Transient ischemia-induced paresis and complete paraplegia displayed distinct reactions of microglia and macrophages

Nakata, Tatsuhiro; Kawachi, Kanji; Nagashima, Mitsugi; Yasugi, Takumi; Izutani, Hironori; Ryugo, Masahiro; Okamura, Toru; Shikata, Fumiaki; Imagawa, Hiroshi; Yano, Hajime; Takahashi, Hiroyuki; Tanaka, Junya

doi:10.1016/j.brainres.2011.08.074

Cited by 25 publications

(16 citation statements)

References 25 publications

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“…In a rat model of spinal cord IRI, a number of bone marrow-derived macrophages were present 7d after IRI [11]. In the animals that suffered from severe paraplegia, a robust accumulation of bone marrow-derived macrophages occupied the entire ischemic gray matter [11].…”

Section: Inflammatory Cells In Spinal Cord Irimentioning

confidence: 99%

“…In the animals that suffered from severe paraplegia, a robust accumulation of bone marrow-derived macrophages occupied the entire ischemic gray matter [11]. In a rabbit model of spinal cord IRI, macrophages were first detected at 8 hours after reperfusion and mainly surrounded the infarction area [12].…”

Section: Inflammatory Cells In Spinal Cord Irimentioning

confidence: 99%

“…Several cell types have been shown to synthesize inflammatory cytokines [1]. Experiments in animal models of spinal cord IRI revealed that macrophages and microglia strongly expressed tumor necrosis factor- α (TNF- α ), interleukin 1 β (IL-1 β ), and other mediators [7, 11, 16]. In a rat model of spinal cord IRI, strong staining of IL-1 β , IL-10, and TNF- α was observed, suggesting a dramatic infiltration of inflammatory cells in both gray matters and peripheral white matters [18].…”

Section: Cytokines In Spinal Cord Irimentioning

confidence: 99%

“…However, data about the pathways and effects of these cytokines in the spinal cord IRI are still limited [9]. In rats that suffered from severe paraplegia induced by spinal cord IRI, TNF- α , IL-1 β , and other mediators were strongly expressed [11]. Lu and colleagues discovered that the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) pathway might play a noxious role in spinal cord IRI via participating in inflammatory reactions and cytokine production [19].…”

Section: Cytokines In Spinal Cord Irimentioning

confidence: 99%

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Development and Treatments of Inflammatory Cells and Cytokines in Spinal Cord Ischemia-Reperfusion Injury

Zhu

Fujino

et al. 2013

Mediators of Inflammation

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During aortic surgery, interruption of spinal cord blood flow might cause spinal cord ischemia-reperfusion injury (IRI). The incidence of spinal cord IRI after aortic surgery is up to 28%, and patients with spinal cord IRI might suffer from postoperative paraplegia or paraparesis. Spinal cord IRI includes two phases. The immediate spinal cord injury is related to acute ischemia. And the delayed spinal cord injury involves both ischemic cellular death and reperfusion injury. Inflammation is a subsequent event of spinal cord ischemia and possibly a major contributor to spinal cord IRI. However, the development of inflammatory mediators is incompletely demonstrated. And treatments available for inflammation in spinal cord IRI are insufficient. Improved understanding about spinal cord IRI and the development of inflammatory cells and cytokines in this process will provide novel therapeutic strategies for spinal cord IRI. Inflammatory cytokines (e.g., TNF-α and IL-1) may play an important role in spinal cord IRI. For treatment of several intractable autoimmune diseases (e.g., rheumatoid arthritis), where inflammatory cytokines are involved in disease progression, anti-inflammatory cytokine antagonist is now available. Hence, there is great potential of anti-inflammatory cytokine antagonist for therapeutic use of spinal cord IRI. We here review the mediators and several possibilities of treatment in spinal cord IRI.

