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(1) Extracellular matrix protein tenascin C increases phagocytosis mediated by CD47 loss of function in glioblastoma.[TOP]

Pubmed ID :30898840
Publication Date : //
Glioblastomas (GBM) are highly infiltrated by myeloid-derived innate immune cells that contribute to the immunosuppressive nature of the brain tumor microenvironment (TME). CD47 has been shown to mediate immune evasion, as the CD47-SIRPα axis prevents phagocytosis of tumor cells by macrophages and other myeloid cells. In this study, we established CD47 homozygous deletion (CD47-/-) in human and mouse GBM cells and investigated the impact of eliminating the "don't eat me" signal on tumor growth and tumor-TME interactions. CD47 knockout (KO) did not significantly alter tumor cell proliferation in vitro but significantly increased phagocytosis of tumor cells by macrophages in co-cultures. Compared with CD47 wild type xenografts, orthotopic xenografts derived from CD47-/- tumor cells grew significantly slower with enhanced tumor cell phagocytosis and increased recruitment of M2-like tumor associated microglia/macrophages (TAM). CD47 KO increased tumor-associated extracellular matrix protein tenascin C (TNC) in xenografts, which was further examined in vitro. CD47 loss-of-function upregulated TNC expression in tumor cells via a Notch pathway-mediated mechanism. Depletion of TNC in tumor cells enhanced the growth of CD47-/- xenografts in vivo and decreased the number of TAM. TNC knockdown also inhibited phagocytosis of CD47-/- tumor cells in co-cultures. Furthermore, TNC stimulated release of pro-inflammatory factors including TNF-α via a toll-like receptor 4 (TLR4) and STAT3-dependent mechanism in human macrophage cells. These results reveal a vital role for TNC in immunomodulation in brain tumor biology and demonstrate the prominence of the TME extracellular matrix in affecting the anti-tumor function of brain innate immune cells.

Authors : Xia Shuli, Ma Ding, Liu Senquan, Lal Bachchu, Wei Shuang, Wang Shuyan, Zhan Daqian, Zhang Hao, Lee Richard S, Gao Peisong, Lopez-Bertoni Hernando, Ying Mingyao, Li Jian Jian, Laterra John, Wilson Mary Ann,

(2) Acetonic Fraction of Enriched for Maturase K Is Able to Control Cerebral Parasite Burden in Mice Experimentally Infected With .[TOP]

Pubmed ID :30895180
Publication Date : //
infection can cause abortions or congenital infection for a vast number of domestic animals and humans, leading to economic loss in veterinary sciences, as well as severe consequences for immunocompromised patients. Linné has been used in ethnopharmacology for treatment of diseases, as malaria, diabetes and hepatitis, in addition to its use as antioxidant, antiallergic, anti-inflammatory, and antiviral. The components of this plant have never been studied before for treatment of toxoplasmosis, and the conventional drugs currently used to treat this disease have high degree of toxicity. Thus, the aim of this study was to evaluate the effect of against , by analyzing a total extract of this plant in parallel with a fraction obtained by precipitation in acetone. Also, it was assessed if the acetonic fraction could present lectinic activity, followed by its identification by mass spectrometry. It was observed with the experimental models designed that both total extract and acetonic fraction of were able to control infection by and experiments, in addition to their low toxicity to host cells. Both total extract and acetonic fraction of this plant display capacity to impair replication of tachyzoites. Interesting, the acetonic fraction treatment for 10 days after infection decreases significantly the number of brain cyst in comparison with controls. The protein isolated from acetonic fraction was characterized as a novel lectin identified as maturase K. Taken together, these findings open new perspectives to treat patients infected by . Future studies will be necessary to investigate the precise mechanism underlying the control of infection to impair the replication of this parasite in the host cells after treatment with maturase K.

Authors : Mota Caroline Martins, Santiago Fernanda Maria, Cardoso Mariana de Resende Damas, Rostkowska Cristina, de Oliveira Taísa Carrijo, Silva Deise Aparecida de Oliveira, Pirovani Carlos Priminho, Mineo Tiago Wilson Patriarca, Mineo José Roberto,

(3) EP Antagonist-Elicited Extracellular Vesicles from Mesenchymal Stem Cells Rescue Cognition/Learning Deficiencies by Restoring Brain Cellular Functions.[TOP]

Pubmed ID :30891948
Publication Date : //
Adult brains have limited regenerative capacity. Consequently, both brain damage and neurodegenerative diseases often cause functional impairment for patients. Mesenchymal stem cells (MSCs), one type of adult stem cells, can be isolated from various adult tissues. MSCs have been used in clinical trials to treat human diseases and the therapeutic potentials of the MSC-derived secretome and extracellular vesicles (EVs) have been under investigation. We found that blocking the prostaglandin E /prostaglandin E receptor 4 (PGE /EP ) signaling pathway in MSCs with EP antagonists increased EV release and promoted the sorting of specific proteins, including anti-inflammatory cytokines and factors that modify astrocyte function, blood-brain barrier integrity, and microglial migration into the damaged hippocampus, into the EVs. Systemic administration of EP antagonist-elicited MSC EVs repaired deficiencies of cognition, learning and memory, inhibited reactive astrogliosis, attenuated extensive inflammation, reduced microglial infiltration into the damaged hippocampus, and increased blood-brain barrier integrity when administered to mice following hippocampal damage. Stem Cells Translational Medicine 2019.

