scholarly journals Recombinant human brain-derived neurotrophic factor prevents neuronal apoptosis in a novel in vitro model of subarachnoid hemorrhage

2017 ◽  
Vol Volume 13 ◽  
pp. 1013-1021 ◽  
Author(s):  
Mingchang Li ◽  
Yuefei Wang ◽  
Wei Wang ◽  
Changlin Zou ◽  
Xin Wang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Human Brain ◽  
Neurotrophic Factor ◽  
Neuronal Apoptosis ◽  
In Vitro Model ◽  
Brain Derived Neurotrophic Factor ◽  
Vitro Model

A Transient Survival Model of Alteration of Electrophysiological Properties Due to Amyloid-Beta Toxicity Based on SH-SY5Y Cell Line

2021 ◽  
Vol 18 ◽  
Author(s):  
M. Abbaszadeh ◽  
M. Sahin ◽  
A. Ozgun ◽  
G. Oncu ◽  
B. Garipcan ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Amyloid Beta ◽  
Neurotrophic Factor ◽  
In Vitro Model ◽  
Brain Derived Neurotrophic Factor ◽  
Survival Model ◽  
Electrophysiological Properties ◽  
Vitro Model

Background: Accumulation of toxic strands of Amyloid Beta (AB), which cause neurofibrillary tangles and, ultimately, cell death, is suspected to be the main culprit behind clinical symptoms of Alzheimer’s disease. Although the mechanism of cell death due to Amyloid-Beta accumulation is well known, the intermediate phase between the start of accumulation and cell death is less known and investigated, partially due to technical challenges in identifying partially affected cells. Objective: First, we aimed to establish an in-vitro model that would show resilience against amyloid-beta toxicity. Then we used morphological, molecular and electrophysiological assays to investigate how the characteristics of the surviving cells changed after amyloid-beta toxicity. Method : To investigate this phase, we used differentiation of SH-SY5Y neuroblastoma stem cells by Retinoic Acid (RA) and Brain Derived Neurotrophic Factor (BDNF) to establish an in-vitro model which would be able to demonstrate various levels of resistance to Amyloid Beta toxicity. We utilized fluorescent microscopy and whole cell patch clamp recordings to investigate behavior of the model. Results: We observed significantly higher morphological resilience against Amyloid Beta toxicity in cells which were differentiated by both Retinoic Acid and Brain Derived Neurotrophic Factor compared to Retinoic Acid only. However, the electrophysiological properties of the Retinoic Acid + Brain-Derived Neurotrophic Factor differentiated cells were significantly altered after Amyloid Beta treatment. Conclusion: We established a transient survival model for amyloid-beta toxicity and observed the effects of Amyloid beta on transmembrane currents of differentiated neurons.

scholarly journals MicroRNA-1297 suppressed the Akt/GSK3β signaling pathway and stimulated neural apoptosis in an in vivo sevoflurane exposure model

2021 ◽  
Vol 49 (4) ◽  
pp. 030006052098210
Author(s):  
Quan Wang ◽  
Jingcong Luo ◽  
Ruiqiang Sun ◽  
Jia Liu
Keyword(s):  
Protein Expression ◽  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
In Vitro Model ◽  
Nervous System Development ◽  
Exposure Model ◽  
Control Group ◽  
Pten Protein ◽  
Vitro Model

Objective Common inhalation anesthetics used for clinical anesthesia (such as sevoflurane) may induce nerve cell apoptosis during central nervous system development. Furthermore, anesthetics can produce cognitive impairments, such as learning and memory impairments, that continue into adulthood. However, the precise mechanism remains largely undefined. We aimed to determine the function of microRNA-1297 (miR-1297) in sevoflurane-induced neurotoxicity. Methods Reverse transcription-polymerase chain reaction assays were used to analyze miR-1297 expression in sevoflurane-exposed mice. MTT and lactate dehydrogenase (LDH) assays were used to measure cell growth, and neuronal apoptosis was analyzed using flow cytometry. Western blot analyses were used to measure PTEN, PI3K, Akt, and GSK3β protein expression. Results In sevoflurane-exposed mice, miR-1297 expression was up-regulated compared with the control group. MiR-1297 up-regulation led to neuronal apoptosis, inhibition of cell proliferation, and increased LDH activity in the in vitro model of sevoflurane exposure. MiR-1297 up-regulation also suppressed the Akt/GSK3β signaling pathway and induced PTEN protein expression in the in vitro model. PTEN inhibition (VO-Ohpic trihydrate) reduced PTEN protein expression and decreased the effects of miR-1297 down-regulation on neuronal apoptosis in the in vitro model. Conclusion Collectively, the results indicated that miR-1297 stimulates sevoflurane-induced neurotoxicity via the Akt/GSK3β signaling pathway by regulating PTEN expression.

