ID2 promotes the expansion and survival of growth-arrested pancreatic beta cells

Hong Hua; Nora Sarvetnick

doi:10.1007/s12020-008-9039-0

ID2 promotes the expansion and survival of growth-arrested pancreatic beta cells

Hong Hua, Nora Sarvetnick

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

Inhibitors of DNA binding proteins (Ids) are implicated in the control of proliferation and differentiation. Herein, we tested the hypothesis that Id2 could stimulate proliferation and survival in differentiated pancreatic beta cells. We showed that Id2-enhanced proliferation of a growth-arrested pancreatic beta cell line (BTC-tet). This was mediated by the Rb pathway, as shown by an E2F1-driven reporter assay and Western immunoblot of phosphorylated Rb protein. Id2 also induced expression of Bcl-2, accompanied by a significant reduction of critical mediators of cytokine stimulation, including p38 MAPK and NFκB, as well as apoptosis markers, caspase-3 and Annexin-V. Overall, our data suggest that Id2 enhances proliferation and survival of growth-arrested BTC-tet cells.

Original language	English (US)
Pages (from-to)	329-337
Number of pages	9
Journal	Endocrine
Volume	32
Issue number	3
DOIs	https://doi.org/10.1007/s12020-008-9039-0
State	Published - Dec 2007
Externally published	Yes

Keywords

BTC
Bcl2
E2F
Id2

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism
Endocrinology

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10.1007/s12020-008-9039-0

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@article{b1a93a1a60d6495896f04931e779906b,

title = "ID2 promotes the expansion and survival of growth-arrested pancreatic beta cells",

abstract = "Inhibitors of DNA binding proteins (Ids) are implicated in the control of proliferation and differentiation. Herein, we tested the hypothesis that Id2 could stimulate proliferation and survival in differentiated pancreatic beta cells. We showed that Id2-enhanced proliferation of a growth-arrested pancreatic beta cell line (BTC-tet). This was mediated by the Rb pathway, as shown by an E2F1-driven reporter assay and Western immunoblot of phosphorylated Rb protein. Id2 also induced expression of Bcl-2, accompanied by a significant reduction of critical mediators of cytokine stimulation, including p38 MAPK and NFκB, as well as apoptosis markers, caspase-3 and Annexin-V. Overall, our data suggest that Id2 enhances proliferation and survival of growth-arrested BTC-tet cells.",

keywords = "BTC, Bcl2, E2F, Id2",

author = "Hong Hua and Nora Sarvetnick",

note = "Funding Information: Acknowledgments This study was generously funded by the Larry L. Hillblom Foundation to HH and NIH grant DK060746 to NS (Scripps manuscript number 18782). We thank the generosity of Jayshree Sarnater and John Kessler for the Id2 construct, Joseph Nevins for the E2F1-luciferase reporter, Shimon Efrat for the BTC-tet cells, and Sandrine Arnaud-Dabernat for the BTC-tet cells expressing the E2F1-luciferase reporter. We also thank members of the Sarvet-nick lab for critical reading of the manuscript.",

year = "2007",

month = dec,

doi = "10.1007/s12020-008-9039-0",

language = "English (US)",

volume = "32",

pages = "329--337",

journal = "Endocrine",

issn = "1355-008X",

publisher = "Humana Press",

number = "3",

}

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T1 - ID2 promotes the expansion and survival of growth-arrested pancreatic beta cells

AU - Hua, Hong

AU - Sarvetnick, Nora

N1 - Funding Information: Acknowledgments This study was generously funded by the Larry L. Hillblom Foundation to HH and NIH grant DK060746 to NS (Scripps manuscript number 18782). We thank the generosity of Jayshree Sarnater and John Kessler for the Id2 construct, Joseph Nevins for the E2F1-luciferase reporter, Shimon Efrat for the BTC-tet cells, and Sandrine Arnaud-Dabernat for the BTC-tet cells expressing the E2F1-luciferase reporter. We also thank members of the Sarvet-nick lab for critical reading of the manuscript.

PY - 2007/12

Y1 - 2007/12

N2 - Inhibitors of DNA binding proteins (Ids) are implicated in the control of proliferation and differentiation. Herein, we tested the hypothesis that Id2 could stimulate proliferation and survival in differentiated pancreatic beta cells. We showed that Id2-enhanced proliferation of a growth-arrested pancreatic beta cell line (BTC-tet). This was mediated by the Rb pathway, as shown by an E2F1-driven reporter assay and Western immunoblot of phosphorylated Rb protein. Id2 also induced expression of Bcl-2, accompanied by a significant reduction of critical mediators of cytokine stimulation, including p38 MAPK and NFκB, as well as apoptosis markers, caspase-3 and Annexin-V. Overall, our data suggest that Id2 enhances proliferation and survival of growth-arrested BTC-tet cells.

AB - Inhibitors of DNA binding proteins (Ids) are implicated in the control of proliferation and differentiation. Herein, we tested the hypothesis that Id2 could stimulate proliferation and survival in differentiated pancreatic beta cells. We showed that Id2-enhanced proliferation of a growth-arrested pancreatic beta cell line (BTC-tet). This was mediated by the Rb pathway, as shown by an E2F1-driven reporter assay and Western immunoblot of phosphorylated Rb protein. Id2 also induced expression of Bcl-2, accompanied by a significant reduction of critical mediators of cytokine stimulation, including p38 MAPK and NFκB, as well as apoptosis markers, caspase-3 and Annexin-V. Overall, our data suggest that Id2 enhances proliferation and survival of growth-arrested BTC-tet cells.

KW - BTC

KW - Bcl2

KW - E2F

KW - Id2

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DO - 10.1007/s12020-008-9039-0

M3 - Article

C2 - 18322822

AN - SCOPUS:46149107878

SN - 1355-008X

VL - 32

SP - 329

EP - 337

JO - Endocrine

JF - Endocrine

IS - 3

ER -

ID2 promotes the expansion and survival of growth-arrested pancreatic beta cells

Abstract

Keywords

ASJC Scopus subject areas

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