Mitochondria are intracellular organelles involved in energy production, cell metabolism and cell signaling. They are essential not only in the process of ATP synthesis, lipid metabolism and nucleic acid metabolism, but also in tumor development and metastasis. Mutations in mtDNA are commonly found in cancer cells to promote the rewiring of bioenergetics and biosynthesis, various metabolites especially oncometabolites in mitochondria regulate tumor metabolism and progression. And mutation of enzymes in the TCA cycle leads to the unusual accumulation of certain metabolites and oncometabolites. Mitochondria have been demonstrated as the target for cancer treatment. Cancer cells rely on two main energy resources: oxidative phosphorylation (OXPHOS) and glycolysis. By manipulating OXPHOS genes or adjusting the metabolites production in mitochondria, tumor growth can be restrained. For example, enhanced complex I activity increases NAD+/NADH to prevent metastasis and progression of cancers. In this review, we discussed mitochondrial function in cancer cell metabolism and specially explored the unique role of mitochondria in cancer stem cells and the tumor microenvironment. Targeting the OXPHOS pathway and mitochondria-related metabolism emerging as a potential therapeutic strategy for various cancers.

/pdf/an-overview-the-diversified-role-of-mitochondria-in-cancer-2m4boj9r.pdf

An Overview: The Diversified Role of Mitochondria in Cancer Metabolism

Epilepsy is a common neurological disorder which affects patients physically and mentally and causes a real burden for the patient, family and society both medically and economically. Currently, more than one-third of epilepsy patients are still under unsatisfied control, even with new anticonvulsants. Other measures may be added to those with drug-resistant epilepsy. Excessive neuronal synchronization is the hallmark of epileptic activity and prolonged epileptic discharges such as in status epilepticus can lead to various cellular events and result in neuronal damage or death. Unbalanced oxidative status is one of the early cellular events and a critical factor to determine the fate of neurons in epilepsy. To counteract excessive oxidative damage through exogenous antioxidant supplements or induction of endogenous antioxidative capability may be a reasonable approach for current anticonvulsant therapy. In this article, we will introduce the critical roles of oxidative stress and further discuss the potential use of antioxidants in this devastating disease.

https://www.mdpi.com/2076-3921/9/11/1029/pdf

Seizure-Induced Oxidative Stress in Status Epilepticus: Is Antioxidant Beneficial?

The natural compound asperosaponin VI has shown potential as an antidepressant, but how it works is unclear. Here, we explored its effects on mice exposed to chronic mild stress (CMS) and the underlying molecular pathways.Mice were exposed to CMS for 3 weeks followed by asperosaponin VI (40 mg/kg) or imipramine (20 mg/kg) for another 3 weeks. Depression-like behaviors were assessed in the forced swimming test (FST), sucrose preference test (SPT), tail suspension test (TST). Microglial phenotypes were evaluated using immunofluorescence staining, real-time quantitative PCR and enzyme-linked immunosorbent assays in hippocampus of mice. In some experiments, stressed animals were treated with the PPAR-γ antagonist GW9662 to examine its involvement in the effects of asperosaponin VI. Blockade of PPAR-γ in asperosaponin VI-treated primary microglia in the presence of lipopolysaccharide (LPS) was executed synchronously. The nuclear transfer of PPAR-γ in microglia was detected by immunofluorescence staining in vitro and in vivo. A co-cultured model of neuron and microglia was used for evaluating the regulation of ASA VI on the microglia-neuron crosstalk molecules.Asperosaponin VI ameliorated depression-like behaviors of CMS mice based on SPT, TST and FST, and this was associated with a switch of hippocampal microglia from a pro-inflammatory (iNOS+-Iba1+) to neuroprotective (Arg-1+-Iba1+) phenotype. CMS reduced the expression levels of PPAR-γ and phosphorylated PPAR-γ in hippocampus, which asperosaponin VI partially reversed. GW9662 treatment prevented the nuclear transfer of PPAR-γ in asperosaponin VI-treated microglia and inhibited the induction of Arg-1+ microglia. Blockade of PPAR-γ signaling also abolished the ability of asperosaponin VI to suppress pro-inflammatory cytokines while elevating anti-inflammatory cytokines in the hippocampus of CMS mice. The asperosaponin VI also promoted interactions between hippocampal microglia and neurons by enhancing CX3CL1/CX3CR1 and CD200/CD200R, and preserved synaptic function based on PSD95, CamKII β and GluA levels, but not in the presence of GW9662. Blockade of PPAR-γ signaling also abolished the antidepressant effects of asperosaponin VI in the SPT, TST and FST.CMS in mice induces a pro-inflammatory microglial phenotype that causes reduced crosstalk between microglia and neuron, inflammation and synaptic dysfunction in the hippocampus, ultimately leading to depression-like behaviors. Asperosaponin VI may ameliorate the effects of CMS by inducing microglia to adopt a PPAR-γ-dependent neuroprotective phenotype. 