β-Asarone Inhibits Neuronal Apoptosis via the CaMKII/CREB/Bcl-2 Signaling Pathway in an in vitro Model and AβPP/PS1 Mice

2013 ◽  
Vol 33 (3) ◽  
pp. 863-880 ◽  
Author(s):  
Gang Wei ◽  
Yun-bo Chen ◽  
Dong-Feng Chen ◽  
Xiao-Ping Lai ◽  
Dong-Hui Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
In Vitro Model ◽  
Vitro Model

Neuronal Apoptosis in an in Vitro Model of Photochemically Induced Oxidative Stress

1995 ◽  
Vol 133 (2) ◽  
pp. 198-206 ◽  
Author(s):  
Hari Manev ◽  
Cinzia M. Cagnoli ◽  
Cagla Atabay ◽  
Elena Kharlamov ◽  
Miloš D. Ikonomović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuronal Apoptosis ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Platelets Alter Gene Expression Profile in Human Brain Endothelial Cells in an In Vitro Model of Cerebral Malaria

PLoS ONE ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. e19651 ◽  
Author(s):  
Mathieu Barbier ◽  
Dorothée Faille ◽  
Béatrice Loriod ◽  
Julien Textoris ◽  
Claire Camus ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Human Brain ◽  
Cerebral Malaria ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
In Vitro Model ◽  
Brain Endothelial Cells ◽  
Vitro Model

scholarly journals Cytosolic Ca2+ Oscillations in Human Cerebrovascular Endothelial Cells after Subarachnoid Hemorrhage

2008 ◽  
Vol 29 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Wolfram Scharbrodt ◽  
Yaser Abdallah ◽  
Sascha A Kasseckert ◽  
Dragan Gligorievski ◽  
Hans M Piper ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
In Vitro Model ◽  
Molecular Mechanisms ◽  
Vascular Inflammation ◽  
Cell Contraction ◽  
Vitro Model ◽  
Cerebrovascular Endothelial Cells

Molecular mechanisms of cerebral vasospasm after subarachnoid hemorrhage (SAH) include specific modes of cell signaling like activation of nuclear factor (NF)-kB and vascular cell adhesion molecules (VCAM)-1 expression. The study's hypothesis is that cisternal cerebral spinal fluid (CSF) from patients after SAH may cause Ca2+ oscillations which induce these modes of vascular inflammation in an in vitro model of human cerebral endothelial cells (HCECs). HCECs were incubated with cisternal CSF from 10 SAH patients with confirmed cerebral vasospasm. The CSF was collected on days 5 and 6 after hemorrhage. Cytosolic Ca2+ concentrations and cell contraction as an indicator of endothelial barrier function were examined by fura-2 microflurometry. Activation of NF-κB and VCAM-1 expression were measured by immunocytochemistry. Incubation of HCEC with SAH-CSF provoked cytosolic Ca2+ oscillations (0.31 ± 0.09 per min), cell contraction, NF-κB activation, and VCAM-1 expression, whereas exposure to native CSF had no significant effect. When endoplasmic reticulum (ER) Ca2+-ATPase and ER inositol trisphosphate (IP3)-sensitive Ca2+ channels were blocked by thapsigargin or xestospongin, the frequency of the Ca2+ oscillations was reduced significantly. In analogy to the reduction of Ca2+ oscillation frequency, the blockers impaired HCEC contraction, NF-κB activation, and VCAM-1 expression. Cisternal SAH-CSF induces cytosolic Ca2+ oscillations in HCEC that results in cellular constriction, NF-κB activation, and VCAM-1 expression. The Ca2+ oscillations depend on the function of ER Ca2+-ATPase and IP3-sensitive Ca2+ channels.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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