MiR-146a-5p Contributes to Microglial Polarization Transitions Associated With AGEs

[1]  M. Nishibori,et al.  Differential contribution of possible pattern‐recognition receptors to advanced glycation end product–induced cellular responses in macrophage‐like RAW264.7 cells , 2020, Biotechnology and applied biochemistry.

[2]  Xiao-qian Dang,et al.  Oral treatment with glycyrrhizin inhibits NLRP3 inflammasome activation and promotes microglial M2 polarization after traumatic spinal cord injury , 2020, Brain Research Bulletin.

[3]  J. Ge,et al.  M2 macrophage-derived exosomes carry microRNA-148a to alleviate myocardial ischemia/reperfusion injury via inhibiting TXNIP and the TLR4/NF-κB/NLRP3 inflammasome signaling pathway. , 2020, Journal of molecular and cellular cardiology.

[4]  Q. Ao,et al.  MicroRNA-152 attenuates neuroinflammation in intracerebral hemorrhage by inhibiting thioredoxin interacting protein (TXNIP)-mediated NLRP3 inflammasome activation. , 2020, International immunopharmacology.

[5]  K. Yin,et al.  MicroRNAs in central nervous system diseases: A prospective role in regulating blood-brain barrier integrity , 2020, Experimental Neurology.

[6]  L. Ye,et al.  The effect of NLRP inflammasome on the regulation of AGEs-induced inflammatory response in human periodontal ligament cells. , 2019, Journal of periodontal research.

[7]  A. Fournier,et al.  microRNA dysregulation in neurodegenerative diseases: A systematic review , 2019, Progress in Neurobiology.

[8]  Pin-Lan Li,et al.  D-Ribose Induces Podocyte NLRP3 Inflammasome Activation and Glomerular Injury via AGEs/RAGE Pathway , 2019, Front. Cell Dev. Biol..

[9]  Y. Chai,et al.  Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway , 2019, Medical science monitor : international medical journal of experimental and clinical research.

[10]  Jianli Liu,et al.  Caffeic Acid Inhibits the Formation of Advanced Glycation End Products (AGEs) and Mitigates the AGEs‐Induced Oxidative Stress and Inflammation Reaction in Human Umbilical Vein Endothelial Cells (HUVECs) , 2019, Chemistry & biodiversity.

[11]  M. Hayden.  Type 2 Diabetes Mellitus Increases the Risk of Late-Onset Alzheimer’s Disease: Ultrastructural Remodeling of the Neurovascular Unit and Diabetic Gliopathy , 2019, Brain sciences.

[12]  Xiao-Liang Wang,et al.  Studies of pathology and pharmacology of diabetic encephalopathy with KK‐Ay mouse model , 2019, CNS neuroscience & therapeutics.

[13]  I. Prokopenko,et al.  miRNAs Identify Shared Pathways in Alzheimer's and Parkinson's Diseases. , 2019, Trends in molecular medicine.

[14]  J. Filosa,et al.  NLRP3 inflammasome inhibition with MCC950 improves diabetes‐mediated cognitive impairment and vasoneuronal remodeling after ischemia , 2019, Pharmacological research.

[15]  Wei-En Yuan,et al.  Nanoparticle-microRNA-146a-5p polyplexes ameliorate diabetic peripheral neuropathy by modulating inflammation and apoptosis. , 2019, Nanomedicine : nanotechnology, biology, and medicine.

[16]  M. Fujimiya,et al.  An enriched environment prevents diabetes-induced cognitive impairment in rats by enhancing exosomal miR-146a secretion from endogenous bone marrow-derived mesenchymal stem cells , 2018, PloS one.

[17]  Naifeng Liu,et al.  Exosomes Derived From Mesenchymal Stromal Cells Pretreated With Advanced Glycation End Product-Bovine Serum Albumin Inhibit Calcification of Vascular Smooth Muscle Cells , 2018, Front. Endocrinol..

[18]  B. Joseph,et al.  Epigenetics Control Microglia Plasticity , 2018, Front. Cell. Neurosci..

[19]  G. Biessels,et al.  Cognitive decline and dementia in diabetes mellitus: mechanisms and clinical implications , 2018, Nature Reviews Endocrinology.

[20]  Soumitra S Ghosh,et al.  Bioenergetic regulation of microglia , 2018, Glia.

[21]  Tuan Leng Tay,et al.  Histone Deacetylases 1 and 2 Regulate Microglia Function during Development, Homeostasis, and Neurodegeneration in a Context‐Dependent Manner , 2018, Immunity.

[22]  Guibo Sun,et al.  Inhibiting the NLRP3 Inflammasome Activation with MCC950 Ameliorates Diabetic Encephalopathy in db/db Mice , 2018, Molecules.

[23]  H. Cai,et al.  AGE-induced neuronal cell death is enhanced in G2019S LRRK2 mutation with increased RAGE expression , 2018, Translational Neurodegeneration.

[24]  Q. Su,et al.  Activation of NLRP3 Inflammasome by Advanced Glycation End Products Promotes Pancreatic Islet Damage , 2017, Oxidative medicine and cellular longevity.

[25]  Souvarish Sarkar,et al.  Mitochondrial impairment in microglia amplifies NLRP3 inflammasome proinflammatory signaling in cell culture and animal models of Parkinson’s disease , 2017, npj Parkinson's Disease.

