Resveratrol Inhibits the Proliferation of Neural Progenitor Cells and Hippocampal Neurogenesis

Park, Hee Ra; Kong, Kyoung Hye; Yu, Byung Pal; Mattson, Mark P.; Lee, Joo Young

doi:10.1074/jbc.m112.406413

Cited by 84 publications

(57 citation statements)

References 69 publications

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“…In our preliminary experiment, we observed that 50 and 100 μmol/L resveratrol decreased NSC viability. Park and Leong reported that resveratrol at high concentrations (20 and 50 μmol/L, 30-120 μmol/L, respectively) inhibited proliferation of NPCs and embryonic cardiomyoblasts [26,27]. Therefore, further studies should investigate whether resveratrol exhibits a dual concentration effect for neurogenesis in different physiological or pathological states.…”

Section: Discussionmentioning

confidence: 99%

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Sonic Hedgehog Signaling Mediates Resveratrol to Increase Proliferation of Neural Stem Cells After Oxygen-Glucose Deprivation/Reoxygenation Injury in Vitro

Cheng

Yu²,

Wang³

et al. 2015

Cell Physiol Biochem

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Background/Aims: There is interest in drugs and rehabilitation methods to enhance neurogenesis and improve neurological function after brain injury or degeneration. Resveratrol may enhance hippocampal neurogenesis and improve hippocampal atrophy in chronic fatigue mice and prenatally stressed rats. However, its effect and mechanism of neurogenesis after stroke is less well understood. Sonic hedgehog (Shh) signaling is crucial for neurogenesis in the embryonic and adult brain, but relatively little is known about the role of Shh signaling in resveratrol-enhanced neurogenesis after stroke. Methods: Neural stem cells (NSCs) before oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro were pretreated with resveratrol with or without cyclopamine. Survival and proliferation of NSCs was assessed by the CCK8 assay and BrdU immunocytochemical staining. The expressions and activity of signaling proteins and mRNAs were detected by immunocytochemistry, Western blotting, and RT-PCR analysis. Results: Resveratrol significantly increased NSCs survival and proliferation in a concentration-dependent manner after OGD/R injury in vitro. At the same time, the expression of Patched-1, Smoothened (Smo), and Gli-1 proteins and mRNAs was upregulated, and Gli-1 entered the nucleus, which was inhibited by cyclopamine, a Smo inhibitor. Conclusion: Shh signaling mediates resveratrol to increase NSCs proliferation after OGD/R injury in vitro.

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Section: Discussionmentioning

confidence: 99%

“…Park et al reported that resveratrol inhibited hippocampal neurogenesis of healthy mice (1-10 mg/kg body weight), and proliferation of NPCs in culture (20 and 50 μmol/L) [26]. Leong et al reported that 30-120 μmol/L resveratrol inhibited the proliferation of embryonic cardiomyoblasts [27].…”

Section: Discussionmentioning

confidence: 99%

Sonic Hedgehog Signaling Mediates Resveratrol to Increase Proliferation of Neural Stem Cells After Oxygen-Glucose Deprivation/Reoxygenation Injury in Vitro

Cheng

Yu²,

Wang³

et al. 2015

Cell Physiol Biochem

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“…Phytochemicals and Adaptive Responses et al, 2013). On the other hand, resveratrol can downregulate CREB activity and BDNF production in the hippocampus of unstressed mice (Park et al, 2012a). This suggests that resveratrol might differentially regulate BDNF expression depending upon the level of stress encountered by neurons.…”

Section: B Trophic Signaling Pathwaysmentioning

confidence: 99%

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

et al. 2014

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“…Park and Leong et al reported that 20 and 50 μmol/L, 30-120 μmol/L, respectively, resveratrol inhibited proliferation of neural progenitor cells and embryonic cardiomyoblasts [45,46]. Sugino's study showed that 10 and 20 μmol/L resveratrol strengthened nerve growth factor-induced neurite outgrowth in PC12 cells [47].Ren and Tang et al reported that 5 μmol/L resveratrol increased proliferation of neural stem cells and promoted synaptogenesis and neurite outgrowth of neurons after OGD/R injury [20,21].…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Activated Sonic Hedgehog Signaling to Enhance Viability of NIH3T3 Cells in Vitro via Regulation of Sirt1

Guo¹,

Liao²,

Liu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Injuries of the brain and spinal cord result in the formation of glial (reactive gliosis) and fibrotic (formed by fibroblasts) scars. Recent studies have shown that the fibrotic scar was much more important for hindering regeneration after brain or spinal cord injury than the astrocytic scar. However, it has been given much less attention for effects and mechanism of fibroblasts during formation of the fibrotic scar. Resveratrol may be a potential anti-scarring agent in burn-related scarring and keloid fibroblasts. However, it is unclear whether and how resveratrol affects formation of the fibrotic scar after brain or spinal cord injury. Earlier studies have shown that the activated Shh signaling has anti-apoptosis, anti-oxidation, anti-inflammation properties. Moreover, resveratrol can activate the Shh signaling. However, it is unclear how resveratrol activates the Shh signaling. Resveratrol is a activator of Sirt1. It is unknown whether resveratrol activates the Shh signaling via Sirt1. Methods: NIH3T3 cells, a fibroblast cell line, were used as model cells and treated with drugs. Cell viability was assessed by Cell Counting Kit 8. The expressions and activity of Shh signaling pathway proteins were evaluated by immunocytochemistry and Western blotting. Transcriptional activity of Gli-1 was detected with Dual-Luciferase Reporter Gene Assay Kit. Results: Resveratrol, Sirt1 agonist STR1720 and recombinant mouse Shh protein, an activator of hedgehog signaling, enhanced the viability of NIH3T3 cells, promoted Smo to translocated to the primary cilia and Gli-1 entered into the nuclei from cytoplasm, and upregulated expressions of Shh, Ptc-1, Smo, and Gli-1 proteins, which can be reversed by Smo antagonist cyclopamine and Sirt1 antagonist Sirtinol. Additionally, resveratrol increased transcriptional activity of Gli-1. Conclusion: We indicate in the first time that it may be mediated by Sirt1 for resveratrol activating the Shh signaling to enhance viability of NIH3T3 cells, and Sirt1 may be a regulator for upstream of the Shh signaling pathway.This study provides a basis for further investigating effects and mechanism of resveratrol during the formation of fibrous scar after brain or spinal cord injury.

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Resveratrol Inhibits the Proliferation of Neural Progenitor Cells and Hippocampal Neurogenesis

Cited by 84 publications

References 69 publications

Sonic Hedgehog Signaling Mediates Resveratrol to Increase Proliferation of Neural Stem Cells After Oxygen-Glucose Deprivation/Reoxygenation Injury in Vitro

Sonic Hedgehog Signaling Mediates Resveratrol to Increase Proliferation of Neural Stem Cells After Oxygen-Glucose Deprivation/Reoxygenation Injury in Vitro

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

Resveratrol Activated Sonic Hedgehog Signaling to Enhance Viability of NIH3T3 Cells in Vitro via Regulation of Sirt1

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