/pdf/asperosaponin-vi-ameliorates-the-cms-induced-depressive-like-1v1wsqel.pdf

Asperosaponin VI ameliorates the CMS-induced depressive-like behaviors by inducing a neuroprotective microglial phenotype in hippocampus via PPAR-γ pathway

Epilepsy is a common neurological disease. The dysregulated long noncoding RNAs (lncRNAs) are implicated in epileptogenesis. The aim of this research is to explore the role and mechanism of lncRNA zinc finger antisense 1 (ZFAS1) in status epilepticus (SE)-induced hippocampal neurons injury. SE mice model was established and primary hippocampal neurons were isolated. The expression levels of ZFAS1 and microRNA-421 (miR-421) were detected in hippocampus and hippocampal neurons via quantitative reverse transcription polymerase chain reaction. Hippocampal neurons viability, apoptosis and autophagy were analyzed via Cell Counting Kit-8, flow cytometry and western blot. The target relationship between ZFAS1 and miR-421 was analyzed via dual-luciferase reporter assay. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway was blocked by LY294002 and related protein levels were detected via western blot. ZFAS1 expression was elevated in hippocampus and hippocampal neurons from SE mice. Knockdown of ZFAS1 increased SE hippocampal neurons viability and decreased apoptosis and autophagy. ZFAS1 could sponge miR-421. MiR-421 expression was declined in SE mice tissues and cells. Down-regulation of miR-421 abolished the suppressive effect of ZFAS1 knockdown on hippocampal neurons apoptosis and autophagy. Silencing of ZFAS1 induced activation of the PI3K/AKT pathway by up-regulating miR-421. Inhibition of the PI3K/AKT pathway reversed the effect of ZFAS1 knockdown on SE hippocampal neurons apoptosis and autophagy. Interference of ZFAS1 attenuated hippocampal neurons apoptosis and autophagy in SE by increasing miR-421 and activating the PI3K/AKT pathway, indicating a new mechanism for understanding the pathogenesis of SE.

Knockdown of ZFAS1 Inhibits Hippocampal Neurons Apoptosis and Autophagy by Activating the PI3K/AKT Pathway via Up-regulating miR-421 in Epilepsy

Extracellular ATP, which is released from damaged cells after ischemia, activates P2 receptors. P2Y1 receptors (P2Y1R) have received considerable attention, especially in astrocytes, because their ...

Neuroprotective effects of microglial P2Y1 receptors against ischemic neuronal injury.

Cell-based assays (CBAs) and radioimmunoprecipitation assay (RIPA) are the most sensitive methods for identifying anti-acetylcholine receptor (AChR) antibody in myasthenia gravis (MG). But CBAs are limited in clinical practice by transient transfection. We established a stable cell line (KL525) expressing clustered AChR by infecting HEK 293T cells with dual lentiviral vectors expressing the genes encoding the human AChR α1, β1, δ, ϵ and the clustering protein rapsyn. We verified the stable expression of human clustered AChR by immunofluorescence, immunoblotting, and real-time PCR. Fluorescence-activated cell sorting (FACS) was used to detect anti-AChR antibodies in 103 MG patients and 58 healthy individuals. The positive results of MG patients reported by the KL525 was 80.6% (83/103), 29.1% higher than the 51.4% (53/103) of RIPA. 58 healthy individuals tested by both the KL525 CBA and RIPA were all negative. In summary, the stable expression of clustered AChR in our cell line makes it highly sensitive and advantageous for broad clinical application in CBAs.

