MiR-184 expression is regulated by AMPK in pancreatic islets

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

MiR-184 expression is regulated by AMPK in pancreatic islets. / Martinez-Sanchez, Aida; Nguyen-Tu, Marie Sophie; Cebola, Ines; Yavari, Arash; Marchetti, Piero; Piemonti, Lorenzo; De Koning, Eelco; Shapiro, A. M.James; Johnson, Paul; Sakamoto, Kei; Smith, David M.; Leclerc, Isabelle; Ashrafian, Houman; Ferrer, Jorge; Rutter, Guy A.

In: FASEB Journal, Vol. 32, No. 5, 05.2018, p. 2587-2600.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Martinez-Sanchez, A, Nguyen-Tu, MS, Cebola, I, Yavari, A, Marchetti, P, Piemonti, L, De Koning, E, Shapiro, AMJ, Johnson, P, Sakamoto, K, Smith, DM, Leclerc, I, Ashrafian, H, Ferrer, J & Rutter, GA 2018, 'MiR-184 expression is regulated by AMPK in pancreatic islets', FASEB Journal, vol. 32, no. 5, pp. 2587-2600. https://doi.org/10.1096/fj.201701100R

APA

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. (2018). MiR-184 expression is regulated by AMPK in pancreatic islets. FASEB Journal, 32(5), 2587-2600. https://doi.org/10.1096/fj.201701100R

Vancouver

Martinez-Sanchez A, Nguyen-Tu MS, Cebola I, Yavari A, Marchetti P, Piemonti L et al. MiR-184 expression is regulated by AMPK in pancreatic islets. FASEB Journal. 2018 May;32(5):2587-2600. https://doi.org/10.1096/fj.201701100R

Author

Martinez-Sanchez, Aida ; Nguyen-Tu, Marie Sophie ; Cebola, Ines ; Yavari, Arash ; Marchetti, Piero ; Piemonti, Lorenzo ; De Koning, Eelco ; Shapiro, A. M.James ; Johnson, Paul ; Sakamoto, Kei ; Smith, David M. ; Leclerc, Isabelle ; Ashrafian, Houman ; Ferrer, Jorge ; Rutter, Guy A. / MiR-184 expression is regulated by AMPK in pancreatic islets. In: FASEB Journal. 2018 ; Vol. 32, No. 5. pp. 2587-2600.

Bibtex

@article{4b1dc34d640f42b78043707575bca86e,
title = "MiR-184 expression is regulated by AMPK in pancreatic islets",
abstract = "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 [β-cell-specific AMPK double-knockout (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 mi RNAs in β AMPKdKO vs. control islets. Gene ontology analysis of targeted transcripts revealed enrichmentinpathways important for β-cell function and identity. The most down-regulated miRNA wasmiR-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 arecentral for there gulation of miR-184 and other miRNAs in is lets and provide a link between energy status and gene expression in β cells.",
keywords = "B cell, Diabetes, Glucose, Mirnas",
author = "Aida Martinez-Sanchez and Nguyen-Tu, {Marie Sophie} and Ines Cebola and Arash Yavari and Piero Marchetti and Lorenzo Piemonti and {De Koning}, Eelco and Shapiro, {A. M.James} and Paul Johnson and Kei Sakamoto and Smith, {David M.} and Isabelle Leclerc and Houman Ashrafian and Jorge Ferrer and Rutter, {Guy A.}",
year = "2018",
month = may,
doi = "10.1096/fj.201701100R",
language = "English",
volume = "32",
pages = "2587--2600",
journal = "F A S E B Journal",
issn = "0892-6638",
publisher = "Federation of American Societies for Experimental Biology",
number = "5",

}

RIS

TY - JOUR

T1 - MiR-184 expression is regulated by AMPK in pancreatic islets

AU - Martinez-Sanchez, Aida

AU - Nguyen-Tu, Marie Sophie

AU - Cebola, Ines

AU - Yavari, Arash

AU - Marchetti, Piero

AU - Piemonti, Lorenzo

AU - De Koning, Eelco

AU - Shapiro, A. M.James

AU - Johnson, Paul

AU - Sakamoto, Kei

AU - Smith, David M.

AU - Leclerc, Isabelle

AU - Ashrafian, Houman

AU - Ferrer, Jorge

AU - Rutter, Guy A.

PY - 2018/5

Y1 - 2018/5

N2 - 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 [β-cell-specific AMPK double-knockout (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 mi RNAs in β AMPKdKO vs. control islets. Gene ontology analysis of targeted transcripts revealed enrichmentinpathways important for β-cell function and identity. The most down-regulated miRNA wasmiR-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 arecentral for there gulation of miR-184 and other miRNAs in is lets and provide a link between energy status and gene expression in β cells.

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 [β-cell-specific AMPK double-knockout (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 mi RNAs in β AMPKdKO vs. control islets. Gene ontology analysis of targeted transcripts revealed enrichmentinpathways important for β-cell function and identity. The most down-regulated miRNA wasmiR-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 arecentral for there gulation of miR-184 and other miRNAs in is lets and provide a link between energy status and gene expression in β cells.

KW - B cell

KW - Diabetes

KW - Glucose

KW - Mirnas

UR - http://www.scopus.com/inward/record.url?scp=85048632168&partnerID=8YFLogxK

U2 - 10.1096/fj.201701100R

DO - 10.1096/fj.201701100R

M3 - Journal article

C2 - 29269398

AN - SCOPUS:85048632168

VL - 32

SP - 2587

EP - 2600

JO - F A S E B Journal

JF - F A S E B Journal

SN - 0892-6638

IS - 5

ER -

ID: 238433779