Authors : Chen Shih-Yin, Lin Meng-Chieh, Tsai Jia-Shiuan, He Pei-Lin, Luo Wen-Ting, Herschman Harvey, Li Hua-Jung,

(4) Experimental Pharmacology in Transgenic Rodent Models of Alzheimer's Disease.[TOP]

Pubmed ID :30886583
Publication Date : //
This Mini Review discusses the merits and shortfalls of transgenic (tg) rodents modeling aspects of the human Alzheimer's disease (AD) pathology and their application to evaluate experimental therapeutics. It addresses some of the differences between mouse and rat tg models for these investigations. It relates, in a condensed fashion, the experience of our research laboratory with the application of anti-inflammatory compounds and S-adenosylmethionine (SAM) at the earliest stages of AD-like amyloid pathology in tg mice. The application of SAM was intended to revert the global brain DNA hypomethylation unleashed by the intraneuronal accumulation of amyloid-β-immunoreactive material, an intervention that restored levels of DNA methylation including of the gene. This review also summarizes experimental pharmacology observations made in the McGill tg rat model of AD-like pathology by applying "nano-lithium" or a drug with allosteric M1 muscarinic and sigma 1 receptor agonistic properties (AF710B). Extremely low doses of lithium (up to 400 times lower than used in the clinic) had remarkable beneficial effects on lowering pathology and improving cognitive functions in tg rats. Likewise, AF710B treatment, even at advanced stages of the pathology, displayed remarkable beneficial effects. This drug, in experimental conditions, demonstrated possible "disease-modifying" properties as pathology was frankly diminished and cognition improved after a month of "wash-out" period. The Mini-Review ends with a discussion on the predictive value of similar experimental pharmacological interventions in current rodent tg models. It comments on the validity of some of these approaches for early interventions at preclinical stages of AD, interventions which may be envisioned once definitive diagnosis of AD before clinical presentation is made possible.

Authors : Cuello A Claudio, Hall Hélène, Do Carmo Sonia,

(5) Assembly of transgenic human P301S Tau is necessary for neurodegeneration in murine spinal cord.[TOP]

Pubmed ID :30885267
Publication Date : //
A pathological pathway leading from soluble monomeric to insoluble filamentous Tau is characteristic of many human neurodegenerative diseases, which also exhibit dysfunction and death of brain cells. However, it is unknown how the assembly of Tau into filaments relates to cell loss. To study this, we first used a mouse line transgenic for full-length human mutant P301S Tau to investigate the temporal relationship between Tau assembly into filaments, assessed using anti-Tau antibody AT100, and motor neuron numbers, in the lumbar spinal cord. AT100 immunoreactivity preceded nerve cell loss. Murine Tau did not contribute significantly to either Tau aggregation or neurodegeneration. To further study the relevance of filament formation for neurodegeneration, we deleted hexapeptides VQIINK and VQIVYK, either singly or in combination, from human 0N4R Tau with the P301S mutation. These hexapeptides are essential for the assembly of Tau into filaments. Homozygous mice transgenic for P301S Tau with the hexapeptide deletions, which expressed Tau at a similar level to the heterozygous line transgenic for P301S Tau, had a normal lifespan, unlike mice from the P301S Tau line. The latter had significant levels of sarkosyl-insoluble Tau in brain and spinal cord, and exhibited neurodegeneration. Mice transgenic for P301S Tau with the hexapeptide deletions failed to show significant levels of sarkosyl-insoluble Tau or neurodegeneration. Recombinant P301S Tau with the hexapeptide deletions failed to form β-sheet structure and filaments following incubation with heparin. Taken together, we conclude that β-sheet assembly of human P301S Tau is necessary for neurodegeneration in transgenic mice.

