| Title |
Inhibition of tumor suppressor p53 preserves glycation-serum induced pancreatic beta-cell demise
|
|---|---|
| Published in |
Endocrine, May 2016
|
| DOI | 10.1007/s12020-016-0979-5 |
| Pubmed ID | |
| Authors |
Y. Li, T. Zhang, Q. Huang, Y. Sun, X. Chang, H. Zhang, Y. Zhu, X. Han |
| Abstract |
Tumor suppressor p53 is a transcriptional factor that determines cell fate in response to multiple stressors, such as oxidative stress and endoplasmic reticulum stress, in the majority of cells. However, its role in pancreatic beta cells is not well documented. Our previous research has revealed that glycation-serum (GS) induced pancreatic beta-cell demise through the AGEs-RAGE pathway. In the present study, we investigated the role of p53 in GS-related beta-cell demise. Using pancreatic islets beta-cell line INS-1 cells, we found that with GS treatment, the transcriptional activity of p53 was significantly evoked due to the increased amount of nuclear p53 protein. Resveratrol (RSV) was capable of further enhancing this transcriptional ability and consequently increased the population of dead beta cells under GS exposure. In contrast, inhibiting this transcriptional activity via p53 interference greatly protected beta cells from the damage provoked by GS, as well as damage strengthened by RSV. However, the pharmacological activation of PPARγ with troglitazone (TRO) only suppressed GS-induced, not RSV-induced, p53 activity. Moreover, the activation of PPARγ greatly preserved beta cells from GS-induced death. This protective effect recurred due to improved mitochondrial function with Bcl2 overexpression. Further, p53 activation could induce cellular apoptosis in primary rat islets. Our findings explore the broader role of p53 in regulating pancreatic beta-cell demise in the presence of GS and may provide a therapeutic target for the treatment and prevention of diabetes. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Australia | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 13 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 13 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Doctoral Student | 2 | 15% |
| Researcher | 2 | 15% |
| Student > Master | 2 | 15% |
| Student > Bachelor | 1 | 8% |
| Unspecified | 1 | 8% |
| Other | 1 | 8% |
| Unknown | 4 | 31% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 3 | 23% |
| Unspecified | 1 | 8% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 8% |
| Nursing and Health Professions | 1 | 8% |
| Agricultural and Biological Sciences | 1 | 8% |
| Other | 1 | 8% |
| Unknown | 5 | 38% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 11 May 2016.
All research outputs
#20,325,615
of 22,869,263 outputs
Outputs from Endocrine
#1,366
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Outputs of similar age
#256,102
of 301,827 outputs
Outputs of similar age from Endocrine
#24
of 31 outputs
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