/pdf/a-stable-cell-line-expressing-clustered-achr-a-novel-cell-39zer9ojq5.pdf

A Stable Cell Line Expressing Clustered AChR: A Novel Cell-Based Assay for Anti-AChR Antibody Detection in Myasthenia Gravis.

Cell trapping is a very useful technique in a variety of cell-based assays and cellular research fields. It requires a high-throughput, high-efficiency operation to isolate cells of interest and immobilize the captured cells at specific positions. In this study, a dentate spiral microfluidic structure is proposed for cell trapping. The structure consists of a main spiral channel connecting an inlet and an out and a large number of dentate traps on the side of the channel. The density of the traps is high. When a cell comes across an empty trap, the cell suddenly makes a turn and enters the trap. Once the trap captures enough cells, the trap becomes closed and the following cells pass by the trap. The microfluidic structure is optimized based on the investigation of the influence over the flow. In the demonstration, 4T1 mouse breast cancer cells injected into the chip can be efficiently captured and isolated in the different traps. The cell trapping operates at a very high flow rate (40 μL/s) and a high trapping efficiency (>90%) can be achieved. The proposed high-throughput cell-trapping technique can be adopted in the many applications, including rapid microfluidic cell-based assays and isolation of rare circulating tumor cells from a large volume of blood sample.

https://www.mdpi.com/2072-666X/12/3/288/pdf

High-Throughput Cell Trapping in the Dentate Spiral Microfluidic Channel.

Aims Activated microglia have been found in the forebrains and hippocampi of temporal lobe epilepsy (TLE) patients and status epileptic (SE) animal models. The peroxisome proliferator-activated receptor γ (PPAR γ) agonist rosiglitazone has been shown to prevent microglial activation. However, its role in pilocarpine-induced status epilepticus remains unknown. We aimed to examine the effect of the PPAR γ agonist rosiglitazone in protecting against pilocarpine-induced status epileptic resulting from over-activation and to explore phenotypic changes in microglia as the underlying mechanism. Methods Male C57BL/6 mice were assigned to three groups: the control group, pilocarpine-induced (SE) group, and rosiglitazone-treated (SE+Rosi) group. Status epileptic mice were administered 300 mg/kg pilocarpine via intraperitoneal injection. SE+Rosi mice were administered rosiglitazone (0.1 mg/kg, i.p.) after SE. Flow cytometry, immunofluorescence staining, and quantitative real-time PCR were used to examine the activation of and phenotypic changes in microglia in the brain and to evaluate neuroinflammation. Results We found that the expression of proinflammatory CD86 and iNOS was increased and that the expression of antiinflammatory CD206 and Arg-1 was decreased in the brains of pilocarpine-induced SE mice compared to control mice. The mRNA levels of proinflammatory and antiinflammatory cytokines were not significantly changed in the brain. Rosiglitazone treatment significantly inhibited the proinflammatory polarization of microglia and rescued neuron loss in the temporal lobe and hippocampi of the brain after SE. Conclusion Rosiglitazone reverses microglial polarization in the brains of SE mice and also affords neuroprotection against pilocarpine-induced status epilepticus without inducing significant changes in brain inflammation.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/cns.13265

Rosiglitazone polarizes microglia and protects against pilocarpine-induced status epilepticus

/pdf/a-3d-printed-standardized-modular-microfluidic-system-for-1jkqevtl.pdf

A 3D-Printed Standardized Modular Microfluidic System for Droplet Generation

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A Stable Cell Line Expressing Clustered AChR: A Novel Cell-Based Assay for Anti-AChR Antibody Detection in Myasthenia Gravis.

High-Throughput Cell Trapping in the Dentate Spiral Microfluidic Channel.

Rosiglitazone polarizes microglia and protects against pilocarpine-induced status epilepticus

A 3D-Printed Standardized Modular Microfluidic System for Droplet Generation