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Studying subcellular signaling events in living microglial cells using fluorescence resonance energy transfer-based nanosensors
Published in Raquel Seruca, Jasjit S. Suri, João M. Sanches, Fluorescence Imaging and Biological Quantification, 2017
Renato Socodato, Camila C. Portugal, Paula Sampaio, João B. Relvas
Microglia are a population of myeloid resident cells in the CNS. It is believed that during early embryogenesis, yolk sac-derived macrophages populate the developing CNS giving rise to microglial cells found in the mature nervous system [7]. Emerging roles of microglia have now established that these cells actively patrol the neuronal parenchyma, monitor synapse functioning, and control neuronal activity [8]. Classically, microglia are known to modulate immune responses and to regulate several branches of the inflammatory process within the neuronal parenchyma, which might also be linked with onset/progression of neurodegenerative disorders [9]. Besides, it is known that specific modulation of microglial function under inflammatory conditions might alleviate neurodegeneration in the CNS. Therefore, the study of signaling pathways in living microglia might be paramount to better understand microglial biology in the healthy and diseased CNS, raising the possibility to delay the onset or halt the progression of neuropathologies.
Huntington’s Disease and Stem Cells
Published in Deepak A. Lamba, Patient-Specific Stem Cells, 2017
Karen Ring, Robert O’Brien, Ningzhe Zhang, Lisa M. Ellerby
Many studies have identified an altered immune response in HD brains even before typical HD symptoms appear. mHTT can induce an inflammatory response, which results in microglial activation. Microglia act as the resident immune cells of the brain. They exist in a quiescent state in normal healthy brains but are activated upon inflammation and neurodegeneration. Microglia activation sets off a cascade of immune responses including overproduction of cytokines, chemokines, and ROS, mitochondrial dysfunction, glutamate-induced excitotoxicity, caspase activation, and ultimately neuronal cell death. Microglia originate from hematopoietic stem cells in the bone marrow, and during development, they cross into the brain through the blood brain barrier where they reside and proliferate upon immune stimuli. mHtt has been implicated in microglial dysfunction in HD mouse models. For instance, the expression of mHTT in primary microglia isolated from postnatal HD mice impaired microglial migration in response to chemotaxic stimuli (61,62). Studies of mHTT expression in microglia reveal impairments in migration in response to laser-induced injury. Migration defects are likely due to defects in actin remodeling caused by mHtt (61). Microglial activation is also used as a presymptomatic biomarker for HD pathogenesis. Correlations between microglial activation and striatal MSN dysfunction and between activated microglial numbers, and HD disease progression were identified (63–65).
Phosphorus-Containing Dendrimers Against Diseases of the Central Nervous System
Published in Anne-Marie Caminade, Cédric-Olivier Turrin, Jean-Pierre Majoral, Phosphorus Dendrimers in Biology and Nanomedicine, 2018
Anne-Marie Caminade, Cedric-Olivier Turrin, Jean-Pierre Majoral
Microglia are cells that function as macrophages in the CNS. They show neurotoxic activity in the presence of abnormal amounts of pro-inflammatory and pro-apoptotic mediators, such as IL-1β, IL-6, IL-12, and TNF-a (a cytokine involved in systemic inflammations). The influence of the cationic PPH dendrimers on the secretion of TNF-a was measured in the mouse microglia cell line BV-2. These cells were incubated with bacterial lipopolysaccharide (LPS) to induce an immune response, in particular a twofold increase in the level of TNF-a secreted. The level of TNF-a in the presence of the PPH dendrimers (0.05 gM) was reduced and comparable to values observed for inactive microglia [21].
The therapeutic effect of nano-zinc on the optic nerve of offspring rats and their mothers treated with lipopolysaccharides
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Eman Mohammed Emara, Hassan Ih El-Sayyad, Amr M Mowafy, Heba a El-Ghaweet
The optic nerve (cranial nerve II) is a central nervous system (CNS) tract that passes through the optic canal to leave the orbit. It is made up of the retinal ganglion cells (RGCs) axons. It allows vision by transmitting neural impulses from the retina to the brain. It is divided into four sections: the intraocular nerve head, the intraorbital, the intracanalicular and the intracranial [6]. The types of glial cells in the optic nerve are oligodendrocytes, astrocytes and microglia. Oligodendrocytes are responsible for producing the myelin sheaths that protect the CNS axons and contact nodes of Ranvier as well as they are the locations where action potentials are propagated and axonal integrity. Astrocytes are responsible for numerous physiological and pathological activities such as potassium homeostasis and metabolism as well as reactive astrogliosis in response to CNS trauma. Microglia are immune cells in CNS and have a significant impact on inflammation and infections [7].
Melatonin attenuates expression of cyclooxygenase-2 (COX-2) in activated microglia induced by lipopolysaccharide (LPS)
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Chunyan Yao, Xiaoling Liu, Zhengyu Zhou, Ying Xiang, Shuai Yuan, Weijia Xie, Meiyu Zhou, Zeyao Hu, Yafei Li, Ailing Ji, Tongjian Cai
Microglia is the major immune cells within the CNS and play key roles in neuroinflammation (Hanisch and Kettenmann 2007). Microglia are distinct from other tissue macrophages in that these cells exhibit unique homeostatic phenotype and tight regulation in CNS microenvironment (Colonna and Butovsky 2017). Under normal physiological conditions, microglia release anti-inflammatory mediators and phagocytose toxic cellular debris to maintain homeostasis in the CNS (Reynolds et al. 2007). It is known that microglia may be activated by numerous factors, including LPS (Dutta, Zhang, and Liu 2008), methylmercury (MeHg) (Ni et al. 2012), manganese (Zhao et al. 2009), lead (Liu et al. 2012), and amyloid β (Doens and Fernandez 2014). The prolonged activation of microglia generates excessive production of inflammatory cytokines, which promote neuroinflammation (Ransohoff and El Khoury 2015). Inhibition of these responses may decrease neuronal degeneration and thus alleviate disease progression.
Application of molecular imaging technology in neurotoxicology research
Published in Journal of Environmental Science and Health, Part C, 2018
Xuan Zhang, Qi Yin, Marc Berridge, Che Wang
MicroPET imaging with [18F]-FEPPA was used to evaluate anesthetic-induced neuronal inflammation and neuronal injury in the developing brain of NHPs.[16,37–39][18F]-FEPPA is an efficient radiotracer that specifically binds to translocator protein (TSPO) on glial cells in CNS, especially in microglia and astrocytes.[40–44] In response to CNS insults, the expression of TSPO will be upregulated in activated glial cells. After exposure to neurotoxins, such as general anesthetics, activated microglia will have morphological changes, accumulating and proliferating at the site of neuronal damage. After onset of neuronal injury, microglia will synthesize proinflammatory cytokines, release toxic molecules, and eliminate damaged neurons.[45–50] Increased expression of TSPO in both astrocytes and microglia in damaged brain areas occurs in a time-dependent and region-specific fashion.[43,51,52]