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Cellular and Molecular Neurobiology

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https://www.readbyqxmd.com/read/30415355/an-in-vitro-model-for-conditioning-lesion-effect
#1
Elif Kaval Oğuz, Gürkan Öztürk
Axons of a peripheral nerve grow faster after an axotomy if it attains a prior injury a few days earlier. This is called conditioning lesion effect (CLE) and very much valued since it may provide new insights into neuron biology and axonal regeneration. There are established in vivo experimental paradigms to study CLE, however, there is a need to have an in vitro conditioning technique where CLE occurs in a maximally controlled environment. Mouse primary sensory neurons were isolated from lumbar 4-5 dorsal root ganglia and incubated at 37 °C on a silicon-coated watch glass that prevents cell attachment...
November 10, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30377908/hypothalamic-inflammation-at-a-crossroad-of-somatic-diseases
#2
REVIEW
Boris Mravec, Lubica Horvathova, Alena Cernackova
Various hypothalamic nuclei function as central parts of regulators that maintain homeostasis of the organism. Recently, findings have shown that inflammation in the hypothalamus may significantly affect activity of these homeostats and consequently participate in the development of various somatic diseases such as obesity, diabetes, hypertension, and cachexia. In addition, hypothalamic inflammation may also affect aging and lifespan. Identification of the causes and mechanisms involved in the development of hypothalamic inflammation creates not only a basis for better understanding of the etiopathogenesis of somatic diseases, but for the development of new therapeutic approaches for their treatment, as well...
October 30, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30361892/research-advances-of-germinal-matrix-hemorrhage-an-update-review
#3
REVIEW
Jinqi Luo, Yujie Luo, Hanhai Zeng, Cesar Reis, Sheng Chen
Germinal matrix hemorrhage (GMH) refers to bleeding that derives from the subependymal (or periventricular) germinal region of the premature brain. GMH can induce severe and irreversible damage attributing to the vulnerable structure of germinal matrix and deleterious circumstances. Molecular mechanisms remain obscure so far. In this review, we summarized the newest preclinical discoveries recent years about GMH to distill a deeper understanding of the neuropathology, and then discuss the potential diagnostic or therapeutic targets among these pathways...
October 25, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30302630/steroids-in-stroke-with-special-reference-to-progesterone
#4
REVIEW
Rachida Guennoun, Xiaoyan Zhu, Magalie Fréchou, Pauline Gaignard, Abdelhamid Slama, Philippe Liere, Michael Schumacher
Both sex and steroid hormones are important to consider in human ischemic stroke and its experimental models. Stroke initiates a cascade of changes that lead to neural cell death, but also activates endogenous protective processes that counter the deleterious consequences of ischemia. Steroids may be part of these cerebroprotective processes. One option to provide cerebroprotection is to reinforce these intrinsic protective mechanisms. In the current review, we first summarize studies describing sex differences and the influence of steroid hormones in stroke...
October 9, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30291573/corticosteroid-receptors-in-the-brain-transcriptional-mechanisms-for-specificity-and-context-dependent-effects
#5
REVIEW
Onno C Meijer, J C Buurstede, Marcel J M Schaaf
Corticosteroid hormones act in the brain to support adaptation to stress via binding to mineralocorticoid and glucocorticoid receptors (MR and GR). These receptors act in large measure as transcription factors. Corticosteroid effects can be highly divergent, depending on the receptor type, but also on brain region, cell type, and physiological context. These differences ultimately depend on differential interactions of MR and GR with other proteins, which determine ligand binding, nuclear translocation, and transcriptional activities...
October 5, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30218404/a-novel-microfluidic-device-based-neurite-outgrowth-inhibition-assay-reveals-the-neurite-outgrowth-promoting-activity-of-tropomyosin-tpm3-1-in-hippocampal-neurons
#6
Holly Stefen, Amin Hassanzadeh-Barforoushi, Merryn Brettle, Sandra Fok, Alexandra K Suchowerska, Nicodemus Tedla, Tracie Barber, Majid Ebrahimi Warkiani, Thomas Fath
Overcoming neurite inhibition is integral for restoring neuronal connectivity after CNS injury. Actin dynamics are critical for neurite growth cone formation and extension. The tropomyosin family of proteins is a regarded as master regulator of actin dynamics. This study investigates tropomyosin isoform 3.1 (Tpm3.1) as a potential candidate for overcoming an inhibitory substrate, as it is known to influence neurite branching and outgrowth. We designed a microfluidic device that enables neurons to be grown adjacent to an inhibitory substrate, Nogo-66...