Authors : Macdonald Jennifer A, Bronner Iraad F, Drynan Lesley, Fan Juan, Curry Annabelle, Fraser Graham, Lavenir Isabelle, Goedert Michel,

(6) Amyotrophic lateral sclerosis.[TOP]

Pubmed ID :30879475
Publication Date : //
Amyotrophic lateral sclerosis (ALS) is caused by selective and progressive loss of spinal, bulbar and cortical motoneurons and leads to irreversible paralysis, loss of speech, inability to swallow and respiratory malfunctions with the eventual death of the affected individual in a rapid disease course. Several suggested molecular pathways are reviewed including SOD1 gene mutation, protein nitrosylation, phosphorylation and oxidative stress, excitotoxicity, glutamate transporter deprivation, mitochondrial involvement, protein aggregation and motor neuron trophic factors. The role of insulin and its receptor in the brain is described. It is very possible that in 90% of the sporadic ALS cases, the cause of the motor neuron degeneration is different or that multiple mechanisms are involved that would need drugs with multiple mechanisms or action. Several marketed drugs have been selected for clinical trials. Only two drugs have been approved by the FDA as showing positive effect in ALS: Riluzole and Edaravone. Two other drugs that have a significant benefit in ALS are Talampanel and Tamoxifen. The results for modulation of the neurotrophic factor Insulin Growth Factor-1 (IGF1) as a potential treatment are inconclusive. Several compounds are discussed that show a positive effect in the mouse model but which have failed in clinical trials. New approaches using different modalities such as peptides, proteins and stem cells are promising. Our ability to design better drugs would be enhanced by investigating the endogenous factors in neuron death, protein aggregation and oxidative stress that would improve our understanding of the potential pathways that result in neurodegeneration.

Authors : Valko Klara, Ciesla Lukasz,

(7) Microglia lacking a peroxisomal β-oxidation enzyme chronically alter their inflammatory profile without evoking neuronal and behavioral deficits.[TOP]

Pubmed ID :30866963
Publication Date : //
Microglia play a central role in most neurological disorders, but the impact of microgliosis on brain environment and clinical functions is not fully understood. Mice lacking multifunctional protein-2 (MFP2), a pivotal enzyme in peroxisomal β-oxidation, develop a fatal disorder characterized by motor problems similar to the milder form of MFP2 deficiency in humans. The hallmark of disease in mice is the chronic proliferation of microglia in the brain, but molecular pathomechanisms that drive rapid clinical deterioration in human and mice remain unknown. In the present study, we identified the effects of specific deletion of MFP2 from microglia in the brain on immune responses, neuronal functioning, and behavior.

Authors : Beckers Lien, Geric Ivana, Stroobants Stijn, Beel Sander, Van Damme Philip, D'Hooge Rudi, Baes Myriam,

(8) CD55 upregulation in astrocytes by statins as potential therapy for AQP4-IgG seropositive neuromyelitis optica.[TOP]

Pubmed ID :30851734
Publication Date : //
Neuromyelitis optica spectrum disorder (herein called NMO) is an inflammatory demyelinating disease that can be initiated by binding of immunoglobulin G autoantibodies (AQP4-IgG) to aquaporin-4 on astrocytes, causing complement-dependent cytotoxicity (CDC) and downstream inflammation. The increased NMO pathology in rodents deficient in complement regulator protein CD59 following passive transfer of AQP4-IgG has suggested the potential therapeutic utility of increasing the expression of complement regulator proteins.

Authors : Tradtrantip Lukmanee, Duan Tianjiao, Yeaman Michael R, Verkman Alan S,

(9) Anti-diabetic properties of different fractions of Korean red ginseng.[TOP]

Pubmed ID :30849506
Publication Date : //
Korean red ginseng (KRG) has been traditionally used to treat diabetes. Ginsenosides are considered as the major bioactive components mediating anti-diabetic effects of KRG. However, considering that ginsenosides account for only about 3-4% of ginsengs, other fractions of KRG may also carry potential anti-diabetic effects. There is no study reporting the differentiated effects of ginsenosides (Spn) and non-saponin fractions (NSpn) of KRG on glycemic control.

Authors : Park Soo Jeong, Nam Jisun, Ahn Chul Woo, Kim YuSik,

(10) In-vitro pre-treatment of cancer cells with TGF-β1: A novel approach of Tail vein lung cancer metastasis mouse model for anti-metastatic studies.[TOP]

Pubmed ID :30848226
Publication Date : //
Aggressive behavior of tumor metastasis comes from certain mutations, changes in cellular metabolic and signaling pathways that are majorly altered by tumor microenvironment (TME), its other components and growth factors like transforming growth factor-β1 (TGF-β1) which is chiefly known for its epithelial to mesenchymal transformation (EMT). EMT is a critical step of metastasis cascade in actual human lung cancer scenario.

Authors : Khan Ghulam Jilany, Sun Li, Abbas Muhammad, Naveed Muhammad, Jamshaid Talha, Baig Mirza Muhammad Faran Ashraf, Yuan Shengtao,