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https://www.readbyqxmd.com/read/29779877/developmental-upregulation-of-ephrin-b1-silences-sema3c-neuropilin-1-signaling-during-post-crossing-navigation-of-corpus-callosum-axons
#1
Erik Mire, Mélanie Hocine, Elsa Bazellières, Thomas Jungas, Alice Davy, Sophie Chauvet, Fanny Mann
The corpus callosum is the largest commissure in the brain, whose main function is to ensure communication between homotopic regions of the cerebral cortex. During fetal development, corpus callosum axons (CCAs) grow toward and across the brain midline and then away on the contralateral hemisphere to their targets. A particular feature of this circuit, which raises a key developmental question, is that the outgoing trajectory of post-crossing CCAs is mirror-symmetric with the incoming trajectory of pre-crossing axons...
May 10, 2018: Current Biology: CB
https://www.readbyqxmd.com/read/29777213/semaphorin-6d-reverse-signaling-controls-macrophage-lipid-metabolism-and-anti-inflammatory-polarization
#2
Sujin Kang, Yoshimitsu Nakanishi, Yoshiyuki Kioi, Daisuke Okuzaki, Tetsuya Kimura, Hyota Takamatsu, Shohei Koyama, Satoshi Nojima, Masayuki Nishide, Yoshitomo Hayama, Yuhei Kinehara, Yasuhiro Kato, Takeshi Nakatani, Tomomi Shimogori, Junichi Takagi, Toshihiko Toyofuku, Atsushi Kumanogoh
Polarization of macrophages into pro-inflammatory or anti-inflammatory states has distinct metabolic requirements, with mechanistic target of rapamycin (mTOR) kinase signaling playing a critical role. However, it remains unclear how mTOR regulates metabolic status to promote polarization of these cells. Here we show that an mTOR-Semaphorin 6D (Sema6D)-Peroxisome proliferator receptor γ (PPARγ) axis plays critical roles in macrophage polarization. Inhibition of mTOR or loss of Sema6D blocked anti-inflammatory macrophage polarization, concomitant with severe impairments in PPARγ expression, uptake of fatty acids, and lipid metabolic reprogramming...
May 18, 2018: Nature Immunology
https://www.readbyqxmd.com/read/29776958/role-of-semaphorin-signaling-during-cardiovascular-development
#3
REVIEW
Qianchuang Sun, Shuyan Liu, Kexiang Liu, Kai Jiao
No abstract text is available yet for this article.
May 18, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29774455/semaphorin-3a-promotes-osteogenic-differentiation-of-bmsc-from-type-2-diabetes-mellitus-rats
#4
Qiao Qiao, Xiaoru Xu, Yingliang Song, Shuang Song, Wenzhong Zhu, Fenglan Li
Bone regeneration is impaired in patients with type 2 diabetes mellitus (T2DM), which leads to non-healing after bone loss. The decreased osteogenic capacity of bone mesenchymal stem cells (BMSCs) might be a main reason. Sema3A, as a powerful protein promoting osteocyte differentiation, shows potential for bone regeneration treatment. BMSCs may be a therapeutic solution. In this study, we divided BMSCs from T2DM rats (BMSCs-D) and normal rats (BMSCs-N), identified their ability to differentiate into different cell types...
May 17, 2018: Journal of Molecular Histology
https://www.readbyqxmd.com/read/29773756/mir126-5p-down-regulation-facilitates-axon-degeneration-and-nmj-disruption-via-a-non-cell-autonomous-mechanism-in-als
#5
Roy Maimon, Ariel Ionescu, Avichai Bonnie, Sahar Sweetat, Shane Wald-Altman, Shani Inbar, Tal Gradus, Davide Trotti, Miguel Weil, Oded Behar, Eran Perlson
Axon degeneration and disruption of neuromuscular junctions (NMJs) are key events in Amyotrophic Lateral Sclerosis (ALS) pathology. Although the disease's etiology is not fully understood, it is thought to involve a non-cell-autonomous mechanism and alterations in RNA metabolism. Here, we identified reduced levels of miR-126-5p in pre-symptomatic ALS male mice models, and an increase in its targets: axon destabilizing type-3 Semaphorins and their co-receptor Neuropilins. Utilizing compartmentalized in vitro co-cultures, we demonstrated that myocytes expressing diverse ALS-causing mutations promote axon degeneration and NMJ dysfunction, which were inhibited by applying Neuropilin1 (NRP1) blocking antibody...