September 14, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30218403/the-beta-hydroxybutyrate-suppresses-the-migration-of-glioma-cells-by-inhibition-of-nlrp3-inflammasome
#7
Sen Shang, Leilei Wang, Yali Zhang, Haixia Lu, Xiaoyun Lu
Activation of inflammasome leads to the formation of an inflammatory microenvironment which plays an important role in the process of cancer development. Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome. Here, we investigated the potential influence of BHB on the in vitro migration of C6 glioma cells and the activation of NLRP3 inflammasome. Our results indicated that administration of BHB suppressed C6 cells migration and NLRP3 inflammasome activation, reducing the levels of activated cysteinyl aspartate-specific proteinase 1 (caspase-1) and mature Interleukin 1β (IL-1β)...
September 14, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30206749/correction-to-posttraumatic-stress-disorder-disturbs-coronary-tone-and-its-regulatory-mechanisms
#8
Svetlana S Lazuko, Olga P Kuzhel, Lyudmila E Belyaeva, Eugenia B Manukhina, H Fred Downey, Olga B Tseilikman, Maria V Komelkova, Vadim E Tseilikman
The original version of this article unfortunately contained a mistake in the co-author name.
September 11, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30187261/allopregnanolone-and-progesterone-in-experimental-neuropathic-pain-former-and-new-insights-with-a-translational-perspective
#9
REVIEW
Susana Laura González, Laurence Meyer, María Celeste Raggio, Omar Taleb, María Florencia Coronel, Christine Patte-Mensah, Ayikoe Guy Mensah-Nyagan
In the last decades, an active and stimulating area of research has been devoted to explore the role of neuroactive steroids in pain modulation. Despite challenges, these studies have clearly contributed to unravel the multiple and complex actions and potential mechanisms underlying steroid effects in several experimental conditions that mimic human chronic pain states. Based on the available data, this review focuses mainly on progesterone and its reduced derivative allopregnanolone (also called 3α,5α-tetrahydroprogesterone) which have been shown to prevent or even reverse the complex maladaptive changes and pain behaviors that arise in the nervous system after injury or disease...
September 5, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30173378/resetting-the-stress-system-with-a-mifepristone-challenge
#10
REVIEW
Sergiu Dalm, Adriaan M Karssen, Onno C Meijer, Joseph K Belanoff, E Ronald de Kloet
Psychotic depression is characterized by elevated circulating cortisol, and high daily doses of the glucocorticoid/progesterone antagonist mifepristone for 1 week are required for significant improvement. Using a rodent model, we find that such high doses of mifepristone are needed because the antagonist is rapidly degraded and poorly penetrates the blood-brain barrier, but seems to facilitate the entry of cortisol. We also report that in male C57BL/6J mice, after a 7-day treatment with a high dose of mifepristone, basal blood corticosterone levels were similar to that of vehicle controls...
September 1, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30117098/mineralocorticoid-receptors-neuroinflammation-and-hypertensive-encephalopathy
#11
REVIEW
Maria Elvira Brocca, Luciana Pietranera, Edo Ronald de Kloet, Alejandro Federico De Nicola
Worldwide, raised blood pressure is estimated to affect 35-40% of the adult population and is a main conditioning factor for cardiovascular diseases and stroke. Animal models of hypertension have provided great advances concerning the pathophysiology of human hypertension, as already shown for the deoxycorticosterone-salt treated rat, the Dahl-salt sensitive rat, the Zucker obese rat and the spontaneously hypertensive rat (SHR). SHR has been widely used to study abnormalities of the brain in chronic hypertension...
