Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2012; Volume 206, Supplement 691
Scandinavian Physiological Society's Annual Meeting
8/24/2012-8/26/2012
Helsinki, Finland


MICRORNAS IN ISCHEMIC DISEASE AND POST-ISCHEMIC VASCULAR REPAIR
Abstract number: S0704

EMANUELI1 C

1Laboratory of Vascular Pathology and Regeneration, School of Clinical Sciences, University of Bristol, Bristol, England

MicroRNAs (miRs) are post-transcriptional inhibitory regulators of gene expression that bind to complementary messenger RNA transcripts. miRs have recently come into focus of cardiovascular research. Because each miR can repress many target mRNAs, it is possible that dysregulation of a single miR might play important roles in complex pathological situations. Our laboratory focuses on the identification of miRs which are involved in ischemic disease and/or post-ischemic vascular repair. We have reported for the first time the importance of miR-503 in diabetes mellitus–associated ischemic disease. miR-503 represses cell cycle–associated genes in endothelial cells. Moreover, new evidences suggest a role of miR-503 in the endothelial cell/pericyte cross-talking. I will present on miR-503 as well as touch on other miRs, which we are elucidating to be relevant for post-ischemic vascular repair. Bone marrow-derived proangiogenic cells (PACs) contribute into post-ischemic vascular repair. We have profiled miR expression in PACs harvested from the peripheral blood of human patients with critical limb ischemia (CLI) and with/out diabetes (controls: healthy donors) and found that member of the extended miR-16 family are deregulated in CLI, thus impairing the PAC capacity to migrate toward proangiogenic stimuli. However, this defect can be corrected ex-vivo by miR therapeutics to enhance the regenerative potential of PACs once transplanted in immunocompromised mice with limb ischemia. Finally, I may be able to present additional data on miR expression in a series of different clinical samples.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 691 :S0704

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE