Current Findings on the Morphological Induction of Synaptogenesis in Neuronal Cells in Vitro

22(R)-hydroxycholesterol for dopaminergic neuronal specification of MSCs and amelioration of Parkinsonian symptoms in rats

Cell Death Discovery ◽

10.1038/s41420-020-00351-6 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Manisha Singh ◽

Manish Jain ◽

Samrat Bose ◽

Ashutosh Halder ◽

Tapas Chandra Nag ◽

...

Keyword(s):

Parkinson’S Disease ◽

Stem Cells ◽

Parkinson's Disease ◽

Dental Pulp ◽

Neuronal Cells ◽

Human Mesenchymal Stem Cells ◽

Wistar Rat ◽

Human Mscs ◽

In Vitro Differentiation

AbstractOxysterols play vital roles in the human body, ranging from cell cycle regulation and progression to dopaminergic neurogenesis. While naïve human mesenchymal stem cells (hMSCs) have been explored to have neurogenic effect, there is still a grey area to explore their regenerative potential after in vitro differentiation. Hence, in the current study, we have investigated the neurogenic effect of 22(R)-hydroxycholesterol (22-HC) on hMSCs obtained from bone marrow, adipose tissue and dental pulp. Morphological and morphometric analysis revealed physical differentiation of stem cells into neuronal cells. Detailed characterization of differentiated cells affirmed generation of neuronal cells in culture. The percentage of generation of non-DA cells in the culture confirmed selective neurogenic potential of 22-HC. We substantiated the efficacy of these cells in neuro-regeneration by transplanting them into Parkinson’s disease Wistar rat model. MSCs from dental pulp had maximal regenerative effect (with 80.20 ± 1.5% in vitro differentiation efficiency) upon transplantation, as shown by various behavioural examinations and immunohistochemical tests. Subsequential analysis revealed that 22-HC yields a higher percentage of functional DA neurons and has differential effect on various tissue-specific primary human MSCs. 22-HC may be used for treating Parkinson’s disease in future with stem cells.

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SIRT1 and SIRT2 modulators reduce LPS-induced inflammation in HAPI microglial cells and protect SH-SY5Y neuronal cells in vitro

Journal of Neural Transmission ◽

10.1007/s00702-021-02331-1 ◽

2021 ◽

Author(s):

Yuqing Zhang ◽

Shailendra Anoopkumar-Dukie ◽

Sanchari Basu Mallik ◽

Andrew K. Davey

Keyword(s):

Neuronal Cells ◽

Microglial Cells

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Mesenchymal Stem Cells (MSCs) Coculture Protects [Ca2+]i Orchestrated Oxidant Mediated Damage in Differentiated Neurons In Vitro

Cells ◽

10.3390/cells7120250 ◽

2018 ◽

Vol 7 (12) ◽

pp. 250 ◽

Cited By ~ 9

Author(s):

Adel Alhazzani ◽

Prasanna Rajagopalan ◽

Zaher Albarqi ◽

Anantharam Devaraj ◽

Mohamed Hessian Mohamed ◽

...

Keyword(s):

Cell Death ◽

Transforming Growth Factor ◽

Neuronal Cells ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Apoptotic Cells ◽

Sequence Of Events ◽

Cox 2 ◽

Anti Inflammatory

Cell-therapy modalities using mesenchymal stem (MSCs) in experimental strokes are being investigated due to the role of MSCs in neuroprotection and regeneration. It is necessary to know the sequence of events that occur during stress and how MSCs complement the rescue of neuronal cell death mediated by [Ca2+]i and reactive oxygen species (ROS). In the current study, SH-SY5Y-differentiated neuronal cells were subjected to in vitro cerebral ischemia-like stress and were experimentally rescued from cell death using an MSCs/neuronal cell coculture model. Neuronal cell death was characterized by the induction of proinflammatory tumor necrosis factor (TNF)-α, interleukin (IL)-1β and -12, up to 35-fold with corresponding downregulation of anti-inflammatory cytokine transforming growth factor (TGF)-β, IL-6 and -10 by approximately 1 to 7 fold. Increased intracellular calcium [Ca2+]i and ROS clearly reaffirmed oxidative stress-mediated apoptosis, while upregulation of nuclear factor NF-B and cyclo-oxygenase (COX)-2 expressions, along with ~41% accumulation of early and late phase apoptotic cells, confirmed ischemic stress-mediated cell death. Stressed neuronal cells were rescued from death when cocultured with MSCs via increased expression of anti-inflammatory cytokines (TGF-β, 17%; IL-6, 4%; and IL-10, 13%), significantly downregulated NF-B and proinflammatory COX-2 expression. Further accumulation of early and late apoptotic cells was diminished to 23%, while corresponding cell death decreased from 40% to 17%. Low superoxide dismutase 1 (SOD1) expression at the mRNA level was rescued by MSCs coculture, while no significant changes were observed with catalase (CAT) and glutathione peroxidase (GPx). Interestingly, increased serotonin release into the culture supernatant was proportionate to the elevated [Ca2+]i and corresponding ROS, which were later rescued by the MSCs coculture to near normalcy. Taken together, all of these results primarily support MSCs-mediated modulation of stressed neuronal cell survival in vitro.