May 17, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29763494/expression-levels-of-semaphorins-3a-3b-4a-and-4d-on-human-peri-implantitis
#6
Marta Ferreira Bastos, Leonardo de Franco, Andressa Cristina Garcia Tebar, Gabriela Giro, Jamil Awad Shibli
PURPOSE: To evaluate the gene expression levels of semaphorins 3A, 3B, 4A, and 4D in both healthy and diseased implants. MATERIALS AND METHODS: Subjects with peri-implantitis presented clinical attachment loss, probing depth ≥ 5 mm, bleeding on probing and/or suppuration, and radiographic bone loss > 4 mm. Peri-implant tissue biopsy specimens were sampled for analysis of the mRNA expression levels for semaphorins 3A, 3B, 4A, and 4D. A real-time polymerase chain reaction was performed, and the gene expression levels of semaphorins in relation to the housekeeping gene were analyzed by using the nonparametric Mann-Whitney test (P < ...
May 2018: International Journal of Oral & Maxillofacial Implants
https://www.readbyqxmd.com/read/29760657/purkinje-cell-signaling-deficits-in-animal-models-of-ataxia
#7
REVIEW
Eriola Hoxha, Ilaria Balbo, Maria Concetta Miniaci, Filippo Tempia
Purkinje cell (PC) dysfunction or degeneration is the most frequent finding in animal models with ataxic symptoms. Mutations affecting intrinsic membrane properties can lead to ataxia by altering the firing rate of PCs or their firing pattern. However, the relationship between specific firing alterations and motor symptoms is not yet clear, and in some cases PC dysfunction precedes the onset of ataxic signs. Moreover, a great variety of ionic and synaptic mechanisms can affect PC signaling, resulting in different features of motor dysfunction...
2018: Frontiers in Synaptic Neuroscience
https://www.readbyqxmd.com/read/29758318/proteome-and-behavioral-alternations-in-phosphorylation-deficient-mutant-collapsin-response-mediator-protein2-knock-in-mice
#8
Haruko Nakamura, Aoi Takahashi-Jitsuki, Hiroko Makihara, Tetsuya Asano, Yayoi Kimura, Jun Nakabayashi, Naoya Yamashita, Yuko Kawamoto, Fumio Nakamura, Toshio Ohshima, Hisashi Hirano, Fumiaki Tanaka, Yoshio Goshima
CRMP2, alternatively designated as DPYSL2, was the first CRMP family member to be identified as an intracellular molecule mediating the signaling of the axon guidance molecule Semaphorin 3A (Sema3A). In Sema3A signaling, cyclin-dependent kinase 5 (Cdk5) primarily phosphorylates CRMP2 at Ser522. Glycogen synthase kinase-3β (GSK-3β) subsequently phosphorylates the residues of Thr509 and Thr514 of CRMP2. Previous studies showed that CRMP2 is involved in pathogenesis of neurological disorders such as Alzheimer's disease...
May 11, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29754498/axonal-guidance-signaling-pathway-is-suppressed-in-human-nasal-polyps
#9
Dawei Wu, Sarina K Mueller, Angela L Nocera, Kristen Finn, Towia A Libermann, Benjamin S Bleier
Background Dysfunctional innervation might contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP), but the state of the axonal outgrowth signaling in CRSwNP is unknown. The purpose of this study was to explore the axonal outgrowth pathway-related protein expression in CRSwNP. Methods Institutional review board approved study in which tissue proteomes were compared between control and CRSwNP patients (n = 10/group) using an aptamer-based proteomic array and confirmed by whole transcriptomic analysis...
January 1, 2018: American Journal of Rhinology & Allergy
https://www.readbyqxmd.com/read/29748532/semaphorin-4d-correlates-with-increased-bone-resorption-hypercalcemia-and-disease-stage-in-newly-diagnosed-patients-with-multiple-myeloma
#10
Evangelos Terpos, Ioannis Ntanasis-Stathopoulos, Dimitrios Christoulas, Tina Bagratuni, Marios Bakogeorgos, Maria Gavriatopoulou, Evangelos Eleutherakis-Papaiakovou, Nikolaos Kanellias, Efstathios Kastritis, Meletios A Dimopoulos
Multiple myeloma (MM) is characterized by bone destruction due to increased bone resorption and decreased bone formation. Semaphorin 4D (CD100, Sema4D) is expressed by osteoclasts, binds to its receptor Plexin-B1, and acts as a mediator of osteoclast-osteoblast interaction that ultimately inhibits osteoblastic bone formation. Preclinical data suggest that Sema4D/Plexin-B1 pathway is implicated in MM-induced bone disease. However, there is no information on the role of Sema4D in MM patients. Thus, we evaluated Sema4D and Plexin-B1 in six myeloma cells lines in vitro; in the bone marrow plasma (BMP) and serum of 72 newly diagnosed symptomatic MM (NDMM) patients and in 25 healthy controls...