August 16, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30361893/correction-to-n-terminal-fusion-potentiates-%C3%AE-synuclein-secretion
#12
Björn H Falkenburger
The original version of this article unfortunately contained a mistake in the article title. The term secretion is missed out in the title. The correct title is: N-terminal fusion potentiates α-synuclein secretion.
November 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30315388/systemic-inflammation-impairs-proliferation-of-hippocampal-type-2-intermediate-precursor-cells
#13
Marlene Sinai Melo-Salas, Martha Pérez-Domínguez, Angélica Zepeda
Neurogenesis is a plastic event modulated by external cues. Systemic inflammation decreases neurogenesis in the dentate gyrus (DG) in part through the proliferative restrain of neural precursor cells (NPCs). To evaluate if inflammation affects the cell cycle progression of particular populations of NPCs, we treated young-adult mice with a single i.p. injection of saline or 1 mg/kg LPS. After 7 days, we analysed proliferation of new BrdU+/DCX+ cells through immunohistochemistry. We extracted the hippocampus and performed a neurosphere assay and a flow cytometric analysis to evaluate proliferation and to identify the phase of the cell cycle in specific populations of DG-derived NPCs...
November 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30315387/pgc-1%C3%AE-mediated-mitochondrial-biogenesis-is-involved-in-cannabinoid-receptor-2-agonist-am1241-induced-microglial-phenotype-amelioration
#14
Lei Ma, Wen Niu, Jianrui Lv, Ji Jia, Miaozhang Zhu, Shuai Yang
Cannabinoid type 2 receptor (CB2R) agonist AM1241 induces anti-inflammation by ameliorating microglial phenotypes, the mechanism, however, is still unknown. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a transcription protein which can regulate mitochondrial biogenesis, and the aim of this study is to investigate whether PGC-1α is involved in AM1241-induced anti-inflammation in N9 microglial cells. We used 10 ng/ml lipopolysaccharide (LPS) plus 10 U/ml interferon γ (IFNγ) to activate microglia into classic activated phenotype (M1 phenotype), and found that co-administration of 10 µM AM1241 increased the expressions of mitochondria biogenesis-associated proteins, including nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (TFAM) and COX IV, and up-regulated the biomarker levels of microglial M2 phenotype, including arginase 1 (Arg-1) and brain-derived neurotrophic factor (BDNF), and down-regulated biomarker levels of M1 phenotype, including inducible nitric oxide synthase (iNOS) and tumor necrosis factor α (TNF-α), compared to the cells treated with LPS plus IFNγ only (P < 0...
November 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30302629/pantoprazole-induces-mitochondrial-apoptosis-and-attenuates-nf-%C3%AE%C2%BAb-signaling-in-glioma-cells
#15
Khamushavalli Geeviman, Deepak Babu, Phanithi Prakash Babu
Gastric H+ /K+ -ATPase or vacuolar-ATPases (V-ATPases) are critical for the cancer cells survival and growth in the ischemic microenvironment by extruding protons from the cell. The drugs which inhibit V-ATPases are known as proton pump inhibitors (PPIs). In the present study, we aimed to evaluate the anticancer efficacy of pantoprazole (PPZ) and its consequences on NF-κB signaling in glioma cells. We have used MTT and clonogenic assay to show PPZ effect on glioma cell growth. Propidium iodide and rhodamine 123 staining were performed to demonstrate cell cycle arrest and mitochondrial depolarization...
