Limits...
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 knockdown MIN6 cells exhibit increased sensitivity to palmitate. Comparison of cell viability between control (MIN6-shc) and Nr2e1 silenced (MIN6-sh2 and MIN6-sh3) cells exposed to palmitate by MTT assay. MIN6-shc, MIN6-sh2, and MIN6-sh3 cells were cultured in complete medium with 0.5 mM palmitate for 48 h. Data represent means ± SD of four observations; ∗P ≤ 0.05 (comparing silenced versus MIN6-shc cells).
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4663339&req=5

fig2: Nr2e1 knockdown MIN6 cells exhibit increased sensitivity to palmitate. Comparison of cell viability between control (MIN6-shc) and Nr2e1 silenced (MIN6-sh2 and MIN6-sh3) cells exposed to palmitate by MTT assay. MIN6-shc, MIN6-sh2, and MIN6-sh3 cells were cultured in complete medium with 0.5 mM palmitate for 48 h. Data represent means ± SD of four observations; ∗P ≤ 0.05 (comparing silenced versus MIN6-shc cells).

Mentions: To investigate the role of Nr2e1 in the survival of MIN6 cells, we investigated cell viability in MIN6 cells exposed to palmitate using MTT analysis. As shown in Figure 2, after 48 hours of palmitate exposure, MIN6-shc, MIN6-sh2, and MIN6-sh3 cells all exhibited decreased cell viability. Compared with the control cells, knockdown of Nr2e1 caused a more significant reduction in the percentage of viable cells.


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 knockdown MIN6 cells exhibit increased sensitivity to palmitate. Comparison of cell viability between control (MIN6-shc) and Nr2e1 silenced (MIN6-sh2 and MIN6-sh3) cells exposed to palmitate by MTT assay. MIN6-shc, MIN6-sh2, and MIN6-sh3 cells were cultured in complete medium with 0.5 mM palmitate for 48 h. Data represent means ± SD of four observations; ∗P ≤ 0.05 (comparing silenced versus MIN6-shc cells).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Nr2e1 knockdown MIN6 cells exhibit increased sensitivity to palmitate. Comparison of cell viability between control (MIN6-shc) and Nr2e1 silenced (MIN6-sh2 and MIN6-sh3) cells exposed to palmitate by MTT assay. MIN6-shc, MIN6-sh2, and MIN6-sh3 cells were cultured in complete medium with 0.5 mM palmitate for 48 h. Data represent means ± SD of four observations; ∗P ≤ 0.05 (comparing silenced versus MIN6-shc cells).
Mentions: To investigate the role of Nr2e1 in the survival of MIN6 cells, we investigated cell viability in MIN6 cells exposed to palmitate using MTT analysis. As shown in Figure 2, after 48 hours of palmitate exposure, MIN6-shc, MIN6-sh2, and MIN6-sh3 cells all exhibited decreased cell viability. Compared with the control cells, knockdown of Nr2e1 caused a more significant reduction in the percentage of viable cells.

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