May 11, 2018: Blood Cancer Journal
https://www.readbyqxmd.com/read/29740048/matrilysin-mmp-7-cleavage-of-perlecan-hspg2-complexed-with-semaphorin-3a-supports-fak-mediated-stromal-invasion-by-prostate-cancer-cells
#11
Brian J Grindel, Jerahme R Martinez, Tristen V Tellman, Daniel A Harrington, Hamim Zafar, Luay Nakhleh, Leland W Chung, Mary C Farach-Carson
Interrupting the interplay between cancer cells and extracellular matrix (ECM) is a strategy to halt tumor progression and stromal invasion. Perlecan/heparan sulfate proteoglycan 2 (HSPG2) is an extracellular proteoglycan that orchestrates tumor angiogenesis, proliferation, differentiation and invasion. Metastatic prostate cancer (PCa) cells degrade perlecan-rich tissue borders to reach bone, including the basement membrane, vasculature, reactive stromal matrix and bone marrow. Domain IV-3, perlecan's last 7 immunoglobulin repeats, mimics native proteoglycan by promoting tumoroid formation...
May 8, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29721238/unresolved-issues-in-hepatitis-c-the-role-of-liver-non-parenchymal-cells-and-semaphorins
#12
Adriana Vince, Neven Papic
No abstract text is available yet for this article.
March 29, 2018: Infectious Disease Reports
https://www.readbyqxmd.com/read/29720701/bidirectional-regulation-of-bone-formation-by-exogenous-and-osteosarcoma-derived-sema3a
#13
Daniëlle de Ridder, Silvia Marino, Ryan T Bishop, Nathalie Renema, Chantal Chenu, Dominique Heymann, Aymen I Idris
Semaphorin 3A (Sema3A), a secreted member of the Semaphorin family, increases osteoblast differentiation, stimulates bone formation and enhances fracture healing. Here, we report a previously unknown role of Sema3A in the regulation of ectopic bone formation and osteolysis related to osteosarcoma. Human recombinant (exogenous) Sema3A promoted the expression of osteoblastic phenotype in a panel of human osteosarcoma cell lines and inhibited the ability of these cells to migrate and enhance osteoclastogenesis in vitro...
May 2, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29715102/pharmacokinetics-biodistribution-and-toxicity-evaluation-of-anti-sema3a-f11-in-in-vivo-models
#14
Jaehyun Lee, Donggeon Kim, Eunju Son, Su-Ji Yoo, Jason K Sa, Yong Jae Shin, Yeup Yoon, DO-Hyun Nam
BACKGROUND/AIM: The aim of our study was to investigate the pharmacokinetics (PK), tissue distribution and toxicity of F11 antibody to semaphorin 3A in mouse models and explore its anti-angiogenic and tumor-inhibitory effect. MATERIALS AND METHODS: Patient-derived xenograft (PDX) models were established via subcutaneous implantation of glioblastoma multiforme (GBM) cells and treated with F11. RESULTS: F11 significantly attenuated tumor growth and angiogenesis in the GBM PDX model...
May 2018: Anticancer Research
https://www.readbyqxmd.com/read/29702282/wedelolactone-inhibits-osteoclastogenesis-but-enhances-osteoblastogenesis-through-altering-different-semaphorins-production
#15
Xue Deng, Li-Na Liang, Di Zhu, Lu-Ping Zheng, Jing-Hua Yu, Xiang-Ling Meng, Yi-Ning Zhao, Xiao-Xin Sun, Tao-Wen Pan, Yan-Qiu Liu
Our previous study showed that wedelolactone, isolated from Ecliptae herba, enhanced osteoblastogenesis but inhibited osteoclastogenesis through Sema3A signaling pathway. This study aims to investigate the role of other semaphorins in wedelolactone-enhanced osteoblastogenesis and -inhibited osteoclastogenesis. Wedelolactone inhibited RANKL-induced Sema4D and Sema7A production, but had no effect on RANKL-reduced Sema6D expression in osteoclastic RAW264.7 cells. In mouse bone marrow mesenchymal stem cells (BMSC), wedelolactone reversed osteogenic medium(OS)-reduced Sema7A expression and OS-enhanced Sema3E mRNA expression, but no effect on OS-reduced Sema3B mRNA expression...
