Imperial College London
Alternate

Dr Aida Martinez-Sanchez

Faculty of Medicine, Department of Metabolism, Digestion and Reproduction

Senior Lecturer
 
 
 
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Contact

 

+44 (0)20 7594 3366a.martinez-sanchez Website

 
 
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Location

 

326ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Martinez-Sanchez:2018:10.1096/fj.201701100R,
author = {Martinez-Sanchez, A and Nguyen-Tu, M-S and Cebola, I and Yavari, A and Marchetti, P and Piemonti, L and de, Koning E and Shapiro, AMJ and Johnson, P and Sakamoto, K and Smith, DM and Leclerc, I and Ashrafian, H and Ferrer, J and Rutter, GA},
doi = {10.1096/fj.201701100R},
journal = {FASEB Journal},
pages = {2587--2600},
title = {MiR-184 expression is regulated by AMPK in pancreatic islets.},
url = {http://dx.doi.org/10.1096/fj.201701100R},
volume = {32},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - AMPK is a critical energy sensor and target for widely used antidiabetic drugs. In β-cells, elevated glucose concentrations lower AMPK activity, and the ablation of both catalytic subunits (βAMPKdKO mice) impairs insulin secretion in vivo and β-cell identity. MicroRNAs (miRNAs) are small RNAs that silence gene expression that are essential for pancreatic β-cell function and identity and altered in diabetes. Here, we have explored the miRNAs acting downstream of AMPK in mouse and human β-cells. We identified 14 down-regulated and 9 up-regulated miRNAs in βAMPKdKO vs. control islets. Gene ontology analysis of targeted transcripts revealed enrichment in pathways important for β-cell function and identity. The most down-regulated miRNA was miR-184 (miR-184-3p), an important regulator of β-cell function and compensatory expansion that is controlled by glucose and reduced in diabetes. We demonstrate that AMPK is a potent regulator and an important mediator of the negative effects of glucose on miR-184 expression. Additionally, we reveal sexual dimorphism in miR-184 expression in mouse and human islets. Collectively, these data demonstrate that glucose-mediated changes in AMPK activity are central for the regulation of miR-184 and other miRNAs in islets and provide a link between energy status and gene expression in β-cells.-Martinez-Sanchez, A., Nguyen-Tu, M.-S., Cebola, I., Yavari, A., Marchetti, P., Piemonti, L., de Koning, E., Shapiro, A. M. J., Johnson, P., Sakamoto, K., Smith, D. M., Leclerc, I., Ashrafian, H., Ferrer, J., Rutter, G. A. MiR-184 expression is regulated by AMPK in pancreatic islets.
AU  - Martinez-Sanchez,A
AU  - Nguyen-Tu,M-S
AU  - Cebola,I
AU  - Yavari,A
AU  - Marchetti,P
AU  - Piemonti,L
AU  - de,Koning E
AU  - Shapiro,AMJ
AU  - Johnson,P
AU  - Sakamoto,K
AU  - Smith,DM
AU  - Leclerc,I
AU  - Ashrafian,H
AU  - Ferrer,J
AU  - Rutter,GA
DO  - 10.1096/fj.201701100R
EP  - 2600
PY  - 2018///
SN  - 0892-6638
SP  - 2587
TI  - MiR-184 expression is regulated by AMPK in pancreatic islets.
T2  - FASEB Journal
UR  - http://dx.doi.org/10.1096/fj.201701100R
UR  - http://hdl.handle.net/10044/1/63379
VL  - 32
ER  -
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