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Features of blood-brain barrier formation affected by the modulation of HIF activity in astroglial and neuronal cells in vitro

Biochemistry (Moscow) Supplement Series B Biomedical Chemistry ◽

10.1134/s1990750817010085 ◽

2017 ◽

Vol 11 (1) ◽

pp. 81-86

Author(s):

V. A. Ruzaeva ◽

A. V. Morgun ◽

E. D. Khilazheva ◽

N. V. Kuvacheva ◽

E. A. Pozhilenkova ◽

...

Keyword(s):

Blood Brain Barrier ◽

Neuronal Cells ◽

Brain Barrier ◽

Blood Brain ◽

Barrier Formation

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Small extracellular vesicles encapsulating CCL2 from activated astrocytes induce microglial activation and neuronal apoptosis after traumatic spinal cord injury

Journal of Neuroinflammation ◽

10.1186/s12974-021-02268-y ◽

2021 ◽

Vol 18 (1) ◽

Author(s):

Yuluo Rong ◽

Chengyue Ji ◽

Zhuanghui Wang ◽

Xuhui Ge ◽

Jiaxing Wang ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Extracellular Vesicles ◽

Neuronal Apoptosis ◽

Microglial Activation ◽

Neuronal Cells ◽

Cell Communication ◽

Bioactive Lipids ◽

Cord Injury

Abstract Background Spinal cord injury (SCI) is a severe traumatic disease which causes high disability and mortality rates. The molecular pathological features after spinal cord injury mainly involve the inflammatory response, microglial and neuronal apoptosis, abnormal proliferation of astrocytes, and the formation of glial scars. However, the microenvironmental changes after spinal cord injury are complex, and the interactions between glial cells and nerve cells remain unclear. Small extracellular vesicles (sEVs) may play a key role in cell communication by transporting RNA, proteins, and bioactive lipids between cells. Few studies have examined the intercellular communication of astrocytes through sEVs after SCI. The inflammatory signal released from astrocytes is known to initiate microglial activation, but its effects on neurons after SCI remain to be further clarified. Methods Electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blotting were applied to characterize sEVs. We examined microglial activation and neuronal apoptosis mediated by astrocyte activation in an experimental model of acute spinal cord injury and in cell culture in vitro. Results Our results indicated that astrocytes activated after spinal cord injury release CCL2, act on microglia and neuronal cells through the sEV pathway, and promote neuronal apoptosis and microglial activation after binding the CCR2. Subsequently, the activated microglia release IL-1β, which acts on neuronal cells, thereby further aggravating their apoptosis. Conclusion This study elucidates that astrocytes interact with microglia and neurons through the sEV pathway after SCI, enriching the mechanism of CCL2 in neuroinflammation and spinal neurodegeneration, and providing a new theoretical basis of CCL2 as a therapeutic target for SCI.

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Haloperidol and Risperidone Induce Apoptosis Neuronal Cell : Invivo Study

Scientia Psychiatrica ◽

10.37275/scipsy.v1i1.5 ◽

2020 ◽

Vol 1 (1) ◽

Author(s):

Ester G Panserga ◽

Cecep S Kristanto ◽

Budi Pratiti ◽

Patricia Wulandari

Keyword(s):

