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Nr2e1 Deficiency Augments Palmitate-Induced Oxidative Stress in Beta Cells.

Shi X, Deng H, Dai Z, Xu Y, Xiong X, Ma P, Cheng J - Oxid Med Cell Longev (2015)

Bottom Line: At the molecular level, Nr2e1 deficiency augments palmitate-induced oxidative stress.Nr2e1 deficiency also resulted in decreases in antioxidant enzymes and expression level of Nrf2.Together, this study indicated a potential protective effect of Nr2e1 on beta cells, which may serve as a target for the development of novel therapies for diabetes.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China.

ABSTRACT
Nuclear receptor subfamily 2 group E member 1 (Nr2e1) has been regarded as an essential regulator of the growth of neural stem cells. However, its function elsewhere is unknown. In the present study, we generated Nr2e1 knockdown MIN6 cells and studied whether Nr2e1 knockdown affected basal beta cell functions such as proliferation, cell death, and insulin secretion. We showed that knockdown of Nr2e1 in MIN6 cells resulted in increased sensitivity to lipotoxicity, decreased proliferation, a partial G0/G1 cell-cycle arrest, and higher rates of apoptosis. Moreover, Nr2e1 deficiency exaggerates palmitate-induced impairment in insulin secretion. At the molecular level, Nr2e1 deficiency augments palmitate-induced oxidative stress. Nr2e1 deficiency also resulted in decreases in antioxidant enzymes and expression level of Nrf2. Together, this study indicated a potential protective effect of Nr2e1 on beta cells, which may serve as a target for the development of novel therapies for diabetes.

No MeSH data available.


Related in: MedlinePlus

Nr2e1 silencing enhanced apoptosis of MIN6 cells. Comparison of cell apoptosis between control (MIN6-shc) and Nr2e1 silenced (MIN6-sh2 and MIN6-sh3) cells exposed to palmitate. MIN6-shc, MIN6-sh2, and MIN6-sh3 cells were cultured in complete medium with 0.5 mM palmitate overnight. Data represent means ± SD of three observations; ∗P ≤ 0.05 (comparing silenced versus MIN6-shc cells exposed to palmitate).
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fig4: Nr2e1 silencing enhanced apoptosis of MIN6 cells. Comparison of cell apoptosis between control (MIN6-shc) and Nr2e1 silenced (MIN6-sh2 and MIN6-sh3) cells exposed to palmitate. MIN6-shc, MIN6-sh2, and MIN6-sh3 cells were cultured in complete medium with 0.5 mM palmitate overnight. Data represent means ± SD of three observations; ∗P ≤ 0.05 (comparing silenced versus MIN6-shc cells exposed to palmitate).

Mentions: We also studied effects of Nr2e1 silencing on MIN6 cells apoptosis in response to palmitate. At basal conditions, MIN6-shc, MIN6-sh2, and MIN6-sh3 cells displayed similar cell apoptosis rates. When stressed by overnight exposure to 0.5 mM palmitate, however, Nr2e1 silencing resulted in augmented cell apoptosis rates compared with control cells (Figure 4).


Nr2e1 Deficiency Augments Palmitate-Induced Oxidative Stress in Beta Cells.

Shi X, Deng H, Dai Z, Xu Y, Xiong X, Ma P, Cheng J - Oxid Med Cell Longev (2015)

Nr2e1 silencing enhanced apoptosis of MIN6 cells. Comparison of cell apoptosis between control (MIN6-shc) and Nr2e1 silenced (MIN6-sh2 and MIN6-sh3) cells exposed to palmitate. MIN6-shc, MIN6-sh2, and MIN6-sh3 cells were cultured in complete medium with 0.5 mM palmitate overnight. Data represent means ± SD of three observations; ∗P ≤ 0.05 (comparing silenced versus MIN6-shc cells exposed to palmitate).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4663339&req=5

fig4: Nr2e1 silencing enhanced apoptosis of MIN6 cells. Comparison of cell apoptosis between control (MIN6-shc) and Nr2e1 silenced (MIN6-sh2 and MIN6-sh3) cells exposed to palmitate. MIN6-shc, MIN6-sh2, and MIN6-sh3 cells were cultured in complete medium with 0.5 mM palmitate overnight. Data represent means ± SD of three observations; ∗P ≤ 0.05 (comparing silenced versus MIN6-shc cells exposed to palmitate).
Mentions: We also studied effects of Nr2e1 silencing on MIN6 cells apoptosis in response to palmitate. At basal conditions, MIN6-shc, MIN6-sh2, and MIN6-sh3 cells displayed similar cell apoptosis rates. When stressed by overnight exposure to 0.5 mM palmitate, however, Nr2e1 silencing resulted in augmented cell apoptosis rates compared with control cells (Figure 4).

Bottom Line: At the molecular level, Nr2e1 deficiency augments palmitate-induced oxidative stress.Nr2e1 deficiency also resulted in decreases in antioxidant enzymes and expression level of Nrf2.Together, this study indicated a potential protective effect of Nr2e1 on beta cells, which may serve as a target for the development of novel therapies for diabetes.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, China.

ABSTRACT
Nuclear receptor subfamily 2 group E member 1 (Nr2e1) has been regarded as an essential regulator of the growth of neural stem cells. However, its function elsewhere is unknown. In the present study, we generated Nr2e1 knockdown MIN6 cells and studied whether Nr2e1 knockdown affected basal beta cell functions such as proliferation, cell death, and insulin secretion. We showed that knockdown of Nr2e1 in MIN6 cells resulted in increased sensitivity to lipotoxicity, decreased proliferation, a partial G0/G1 cell-cycle arrest, and higher rates of apoptosis. Moreover, Nr2e1 deficiency exaggerates palmitate-induced impairment in insulin secretion. At the molecular level, Nr2e1 deficiency augments palmitate-induced oxidative stress. Nr2e1 deficiency also resulted in decreases in antioxidant enzymes and expression level of Nrf2. Together, this study indicated a potential protective effect of Nr2e1 on beta cells, which may serve as a target for the development of novel therapies for diabetes.

No MeSH data available.


Related in: MedlinePlus