Microglia at brain stab wounds express connexin 43 and<i>in vitro</i>form functional gap junctions after treatment with interferon-γ and tumor necrosis factor-α

Eugenín, Eliseo A.; Eckardt, Dominik; Theis, Martin; Willecke, Klaus; Bennett, Michael V. L.; Sáez, Juan C.

doi:10.1073/pnas.051634298

Cited by 210 publications

(222 citation statements)

References 46 publications

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“…Our in vitro data, LPS plus IFN-γ, but not either proinflammatory agent alone, induced gap junctional communication in a similar extent as previously described for macrophages/ monocytes and microglia (14,15). LPS plus IFN-γ treatment induced intercellular dye transfer in ~30% KCs and induced ~45% incidence of dye coupling in macrophages/monocytes and microglia (14,15).…”

Section: Discussionsupporting

confidence: 88%

“…Differences in cell surface receptor densities might explain why only a fraction of cells respond to LPS plus IFN-γ. In agreement with this interpretation, treatment of microglia with a Ca 2+ ionophore that bypasses membrane receptors induces a much higher incidence of gap junctional communication (~75%) (35) as compared to LPS plus IFN-γ (~45%) (15).…”

Section: Discussionmentioning

confidence: 59%

“…LPS plus IFN-γ treatment induced intercellular dye transfer in ~30% KCs and induced ~45% incidence of dye coupling in macrophages/monocytes and microglia (14,15). Similarly, peptidoglycan, another proinflammatory agent, induces dye coupling in ~45% microglia (33).…”

Section: Discussionmentioning

confidence: 99%

“…Since previous studies in monocytes/macrophages and microglia have demonstrated induction of dye coupling after treatment with LPS plus IFN-γ (14,15), the possibility that these proinflammatory agents induce dye transfer between KCs was evaluated. The effect of these agents was tested on KCs isolated from normal rats plated and kept in culture for 2 hours before treatment with the proinflammatory agents.…”

Section: Treatment With Lps Plus Ifn-γ Induces Intercellular Communicmentioning

confidence: 99%

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Inflammatory conditions induce gap junctional communication between rat Kupffer cells both in vivo and in vitro

Eugenín

González

Sánchez

et al. 2007

Cellular Immunology

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Connexin43 (Cx43), a gap junction protein subunit, has been previously detected in Kupffer cells (KCs) during liver inflammation, however, KCs phagocytose cell debris that may include Cx43 protein, which could explain the detection of Cx43 in KCs. We determined that KCs express Cx43 and form gap junctions both in vivo and in vitro. In liver sections of animals treated with LPS, Cx43 was detected at ED2+ cells interfaces, indicating formation of GJ between KCs in vivo. In vitro, unstimulated KCs cultures did not form functional GJs, and expressed low levels of Cx43 that showed a diffuse intracellular distribution. In contrast, KCs treated with LPS plus IFN-γ, expressed a greater amount of Cx43 at both the, protein and mRNA levels, and showed Cx43 at cell-cell contacts associated with higher dye coupling. In conclusion, activation of KCs in vivo or in vitro resulted in enhanced Cx43 expression levels and formation of GJ that might play relevant roles during liver inflammation.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Treatment With Lps Plus Ifn-γ Induces Intercellular Communicmentioning

confidence: 99%

See 2 more Smart Citations

Inflammatory conditions induce gap junctional communication between rat Kupffer cells both in vivo and in vitro

Eugenín

González

Sánchez

et al. 2007

Cellular Immunology

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“…In this case, Cx43 is observed at the interfaces between activated cells, which become dye-coupled through gap junctions. 40 The expression of glial connexins is affected in brain inflammation. Brain inflammation is a hallmark of many brain diseases and it is characterised by a reactive gliosis associated with phenotypic changes and proliferation of glial cells (mainly astrocytes and microglia).…”