Cell Apoptosis ◽

Wistar Rats ◽

Caspase 3 ◽

Neuronal Cells ◽

Neuronal Cell ◽

Total Percentage ◽

White Rats ◽

Male Wistar Rats ◽

Group B

Abstract Introduction Antipsychotics are drugs that are widely prescribed for mental disorders, such as schizophrenia and psychosis. Recent in vitro studies show antipsychotics play a role in the initiation of neuronal cell apoptosis. This study aims to determine the effect of haloperidol and risperidone on neuronal cell apoptosis in Wistar white rats. Methods Male wistar rats aged 8 weeks (n = 30) were used in this study. Wistar rats were randomized into 6 groups. Group A: 5 wistar rats as a control without induced schizophrenia, aquades and drugs. Group B: 5 Wistar-induced psychotic mice (using 30 mg / kgBB ketamine, intraperitoneal injection for 5 days) and aquadest. Group C: 5 rats were induced psychotic and were given haloperidol or 0.05 mg / kgBB orally, for 28 days. Group D: 5 mice were induced psychotic and were given haloperidol 0.1 mg / kg orally, for 28 days. Group E: 5 mice were induced psychotic and were given risperidone 0.05 mg / kgBB orally, for 28 days. Group F: 5 mice were induced psychotic and given risperidone 0.1 mg / kgBB orally, for 28 days. Apoptosis of neuronal cells in the ventral tegmental area was assessed by caspase-3 immunohistochemistry. The colored area will be calculated as a total percentage using the imageJ program. Results Risperidone and haloperidol increase caspase-3 activity, but haloperidol increases caspase-3 activity more than risperidone. Conclussion Risperidone and haloperidol induce apoptosis of neuronal cells and tardive dyskinesia in Wistar rats with psychotic models.

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The natural product 4,10-aromadendranediol induces neuritogenesis in neuronal cells in vitro through activation of the ERK pathway

Acta Pharmacologica Sinica ◽

10.1038/aps.2016.115 ◽

2016 ◽

Vol 38 (1) ◽

pp. 29-40 ◽

Cited By ~ 6

Author(s):

Sai Chang ◽

Wen-chen Ruan ◽

Ya-zhou Xu ◽

Yun-jie Wang ◽

Jie Pang ◽

...

Keyword(s):

Natural Product ◽

Neuronal Cells ◽

Erk Pathway

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Poliovirus Internal Ribosome Entry Segment Structure Alterations That Specifically Affect Function in Neuronal Cells: Molecular Genetic Analysis

Journal of Virology ◽

10.1128/jvi.76.21.10617-10626.2002 ◽

2002 ◽

Vol 76 (21) ◽

pp. 10617-10626 ◽

Cited By ~ 37

Author(s):

Cécile E. Malnou ◽

Tuija A. A. Pöyry ◽

Richard J. Jackson ◽

Katherine M. Kean

Keyword(s):

Secondary Structure ◽

Neuronal Cells ◽

Neuronal Cell ◽

In Vitro Translation ◽

Internal Ribosome Entry ◽

Cell Extracts ◽

Internal Ribosome Entry Segment ◽

Domain V ◽

Bulge Loop

ABSTRACT Translation of poliovirus RNA is driven by an internal ribosome entry segment (IRES) present in the 5′ noncoding region of the genomic RNA. This IRES is structured into several domains, including domain V, which contains a large lateral bulge-loop whose predicted secondary structure is unclear. The primary sequence of this bulge-loop is strongly conserved within enteroviruses and rhinoviruses: it encompasses two GNAA motifs which could participate in intrabulge base pairing or (in one case) could be presented as a GNRA tetraloop. We have begun to address the question of the significance of the sequence conservation observed among enterovirus reference strains and field isolates by using a comprehensive site-directed mutagenesis program targeted to these two GNAA motifs. Mutants were analyzed functionally in terms of (i) viability and growth kinetics in both HeLa and neuronal cell lines, (ii) structural analyses by biochemical probing of the RNA, and (iii) translation initiation efficiencies in vitro in rabbit reticulocyte lysates supplemented with HeLa or neuronal cell extracts. Phenotypic analyses showed that only viruses with both GNAA motifs destroyed were significantly affected in their growth capacities, which correlated with in vitro translation defects. The phenotypic defects were strongly exacerbated in neuronal cells, where a temperature-sensitive phenotype could be revealed at between 37 and 39.5°C. Biochemical probing of mutated domain V, compared to the wild type, demonstrated that such mutations lead to significant structural perturbations. Interestingly, revertant viruses possessed compensatory mutations which were distant from the primary mutations in terms of sequence and secondary structure, suggesting that intradomain tertiary interactions could exist within domain V of the IRES.

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