cells of 14 IGT subjects. The in vitro effect of pioglitazone (10 µM) with/without PPARγ-antagonist GW9662 (1 µM) was assessed on EPC viability, apoptosis, ability to form tubular-like structures and pro-inflammatory molecule expression.<h4>Results</h4>Pioglitazone increased early and late-outgrowth EPC viability, with negligible effects on apoptosis. The capacity of EPCs to form tubular-like structures was improved by pioglitazone in early (mean increase 28%; p=0.005) and late-outgrowth (mean increase 30%; p=0.037) EPCs. Pioglitazone reduced ICAM-1 and VCAM-1 adhesion molecule expression in both early (p=0.001 and p=0.012 respectively) and late-outgrowth (p=0.047 and p=0.048, respectively) EPCs. Similarly, pioglitazone reduced TNFα gene and protein expression in both early (p=0.034;p=0.022) and late-outgrowth (p=0.026;p=0.017) EPCs compared to control. These effects were prevented by incubation with the PPARγ-antagonist GW9662.<h4>Conclusion</h4>Pioglitazone exerts beneficial effects in vitro on EPCs isolated from IGT subjects, supporting the potential implication of pioglitazone as a CV protective agents.Valentina SpigoniAngela PicconiMonia CitoValentina RidolfiSabrina BonominiChiara CasaliIvana ZavaroniLuigi GnudiMarco MetraAlessandra Dei CasPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 11, p e48283 (2012) |
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Medicine R Science Q Valentina Spigoni Angela Picconi Monia Cito Valentina Ridolfi Sabrina Bonomini Chiara Casali Ivana Zavaroni Luigi Gnudi Marco Metra Alessandra Dei Cas Pioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance. |
| description |
<h4>Background</h4>Evidence suggests that the PPARγ-agonist insulin sensitizer pioglitazone, may provide potential beneficial cardiovascular (CV) effects beyond its anti-hyperglycaemic function. A reduced endothelial progenitor cell (EPC) number is associated with impaired glucose tolerance (IGT) or diabetes, conditions characterised by increased CV risk.<h4>Aim</h4>To evaluate whether pioglitazone can provide benefit in vitro in EPCs obtained from IGT subjects.<h4>Materials and methods</h4>Early and late-outgrowth EPCs were obtained from peripheral blood mononuclear cells of 14 IGT subjects. The in vitro effect of pioglitazone (10 µM) with/without PPARγ-antagonist GW9662 (1 µM) was assessed on EPC viability, apoptosis, ability to form tubular-like structures and pro-inflammatory molecule expression.<h4>Results</h4>Pioglitazone increased early and late-outgrowth EPC viability, with negligible effects on apoptosis. The capacity of EPCs to form tubular-like structures was improved by pioglitazone in early (mean increase 28%; p=0.005) and late-outgrowth (mean increase 30%; p=0.037) EPCs. Pioglitazone reduced ICAM-1 and VCAM-1 adhesion molecule expression in both early (p=0.001 and p=0.012 respectively) and late-outgrowth (p=0.047 and p=0.048, respectively) EPCs. Similarly, pioglitazone reduced TNFα gene and protein expression in both early (p=0.034;p=0.022) and late-outgrowth (p=0.026;p=0.017) EPCs compared to control. These effects were prevented by incubation with the PPARγ-antagonist GW9662.<h4>Conclusion</h4>Pioglitazone exerts beneficial effects in vitro on EPCs isolated from IGT subjects, supporting the potential implication of pioglitazone as a CV protective agents. |
| format |
article |
| author |
Valentina Spigoni Angela Picconi Monia Cito Valentina Ridolfi Sabrina Bonomini Chiara Casali Ivana Zavaroni Luigi Gnudi Marco Metra Alessandra Dei Cas |
| author_facet |
Valentina Spigoni Angela Picconi Monia Cito Valentina Ridolfi Sabrina Bonomini Chiara Casali Ivana Zavaroni Luigi Gnudi Marco Metra Alessandra Dei Cas |
| author_sort |
Valentina Spigoni |
| title |
Pioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance. |
| title_short |
Pioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance. |
| title_full |
Pioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance. |
| title_fullStr |
Pioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance. |
| title_full_unstemmed |
Pioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance. |
| title_sort |
pioglitazone improves in vitro viability and function of endothelial progenitor cells from individuals with impaired glucose tolerance. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2012 |
| url |
https://doaj.org/article/d0c2c141123543ff8cc35f48394d56ee |
| work_keys_str_mv |
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