April 24, 2018: International Immunopharmacology
https://www.readbyqxmd.com/read/29696565/emerging-role-of-semaphorin-3a-in-autoimmune-diseases
#16
REVIEW
Li-Na Liu, Xiao-Mei Li, Dong-Qing Ye, Hai-Feng Pan
Autoimmune diseases (ADs) are featured by the body's immune responses being directed against its own tissues, resulting in prolonged inflammation and subsequent tissue damage. Currently, the exact pathogenesis of ADs remains not fully elucidated. Semaphorin-3A (Sema3A), a secreted member of semaphorin family, is a potent immunoregulator during all immune response stages. Sema3A has wide expression, such as in bone, connective tissue, kidney, neurons, and cartilage. Sema3A can downregulate ADs by suppressing the over-activity of both T-cell and B-cell autoimmunity...
April 25, 2018: Inflammopharmacology
https://www.readbyqxmd.com/read/29666369/lithium-associated-transcriptional-regulation-of-crmp1-in-patient-derived-olfactory-neurons-and-symptom-changes-in-bipolar-disorder
#17
Charlee K McLean, Soumya Narayan, Sandra Y Lin, Narayan Rai, Youjin Chung, MariaMananita S Hipolito, Nicola G Cascella, John I Nurnberger, Koko Ishizuka, Akira S Sawa, Evaristus A Nwulia
There is growing evidence that lithium used in the treatment of bipolar disorder (BD) affects molecular targets that are involved in neuronal growth, survival, and maturation, but it remains unclear if neuronal alterations in any of these molecules predict specific symptom changes in BD patients undergoing lithium monotherapy. The goals of this study were to (a) determine which molecular changes in the olfactory neurons of symptomatic patients receiving lithium are associated with antimanic or antidepressant response, and (b) uncover novel intraneuronal regulatory mechanisms of lithium therapy...
April 18, 2018: Translational Psychiatry
https://www.readbyqxmd.com/read/29661844/plexin-a4-plexin-d1-complexes-convey-semaphorin-3c-signals-to-induce-cytoskeletal-collapse-in-the-absence-of-neuropilins
#18
Tatyana Smolkin, Inbal Nir-Zvi, Nerri Duvshani, Yelena Mumblat, Ofra Kessler, Gera Neufeld
Class-3 semaphorin guidance factors bind to receptor complexes containing neuropilin and plexin receptors. A semaphorin may bind to several receptor complexes containing somewhat different constituents, resulting in diverse effects on cell migration. U87MG glioblastoma cells express both neuropilins and the four class-A plexins. They respond by cytoskeletal collapse and cell contraction to sema3A or sema3B but fail to contract in response to Sema3C, Sema3D, Sema3G or sema3E even when class-A plexins are over-expressed in the cells...
April 16, 2018: Journal of Cell Science
https://www.readbyqxmd.com/read/29642487/semaphorin-3c-and-its-receptors-in-cancer-and-cancer-stem-like-cells
#19
REVIEW
Jing Hao, Jennifer S Yu
Neurodevelopmental programs are frequently dysregulated in cancer. Semaphorins are a large family of guidance cues that direct neuronal network formation and are also implicated in cancer. Semaphorins have two kinds of receptors, neuropilins and plexins. Besides their role in development, semaphorin signaling may promote or suppress tumors depending on their context. Sema3C is a secreted semaphorin that plays an important role in the maintenance of cancer stem-like cells, promotes migration and invasion, and may facilitate angiogenesis...
April 8, 2018: Biomedicines
https://www.readbyqxmd.com/read/29618514/activation-of-stimulator-of-interferon-genes-sting-induces-adam17-mediated-shedding-of-the-immune-semaphorin-sema4d
#20
Kou Motani, Hidetaka Kosako
Stimulator of interferon genes (STING) is an endoplasmic reticulum (ER)-resident membrane protein that mediates cytosolic pathogen DNA-induced innate immunity and inflammatory responses in host defenses. STING is activated by cyclic di-nucleotides and is then translocated to the Golgi apparatus, an event that triggers STING assembly with the downstream enzyme TANK-binding kinase 1 (TBK1). This assembly leads to the phosphorylation of the transcription factor interferon regulatory factor 3 (IRF3), which, in turn, induces expression of type-I interferon (IFN) and chemokine genes...
April 4, 2018: Journal of Biological Chemistry
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