Insulin Secretion Enhanced by Beta Cell Senescence
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By LabMedica International staff writers Posted on 16 Mar 2016 |
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Image: Human beta cells grown in culture (blue). Cells on right were induced to undergo senescence, causing them to secrete more insulin, stained in red (Photo courtesy of Dr. Ronny Helman, the Hebrew University of Jerusalem).
Cellular senescence, a condition of permanent cell cycle arrest that is considered a safeguard mechanism preventing aged or abnormal cells from further expansion, has been found to increase the insulin-producing capability of pancreatic beta cells.
The cyclin-dependent kinase (CDK) p16Ink4a (cyclin-dependent kinase inhibitor 2A) is a tumor suppressor protein, which in humans is encoded by the CDKN2A gene. This gene is frequently mutated or deleted in a wide variety of tumors. p16Ink4a plays an important role in cell cycle regulation by slowing the progression from G1 phase to S phase, and is implicated in the prevention of cancers, notably melanoma, oropharyngeal squamous cell carcinoma, cervical cancer, and esophageal cancer. In addition, p16Ink4a is expressed in pancreatic beta cells during aging and limits their proliferative potential; however, its effects on beta cell function are poorly characterized.
Investigators at the Hebrew University of Jerusalem (Israel) worked with transgenic mice and with human beta cells growing in culture. They reported in the March 7, 2016, online edition of the journal Nature Medicine that beta cell-specific activation of p16Ink4a in transgenic mice enhanced glucose-stimulated insulin secretion (GSIS). In mice with diabetes, this led to improved glucose homeostasis, providing an unexpected functional benefit.
Expression of p16Ink4a in beta cells induced characteristics of senescence—including cell enlargement, greater glucose uptake, and increased mitochondrial activity—that promoted increased insulin secretion. GSIS increased during the normal aging of mice and was driven by elevated p16Ink4a activity. Furthermore, islets from human adults contained p16Ink4a-expressing senescent beta cells, and senescence induced by p16Ink4a in a human beta cell line increased insulin secretion.
“Senescence of cells is generally thought to represent a state in which cells lose their functionality, and contribute to tissue aging and disease. It was therefore very striking to observe that when beta cells enter this state during normal aging, the program allows them to function better, rather than worse,” said senior author Dr. Ittai Ben-Porath, senior lecturer in the department of developmental biology and cancer research at The Hebrew University of Jerusalem (Israel).
Related Links:
Hebrew University of Jerusalem
The cyclin-dependent kinase (CDK) p16Ink4a (cyclin-dependent kinase inhibitor 2A) is a tumor suppressor protein, which in humans is encoded by the CDKN2A gene. This gene is frequently mutated or deleted in a wide variety of tumors. p16Ink4a plays an important role in cell cycle regulation by slowing the progression from G1 phase to S phase, and is implicated in the prevention of cancers, notably melanoma, oropharyngeal squamous cell carcinoma, cervical cancer, and esophageal cancer. In addition, p16Ink4a is expressed in pancreatic beta cells during aging and limits their proliferative potential; however, its effects on beta cell function are poorly characterized.
Investigators at the Hebrew University of Jerusalem (Israel) worked with transgenic mice and with human beta cells growing in culture. They reported in the March 7, 2016, online edition of the journal Nature Medicine that beta cell-specific activation of p16Ink4a in transgenic mice enhanced glucose-stimulated insulin secretion (GSIS). In mice with diabetes, this led to improved glucose homeostasis, providing an unexpected functional benefit.
Expression of p16Ink4a in beta cells induced characteristics of senescence—including cell enlargement, greater glucose uptake, and increased mitochondrial activity—that promoted increased insulin secretion. GSIS increased during the normal aging of mice and was driven by elevated p16Ink4a activity. Furthermore, islets from human adults contained p16Ink4a-expressing senescent beta cells, and senescence induced by p16Ink4a in a human beta cell line increased insulin secretion.
“Senescence of cells is generally thought to represent a state in which cells lose their functionality, and contribute to tissue aging and disease. It was therefore very striking to observe that when beta cells enter this state during normal aging, the program allows them to function better, rather than worse,” said senior author Dr. Ittai Ben-Porath, senior lecturer in the department of developmental biology and cancer research at The Hebrew University of Jerusalem (Israel).
Related Links:
Hebrew University of Jerusalem
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