Brain Microglia and Microglial Markers

Коржевский, Д. Э.; Кирик, О. В.

doi:10.1007/s11055-016-0231-z

Cited by 113 publications

(87 citation statements)

References 49 publications

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“…Placental tissues were incubated with endothelial markers, rabbit anti‐vimentin antibody 1:200, Abcam), and rat anti‐CD31 (1:200, Abcam) . Ionized calcium‐binding adaptor molecule 1 IBA1) is a marker of fetal brain injury . Fetal brains were incubated with IBA1 antibody (1:400, Wako Chemicals) .…”

Section: Methodssupporting

confidence: 87%

Melatonin for prevention of placental malperfusion and fetal compromise associated with intrauterine inflammation‐induced oxidative stress in a mouse model

Lee

Shin

et al. 2019

Journal of Pineal Research

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Melatonin has been shown to reduce oxidative stress and mitigate hypercoagulability. We hypothesized that maternally administered melatonin may reduce placental oxidative stress and hypercoagulability associated with exposure to intrauterine inflammation (IUI) and consequently improve fetoplacental blood flow and fetal sequelae. Mice were randomized to the following groups: control (C), melatonin (M), lipopolysaccharide (LPS; a model of IUI) (L), and LPS with melatonin (ML). The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro‐inflammatory mediators was significantly increased in L compared to C and ML. The systolic/diastolic ratio, resistance index, and pulsatility index in uterine artery (UtA) and umbilical artery (UA) were significantly increased in L compared with other groups when analyzed by Doppler ultrasonography. The expression of antioxidant mediators in the placenta was significantly decreased, while that of pro‐inflammatory mediators was significantly increased in L compared to C and ML. Vascular endothelial damage and thrombi formation, as evidenced by fibrin deposits, were similarly increased in L compared to other groups. Maternal pretreatment with melatonin appears to modulate maternal placental malperfusion, fetal cardiovascular compromise, and fetal neuroinflammation induced by IUI through its antioxidant properties.

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Section: Methodssupporting

confidence: 87%

Melatonin for prevention of placental malperfusion and fetal compromise associated with intrauterine inflammation‐induced oxidative stress in a mouse model

Lee

Shin

et al. 2019

Journal of Pineal Research

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“…To expand on the social modulation of microglial reactivity to cerebral ischemia, we stained brain slices with ionized calcium-binding adaptor 1 (Iba-1; Figure 4). Myeloid cells, microglia and macrophages, are often labeled with constitutive marker Iba-1 to obtain information regarding their morphological and activational state (Kettenmann, et al 2011; Korzhevskii and Kirik, 2015). The retraction of processes and an increase in cell body area are characteristic of microglial activation (Kettenmann, et al 2011; Beynon and Walker, 2012).…”

Section: Discussionmentioning

confidence: 99%

Social interaction modulates the neuroinflammatory response to global cerebral ischemia in male mice

et al. 2017

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Social isolation is a risk factor for cardiovascular and cerebrovascular diseases, although the underlying mechanisms remain underspecified. Considering the potential of microglia to become sensitized by stressors and their role in neuroinflammation, we hypothesized that social isolation primes microglia, resulting in an exaggerated neuroimmune response to experimental cerebral ischemia. First, major histocompatibility complex II (MHC II) gene expression, an indicator of microglial priming, was compared between mice that were socially isolated or pair-housed. MHC II increased in the hippocampus and cortex of socially isolated mice, which is suggestive of isolation-induced microglial priming. In experiment 2, isolated and pair-housed mice underwent ~8 minutes of global cerebral ischemia. Hippocampal mRNA expression of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) was significantly increased among both isolated and pair-housed ischemia groups relative to sham controls. Hippocampal expression of interleukin 1 beta (IL-1β) and cortical TNF-α, IL-1β and IL-6, were significantly increased 24-hours post ischemia in isolated mice, but not pair-housed mice, relative to controls. Ischemia-induced increases in microglial cell body area and percent area fraction of ionized calcium binding adaptor molecule 1 (Iba-1) positive staining were also observed in isolated, but not pair-housed mice, relative to controls. For experiment 3, brain sections from socially isolated and pair-housed mice underwent 15 minutes of oxygen glucose deprivation (OGD), an ex vivo model of cerebral ischemia. IL-6 gene expression was significantly elevated following OGD only in hippocampi from mice that had been socially isolated, indicating that isolation prior to ischemia is sufficient to modulate the neuroinflammatory response. Together, these data suggest microglial priming as a possible mechanism underlying the detrimental effects of social isolation on cerebral ischemia outcome.

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“…Examples are Ionized calcium Binding Adapter molecule 1 (Iba1) and the glycoproteins Cluster of Differentiation 11b, 68 and 45 (CD11b/68/45), that are used to visualize microglia and detect the cells in different functional activation states (see Korzhevskii and Kirik, 2016). Usually it is difficult to distinguish between CNS resident microglia and infiltrating monocytes since many microglial markers—proteins are expressed by blood-borne monocytes.…”

Section: Microglia—the First Glial Cells To Enter the Brainmentioning

confidence: 99%

The Indispensable Roles of Microglia and Astrocytes during Brain Development

Reemst

Noctor

Lucassen

et al. 2016

Front. Hum. Neurosci.

437

387

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Glia are essential for brain functioning during development and in the adult brain. Here, we discuss the various roles of both microglia and astrocytes, and their interactions during brain development. Although both cells are fundamentally different in origin and function, they often affect the same developmental processes such as neuro-/gliogenesis, angiogenesis, axonal outgrowth, synaptogenesis and synaptic pruning. Due to their important instructive roles in these processes, dysfunction of microglia or astrocytes during brain development could contribute to neurodevelopmental disorders and potentially even late-onset neuropathology. A better understanding of the origin, differentiation process and developmental functions of microglia and astrocytes will help to fully appreciate their role both in the developing as well as in the adult brain, in health and disease.

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Brain Microglia and Microglial Markers

Cited by 113 publications

References 49 publications

Melatonin for prevention of placental malperfusion and fetal compromise associated with intrauterine inflammation‐induced oxidative stress in a mouse model

Melatonin for prevention of placental malperfusion and fetal compromise associated with intrauterine inflammation‐induced oxidative stress in a mouse model

Social interaction modulates the neuroinflammatory response to global cerebral ischemia in male mice

The Indispensable Roles of Microglia and Astrocytes during Brain Development

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