Rapamycin inhibits oxidative/nitrosative stress and enhances angiogenesis in high glucose-treated human umbilical vein endothelial cells: Role of autophagy

Rezabakhsh, Aysa; Ahmadi, Mahdi; Khaksar, Majid; Montaseri, Azadeh; Malekinejad, Hassan; Rahbarghazi‬, Reza; Garjani, Alireza

doi:10.1016/j.biopha.2017.07.044

Cited by 56 publications

(36 citation statements)

References 47 publications

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“…Studies have also reported that HG contributes to autophagy in retinal cells and placenta . However, HG has also been shown to impair autophagy in endothelial progenitor cells and umbilical vein endothelial cells . These different results indicate that modulation of autophagy is complex and possibly dependent on the tissues and the pathologic conditions.…”

Section: Discussionmentioning

confidence: 99%

Melatonin Enhances Proliferation and Modulates Differentiation of Neural Stem Cells Via Autophagy in Hyperglycemia

Zhang

Liu

et al. 2019

Stem Cells

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Dysfunction of neural stem cells (NSCs) has been linked to fetal neuropathy, one of the most devastating complications of gestational diabetes. Several studies have demonstrated that melatonin (Mel) exerted neuroprotective actions in various stresses. However, the role of autophagy and the involvement of Mel in NSCs in hyperglycemia (HG) have not yet been fully established. Here, we found that HG increased autophagy and autophagic flux of NSCs as evidenced by increasing LC3B II/I ratio, Beclin-1 expression, and autophagosomes. Moreover, Mel enhanced NSCs proliferation and self-renewal in HG with decreasing autophagy and activated mTOR signaling. Consistently, inhibition of autophagy by 3-Methyladenine (3-Ma) could assist Mel effects above, and induction of autophagy by Rapamycin (Rapa) could diminish Mel effects. Remarkably, HG induced premature differentiation of NSCs into neurons (Map2 positive cells) and astrocytes (GFAP positive cells). Furthermore, Mel diminished HG-induced premature differentiation and assisted NSCs in HG differentiation as that in normal condition. Coincidentally, inhibiting of NSCs autophagy by 3-Ma assisted Mel to modulate differentiation. However, increasing NSCs autophagy by Rapa disturbed the Mel effects and retarded NSCs differentiation. These findings suggested that Mel supplementation could contribute to mimicking normal NSCs proliferation and differentiation in fetal central nervous system by inhibiting autophagy in the context of gestational diabetes. STEM CELLS 2019;37:504-515 SIGNIFICANCE STATEMENTNeural stem cells play important roles in fetal neurodevelopment. The incidences of gestational diabetes are rising in the world and prevention of fetal neuropathy in gestational diabetes mellitus (GDM) needs to be deeply explored. In addition, autophagy of NSCs in HG is still unclear. Here, it is reported that HG inhibits proliferation and induces premature differentiation of NSCs by promoting autophagy and autophagic flux. The naturally occurring hormone melatonin (Mel) antagonized HG-mediated effects and maintained normal proliferation and differentiation in NSCs by modulating autophagy, which protected NSCs mainly by downregulating Beclin-1 and up modulating mTORC1 signaling. This work indicates that Mel could be used as a potential drug to aid in fetal central nervous system (CNS) development in GDM patients.

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Section: Discussionmentioning

confidence: 99%

Melatonin Enhances Proliferation and Modulates Differentiation of Neural Stem Cells Via Autophagy in Hyperglycemia

Zhang

Liu

et al. 2019

Stem Cells

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“…Finally, in the reaction with sulfanilamide, HNO2 forms a diazonium salt, which reacts with N-(1-naphthyl) ethylenediamine 2HCl to form an azo dye which its absorbance was detected at 540 nm. NOx levels were expressed as nmol and sodium nitrite was used as a standard (Rezabakhsh et al 2017).…”

Section: Methodsmentioning

confidence: 99%

Evaluation of ameliorative effect of sodium nitrate in experimental model of streptozotocin-induced diabetic neuropathy in male rats

Oghbaei

Alipour

Mohaddes

et al. 2019

Endocrine Regulations

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Objective. Diabetes induces sensory symptoms of neuropathy as positive (hyperalgesia), negative (hypoalgesia), or both.Methods. In the present study, fifty male Wistar rats were allocated to five groups: control, control+nitrate, diabetes, diabetes+insulin, and diabetes+nitrate. Thirty days after diabetes confirmation, insulin (2-4 U/day) was injected subcutaneously in diabetes+insulin group and nitrate (100 mg/l) was added into drinking water of the control+nitrate and diabetes+nitrate groups for a period of 2 months. In order to assess the mechanical and thermal algesia, tail immersion, hot plate, and von Frey tests were performed. The serum insulin levels were determined with insulin ELISA Kit. Serum level of NOx was determined by the Griess method.Results. Both thermal and mechanical nociceptive thresholds showed a significant decrease (p<0.05) which was followed by a significant increase (p<0.01) in the thermal nociceptive threshold in the diabetes group. Chronic nitrate or insulin treatment led to a significant decrease (p<0.01) in blood glucose levels, as well as a significant (p<0.05) increase in the body weight and serum NOx. Moreover, nitrate treatment significantly increased serum insulin levels (p<0.001) compared to the other groups.Conclusion. Chronic nitrate treatment modified the thermal and mechanical sensitivities in diabetic animals.

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“…18 Briefly, 1 × 10 4 cells were plated in each well of 96-well plates. 18 Briefly, 1 × 10 4 cells were plated in each well of 96-well plates.…”

Section: Measuring the Levels Of Pge 2 And Il-6 By Enzyme-linked Immentioning

confidence: 99%

“…The content of NO was determined by the colorimetric method in the supernatant using Griess reagent according to previous protocols. 18 Briefly, 1 × 10 4 cells were plated in each well of 96-well plates. After treatment procedure and collection of the supernatant, 150 μL of each sample was incubated for 10 minutes with 15 μL of Griess A solution and 20 minutes with 15 μL of Griess B reagent.…”

Section: Measuring the Levels Of Pge 2 And Il-6 By Enzyme-linked Immentioning

confidence: 99%

Docosahexaenoic acid reversed atherosclerotic changes in human endothelial cells induced by palmitic acid in vitro

Karbasforush

Nourazarian

Darabi

et al. 2018

Cell Biochemistry & Function

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The current experiment showed that docosahexaenoic acid could reverse atherosclerotic changes in human endothelial cells induced by palmitic acid. The increased levels of interleukin-6 and prostaglandin E in atherosclerotic cells were returned to near-to-normal status. Gene expression analysis showed a reduced activity of genes participating in atherosclerotic endothelial cells treated by docosahexaenoic acid. The expression of genes related to cell clotting activity was also similar to that of normal cells.

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Rapamycin inhibits oxidative/nitrosative stress and enhances angiogenesis in high glucose-treated human umbilical vein endothelial cells: Role of autophagy

Cited by 56 publications

References 47 publications

Melatonin Enhances Proliferation and Modulates Differentiation of Neural Stem Cells Via Autophagy in Hyperglycemia

Melatonin Enhances Proliferation and Modulates Differentiation of Neural Stem Cells Via Autophagy in Hyperglycemia

Evaluation of ameliorative effect of sodium nitrate in experimental model of streptozotocin-induced diabetic neuropathy in male rats

Docosahexaenoic acid reversed atherosclerotic changes in human endothelial cells induced by palmitic acid in vitro

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