Ginsenoside Rg1 Promotes the Migration of Olfactory Ensheathing Cells &lt;i&gt;via&lt;/i&gt; the PI3K/Akt Pathway to Repair Rat Spinal Cord Injury

Jiang

Stem Cells International

et al. 2020

Objectives. To demonstrate the effect of Ginsenoside Rg1 on the differentiation of human bone marrow-derived mesenchymal stem cells (hBM-MSCs). Subsequently, a rational mechanism for the detection of Rg1 which affects mesenchymal stem cell differentiation was explored. Methods. Flow cytometry is used for cell identification. The differentiation ability of hBM-MSCs was studied by differentiation culture. SA-β-gal staining is used to detect cell senescence levels. Western blot and immunofluorescence were used to determine protein expression levels. RT-qPCR is used to detect mRNA expression levels. Results. Rg1 regulates the differentiation of hBM-MSCs. Differentiation culture analysis showed that Rg1 promoted cells to osteogenesis and chondrogenesis. Western blot results showed that Rg1 regulated the overactivation of the β-catenin signaling pathway and significantly adjusted the phosphorylation of GSK-3β. GSK-3β inhibitor (Licl) significantly increased Rg1-induced phosphorylation of GSK-3β, which in turn reduced Rg1-induced differentiation of hBM-MSCs. Conclusion. Ginsenoside Rg1 can reduce the excessive activation of the Wnt pathway in senescent cells by inhibiting the phosphorylation of GSK-3β and regulate the mesenchymal stem cell differentiation ability.

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg1 Improves Differentiation by Inhibiting Senescence of Human Bone Marrow Mesenchymal Stem Cell via GSK-3β and β-Catenin

Jiang

Stem Cells International

et al. 2020

J of Cellular Biochemistry

“…NCAM1 knockdown could decrease the neural invasion and paralysis . Moreover, NCAM1 is defined as one of the migration‐related factors of olfactory ensheathing cells …”

Section: Discussionmentioning

confidence: 99%

siRNA‐mediated NCAM1 gene silencing suppresses oxidative stress in pre‐eclampsia by inhibiting the p38MAPK signaling pathway

Zhang

Han

2019

Pre‐eclampsia (PE), whose pathophysiology and etiology remain undefined, represents a leading consequence of fetal and maternal mortality and morbidity. Oxidative stress (OS) is recognized to involve in this disorder. In this study, we hypothesized that neural cell adhesion molecule 1 (NCAM1) gene silencing would suppress the OS in the pregnancy complicated by PE. Initially, clinical samples were collected for determination of NCAM1 expression in placental tissues and levels of OS products in blood. To assess the regulatory mechanism of NCAM1 knockdown on OS, we used small interfering RNA (siRNA) to silence NCAM1 expression in human umbilical vein endothelial cells (HUVECs). Next, cells were treated with or without hypoxia/reoxygenation to observe the level changes of OS products and p38 mitogen‐activated protein kinase (p38MAPK) pathway‐related genes. Finally, an evaluation of HUVEC migration and invasion abilities was conducted by wound‐healing and transwell assays. Placenta of pregnancy with PE presented significantly increased NCAM1 expression in comparison to placenta of normal pregnancy. Meanwhile, enhanced OS in blood of pregnant women with PE was observed relative to women with normal pregnancy. siRNA‐mediated knockdown of NCAM1 gene could inhibit the p38MAPK signaling pathway, repress OS, and promote cell migration and invasion in HUVECs, indicating that NCAM1 inhibition could reduce the influence of PE. Importantly, blocking the p38MAPK signaling pathway reversed the inhibitory role of NCAM1 gene silencing on PE. Collectively, this study defines potential role of NCAM1 gene silencing as a therapeutic target in PE through inhibiting OS and enhancing HUVEC migration and invasion by disrupting the p38MAPK signaling pathway.

Cell Stress and Chaperones

“…The present study highlights the mechanism controlling mitochondrial homeostasis in the presence of LPSrelated inflammation stress. Notably, several signaling pathways have been found to be associated with OEG viability, such as TGFβ1 (Li et al 2017b), Nurr1 (Liu et al 2018), PI3K/Akt (Tang et al 2017), and Runx1/3 (Wang and Stifani 2017). Additional studies are required to explore whether these pathways are involved in the inflammationmediated OEG damage.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide induces human olfactory ensheathing glial apoptosis by promoting mitochondrial dysfunction and activating the JNK-Bnip3-Bax pathway

Xiang

et al. 2019

Olfactory ensheathing glia (OEG) play an important role in regulating the regeneration of an injured nervous system. However, chronic inflammation damage reduces the viability of OEG via poorly understood mechanisms. We aimed to investigate the pathological responses of OEG in response to LPS-mediated inflammation stress in vitro. The results indicated that lipopolysaccharide (LPS) treatment significantly reduced the viability of OEG in a dose-dependent fashion. Mechanistically, LPS stimuli induced mitochondrial oxidative damage, mitochondrial fragmentation, mitochondrial metabolism disruption, and mitochondrial apoptosis activation. Furthermore, we verified that LPS modulated mitochondrial apoptosis by promoting Bax upregulation, and this process was regulated by the JNK-Bnip3 pathway. Inhibition of the JNK-Bnip3 pathway prevented LPS-mediated Bax activation, thus attenuating OEG apoptosis. Altogether, our data illustrated that LPS-mediated inflammation injury evoked mitochondrial abnormalities in OEG damage via the JNK-Bnip3-Bax pathway. This finding provides a potential target to protect OEG against chronic inflammation stress.