@misc{10498/34804,
year = {2015},
month = {3},
url = {http://hdl.handle.net/10498/34804},
abstract = {Activation of pancreatic β-cell proliferation has been proposed as an approach to replace reduced functional β-cell mass in diabetes. Quiescent fibroblasts exit from G0 (quiescence) to G1 through pRb phosphorylation mediated by cyclin C/cdk3 complexes. Overexpression of cyclin D1, D2, D3, or cyclin E induces pancreatic β-cell proliferation. We hypothesized that cyclin C overexpression would induce β-cell proliferation through G0 exit, thus being a potential therapeutic target to recover functional β-cell mass. We used isolated rat and human islets transduced with adenovirus expressing cyclin C. We measured multiple markers of proliferation: [(3)H]thymidine incorporation, BrdU incorporation and staining, and Ki67 staining. Furthermore, we detected β-cell death by TUNEL, β-cell differentiation by RT-PCR, and β-cell function by glucose-stimulated insulin secretion. Interestingly, we have found that cyclin C increases rat and human β-cell proliferation. This augmented proliferation did not induce β-cell death, dedifferentiation, or dysfunction in rat or human islets. Our results indicate that cyclin C is a potential target for inducing β-cell regeneration.},
keywords = {cell cycle},
keywords = {cyclin C},
keywords = {pancreatic β-cell},
keywords = {proliferation},
title = {Cyclin C stimulates β-cell proliferation in rat and human pancreatic β-cells},
doi = {10.1152/ajpendo.00260.2014},
author = {Jiménez Palomares, Margarita and Lopez-Acosta, José Francisco and Villa-Pérez, Pablo and Moreno-Amador, José Luis and Muñoz-Barrera, Jennifer and Fernandez-Luis, Sara and Heras-Pozas, Blanca and Perdomo, Germán and Bernal-Mizrachi, Ernesto and Cozar-Castellano, Irene},
}