November 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30302628/oxidative-imbalance-nitrative-stress-and-inflammation-in-c6-glial-cells-exposed-to-hexacosanoic-acid-protective-effect-of-n-acetyl-l-cysteine-trolox-and-rosuvastatin
#16
Desirèe Padilha Marchetti, Luiza Steffens, Carlos E Jacques, Gilian B Guerreiro, Caroline P Mescka, Marion Deon, Daniella M de Coelho, Dinara J Moura, Alice G Viario, Fernanda Poletto, Adriana S Coitinho, Laura B Jardim, Carmen R Vargas
X-linked adrenoleukodystrophy (X-ALD) is an inherited neurometabolic disorder caused by disfunction of the ABCD1 gene, which encodes a peroxisomal protein responsible for the transport of the very long-chain fatty acids from the cytosol into the peroxisome, to undergo β-oxidation. The mainly accumulated saturated fatty acids are hexacosanoic acid (C26:0) and tetracosanoic acid (C24:0) in tissues and body fluids. This peroxisomal disorder occurs in at least 1 out of 20,000 births. Considering that pathophysiology of this disease is not well characterized yet, and glial cells are widely used in studies of protective mechanisms against neuronal oxidative stress, we investigated oxidative damages and inflammatory effects of vesicles containing lecithin and C26:0, as well as the protection conferred by N-acetyl-L-cysteine (NAC), trolox (TRO), and rosuvastatin (RSV) was assessed...
November 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30288631/secretion-and-uptake-of-%C3%AE-synuclein-via-extracellular-vesicles-in-cultured-cells
#17
Gabriel Gustafsson, Camilla Lööv, Emma Persson, Diana F Lázaro, Shuko Takeda, Joakim Bergström, Anna Erlandsson, Dag Sehlin, Leonora Balaj, Bence György, Martin Hallbeck, Tiago F Outeiro, Xandra O Breakefield, Bradley T Hyman, Martin Ingelsson
In Parkinson's disease and other Lewy body disorders, the propagation of pathology has been accredited to the spreading of extracellular α-synuclein (α-syn). Although the pathogenic mechanisms are not fully understood, cell-to-cell transfer of α-syn via exosomes and other extracellular vesicles (EVs) has been reported. Here, we investigated whether altered molecular properties of α-syn can influence the distribution and secretion of α-syn in human neuroblastoma cells. Different α-syn variants, including α-syn:hemi-Venus and disease-causing mutants, were overexpressed and EVs were isolated from the conditioned medium...
November 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30288630/n-terminal-fusion-potentiates-%C3%AE-synuclein-secretion
#18
REVIEW
Björn H Falkenburger
No abstract text is available yet for this article.
November 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30155758/curcumin-attenuates-gp120-induced-microglial-inflammation-by-inhibiting-autophagy-via-the-pi3k-pathway
#19
Guiling Chen, Sisi Liu, Rui Pan, Guangming Li, Haijie Tang, Mingliang Jiang, Yanyan Xing, Fujun Jin, Liqing Lin, Jun Dong
Microglial inflammation plays an essential role in the pathogenesis of HIV-associated neurocognitive disorders. A previous study indicated that curcumin relieved microglial inflammatory responses. However, the mechanism of this process remained unclear. Autophagy is a lysosome-mediated cell content-dependent degradation pathway, and uncontrolled autophagy leads to enhanced inflammation. The role of autophagy in curcumin-attenuating BV2 cell inflammation caused by gp120 was investigated with or without pretreatment with the autophagy inhibitor 3-MA and blockers of NF-κB, IKK, AKT, and PI3K, and we then detected the production of the inflammatory mediators monocyte chemoattractant protein-1 (MCP-1) and IL17 using ELISA, and autophagy markers ATG5 and LC3 II by Western Blot...
November 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/30136167/possible-involvement-of-pten-signaling-pathway-in-the-anti-apoptotic-effect-of-electroacupuncture-following-ischemic-stroke-in-rats
#20
Ying Xing, Man-Man Wang, Ya-Shuo Feng, Fang Dong, Feng Zhang
As a traditional therapeutic method, electroacupuncture (EA) has been adopted as an alternative therapy for stroke recovery. Here, we aimed to evaluate whether EA therapy at points of Quchi (LI11) and Zusanli (ST36) alleviated neuronal apoptosis by PTEN signaling pathway after ischemic stroke. A total of 72 male Sprague-Dawley rats were randomized into three groups, including sham group, MCAO group, and EA group. EA was initiated after 24 h of reperfusion for 3 consecutive days. At 72 h following ischemia/reperfusion, neurological deficits, infarct volumes, and TUNEL staining were evaluated and the PTEN pathway-related proteins together with apoptosis-related proteins were detected...
November 2018: Cellular and Molecular Neurobiology
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