Section: Intercellular Communication In Glia and Neuroprotectionmentioning

confidence: 99%

Glia: the fulcrum of brain diseases

et al. 2007

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Neuroglia represented by astrocytes, oligodendrocytes and microglial cells provide for numerous vital functions. Glial cells shape the micro-architecture of the brain matter; they are involved in information transfer by virtue of numerous plasmalemmal receptors and channels; they receive synaptic inputs; they are able to release 'glio'transmitters and produce long-range information exchange; finally they act as pluripotent neural precursors and some of them can even act as stem cells, which provide for adult neurogenesis. Recent advances in gliology emphasised the role of glia in the progression and handling of the insults to the nervous system. The brain pathology, is, to a very great extent, a pathology of glia, which, when falling to function properly, determines the degree of neuronal death, the outcome and the scale of neurological deficit. Glial cells are central in providing for brain homeostasis. As a result glia appears as a brain warden, and as such it is intrinsically endowed with two opposite features: it protects the nervous tissue as long as it can, but it also can rapidly assume the guise of a natural killer, trying to eliminate and seal the damaged area, to save the whole at the expense of the part. The sudden emergence of an intellect, and therefore a human being, which materialised only around a million years ago, remains the main mystery for our self-understanding. Similarly, we still do not know by which steps or transitions the human intellect emerged from the animal kingdom and where the fundamental difference between a man and an animal lies. According to the neuronal doctrine, which governs modern neuroscience since the beginning of the twentieth century, 1,2 the neurone is regarded as a basic information processing unit consisting of dendrites and axons with a unidirectional flow of information from the receiving dendrites via the integrating cell body to the terminal branches of the axon. Neuronal networks, connected through synaptic contacts, are generally considered as the substrate of our intellect.The number and size of neural cells increase with the size of the body and of the brain of mammals. This increasing quantity eventually has caused the generation of a new quality, the intellect. Rather amazingly, however, there is a relatively little difference in the morphology and physiology of neurones between humans and beasts; similarly the density of synaptic contacts in the brains of rodents and humans is more or less constant at around 1100-1300 millions/mm 3 . 3 On the contrary, evolution of the nervous system resulted in great changes in the second type of neural cells, the neuroglia. 4 Indeed, phylogenetic advance in brain complexity and capabilities coincided with a remarkable increase in the number of glial cells: in the rodent cortex the glial to neurone ratio is about 0.3 : 1, whereas in humans the same ratio is several times higher being B1.65:1, 5 while the total number of glial cells in the human brain is B10 (or even more) times larger than in lesser mammals. Astrocytes ...

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Zwitterionic Polymer Coating Suppresses Microglial Encapsulation to Neural Implants In Vitro and In Vivo

Yang

Eles

et al. 2020

Adv. Biosys.

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For brain computer interfaces (BCI), the immune response to implanted electrodes is a major biological cause of device failure. Bioactive coatings such as neural adhesion molecule L1 have been shown to improve the biocompatibility, but are difficult to handle or produce in batches. Here, a synthetic zwitterionic polymer coating, poly(sulfobetaine methacrylate) (PSBMA) is developed for neural implants with the goal of reducing the inflammatory host response. In tests in vitro, the zwitterionic coating inhibits protein adsorption and the attachment of fibroblasts and microglia, and remains stable for at least 4 weeks. In vivo two‐photon microscopy on CX3CR1‐GFP mice shows that the zwitterionic coating significantly suppresses the microglial encapsulation of neural microelectrodes over a 6 h observation period. Furthermore, the lower microglial encapsulation on zwitterionic polymer‐coated microelectrodes is revealed to originate from a reduction in the size but not the number of microglial end feet. This work provides a facile method for coating neural implants with zwitterionic polymers and illustrates the initial interaction between microglia and coated surface at high temporal and spatial resolution.

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Microglia at brain stab wounds express connexin 43 andin vitroform functional gap junctions after treatment with interferon-γ and tumor necrosis factor-α

Cited by 210 publications

References 46 publications

Inflammatory conditions induce gap junctional communication between rat Kupffer cells both in vivo and in vitro

Inflammatory conditions induce gap junctional communication between rat Kupffer cells both in vivo and in vitro

Glia: the fulcrum of brain diseases

Zwitterionic Polymer Coating Suppresses Microglial Encapsulation to Neural Implants In Vitro and In Vivo

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