[26]  M. Chopp,et al.  MicroRNA-146a Mimics Reduce the Peripheral Neuropathy in Type 2 Diabetic Mice , 2017, Diabetes.

[27]  A. Kalsbeek,et al.  Dietary sugars, not lipids, drive hypothalamic inflammation , 2017, Molecular metabolism.

[28]  M. Lasaga,et al.  Neuropeptides and Microglial Activation in Inflammation, Pain, and Neurodegenerative Diseases , 2017, Mediators of inflammation.

[29]  X. Ni,et al.  NLRP3 inflammasome activation mediates estrogen deficiency-induced depression- and anxiety-like behavior and hippocampal inflammation in mice , 2016, Brain, Behavior, and Immunity.

[30]  S. Matsubara,et al.  AGEs and HMGB1 Increase Inflammatory Cytokine Production from Human Placental Cells, Resulting in an Enhancement of Monocyte Migration , 2016, American journal of reproductive immunology.

[31]  S. Razavi,et al.  The Effect of Diabetes Mellitus on Apoptosis in Hippocampus: Cellular and Molecular Aspects , 2016, International journal of preventive medicine.

[32]  W. Le,et al.  Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases , 2016, Molecular Neurobiology.

[33]  R. Mastrocola,et al.  High-fructose intake as risk factor for neurodegeneration: Key role for carboxy methyllysine accumulation in mice hippocampal neurons , 2016, Neurobiology of Disease.

[34]  Jia Liu,et al.  miR-146a-5p Antagonized AGEs- and P.g-LPS-Induced ABCA1 and ABCG1 Dysregulation in Macrophages via IRAK-1 Downregulation , 2015, Inflammation.

[35]  Yi Zhang,et al.  NLRP3 Inflammasome Mediates Chronic Mild Stress-Induced Depression in Mice via Neuroinflammation , 2015, The international journal of neuropsychopharmacology.

[36]  D. Yoo,et al.  Activation of microglia and induction of pro-inflammatory cytokines in the hippocampus of type 2 diabetic rats , 2014, Neurological research.

[37]  F. Sutterwala,et al.  Mechanism of NLRP3 inflammasome activation , 2014, Annals of the New York Academy of Sciences.

[38]  S. Phipps,et al.  RAGE and TLRs: relatives, friends or neighbours? , 2013, Molecular immunology.

[39]  V. Perry,et al.  Review: Activation patterns of microglia and their identification in the human brain , 2013, Neuropathology and applied neurobiology.

[40]  M. Heneka,et al.  NLRP3 is activated in Alzheimer´s disease and contributes to pathology in APP/PS1 mice , 2012, Nature.

[41]  Nathan T. Ross,et al.  A multimodal RAGE-specific inhibitor reduces amyloid β-mediated brain disorder in a mouse model of Alzheimer disease. , 2012, The Journal of clinical investigation.

[42]  P. Tobias,et al.  Knockout of toll-like receptor-4 attenuates the pro-inflammatory state of diabetes. , 2011, Cytokine.

[43]  Xi-sha Chen,et al.  MicroRNA‐146a and Human Disease , 2010, Scandinavian journal of immunology.

[44]  L. Lue,et al.  Microglia Activation and Anti-inflammatory Regulation in Alzheimer’s Disease , 2010, Molecular Neurobiology.

[45]  J. Williamson,et al.  Cognitive decline and dementia in diabetes—systematic overview of prospective observational studies , 2005, Diabetologia.

[46]  S. McMahon,et al.  Role of the Immune system in chronic pain , 2005, Nature Reviews Neuroscience.

[47]  W. Gan,et al.  ATP mediates rapid microglial response to local brain injury in vivo , 2005, Nature Neuroscience.

[48]  F. Helmchen,et al.  Resting Microglial Cells Are Highly Dynamic Surveillants of Brain Parenchyma in Vivo , 2005, Science.

[49]  G. Münch,et al.  Signal transduction pathways in mouse microglia N‐11 cells activated by advanced glycation endproducts (AGEs) , 2003, Journal of neurochemistry.

[50]  T. Niwa.  Dialysis‐Related Amyloidosis: Pathogenesis Focusing on AGE Modification , 2001, Seminars in dialysis.

[51]  S. Horiuchi,et al.  Glycoxidative modification of AA amyloid deposits in renal tissue. , 2000, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.

[52]  T. Toyomura,et al.  [Regulation of inflammatory response based on interaction among AGEs, DAMPs, and/or cytokines]. , 2022, Nihon yakurigaku zasshi. Folia pharmacologica Japonica.

[53]  H. Jia,et al.  [The Effect of Interference of NLRP3 with shRNA on AGEs-induced Inflammatory Response in Myocardial Cell]. , 2019, Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition.

[54]  Jiun-Rong Chen,et al.  Long-term administration of advanced glycation end-product stimulates the activation of NLRP3 inflammasome and sparking the development of renal injury. , 2017, The Journal of nutritional biochemistry.

[55]  P. Cimflova,et al.  microRNAs in Cerebrovascular Disease. , 2015, Advances in experimental medicine and biology.

[56]  H. Sauer,et al.  Pentosidine and N(epsilon)-(carboxymethyl)-lysine in Alzheimer's disease and vascular dementia. , 2003, Neurobiology of aging.