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Section: Inflammatory Cells In Spinal Cord Irimentioning

confidence: 99%

Section: Inflammatory Cells In Spinal Cord Irimentioning

confidence: 99%

Section: Cytokines In Spinal Cord Irimentioning

confidence: 99%

Section: Cytokines In Spinal Cord Irimentioning

confidence: 99%

See 2 more Smart Citations

Development and Treatments of Inflammatory Cells and Cytokines in Spinal Cord Ischemia-Reperfusion Injury

Zhu

Fujino

et al. 2013

Mediators of Inflammation

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“…Activated microglia plays a neuroprotective role via up-regulating expression of neurotrophic factors; however, activated microglia can also release a large amount of inflammatory factors [32,33]. Excessive inflammatory cytokines may participate in the activation of neurons microglia and astrocytes, and could lead to the death of cells in septic brains.…”

Section: Discussionmentioning

confidence: 98%

Role of HMGB1 translocation to neuronal nucleus in rat model with septic brain injury

et al. 2017

Neuroscience Letters

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High-mobility Group Box-1 (HMGB1) is a central late proinflammatory cytokine that triggers the inflammatory response during sepsis. However, whether HMGB1 is involved in the pathogenesis of septic brain damage is unknown. In this study, we investigated the role of HMGB1 in regulating brain injury in a rat model of sepsis. Wistar rats were subjected to cecal ligation and puncture (CLP) to induce septic brain injury. Hematoxylin and eosin staining was used to detect pathological changes in the cortex. The cellular localization of HMGB1 was determined using immunostaining. Cortical levels of HMGB1, its receptor for advanced glycation end-products (RAGE), and downstream effecter, nuclear factor kappa-B (NF-κB) subunit p65, were detected via western blot.HMGB1was increased in the cytoplasm via translocation from the nucleus predominantly in neurons. Moreover, RAGE and NF-κB p65 were upregulated after septic brain injury. Ethyl pyruvate, an inhibitor of HMGB1, down-regulated the expression of RAGE and NF-κB p65via inhibiting HMGB1 expression in the cytoplasm. Collectively, our findings suggest that HMGB1 and its signaling transduction have critical roles in the pathogenesis of septic brain injury. HMGB1 inhibition might be a potential new therapeutic target for septic brain injury.

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Expression of MCP‐1 and fractalkine on endothelial cells and astrocytes may contribute to the invasion and migration of brain macrophages in ischemic rat brain lesions

Tei

Tanaka

Sugimoto

et al. 2013

J of Neuroscience Research

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Some macrophages expressing NG2 chondroitin sulfate proteoglycan (NG2) and the macrophage marker Iba1 accumulate in the ischemic core of a rat brain subjected to transient middle cerebral artery occlusion (MCAO) for 90 min. These cells are termed BINCs (for brain Iba1(+) /NG2(+) cells) and may play a neuroprotective role. Because BINCs are bone marrow-derived cells, they are able to invade ischemic tissue after the onset of an ischemic insult. In this study, chemokine-based mechanisms underlying the invasion of BINCs or their progenitor cells were investigated. We found that isolated BINCs expressed mRNA encoding CCR2 and CX3CR1 at high levels. Cultured astrocytes expressed mRNA encoding their ligands, MCP-1 and fractalkine. Recombinant MCP-1 and/or fractalkine, as well as astrocytes, induced the migration of BINCs in vitro. mRNA for MCP-1, fractalkine, CCR2, and CX3CR1 was expressed in the ischemic core during the acute phase of the ischemic event. Immunohistochemical studies revealed that vascular endothelial cells and astrocytic endfeet expressed MCP-1 and fractalkine, respectively, in the ischemic core during the acute phase. CCR2(+) /Iba1(+) monocytes attached to the inside of the vascular wall at 1 day postreperfusion (dpr), and there were CCR2(+) /CX3CR1(+) macrophage-like cells in the parenchyma in the ischemic lesion core at 2 dpr, which may be the progenitors for BINCs. These results suggest that CCR2(+) monocytes are first attracted to the ischemic lesion by MCP-1(+) endothelial cells and migrate toward fractalkine(+) astrocytic endfeet through the disrupted blood-brain barrier. Thus, chemokines may play a critical role in the accumulation of neuroprotective BINCs. © 2013 Wiley Periodicals, Inc.

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Transient ischemia-induced paresis and complete paraplegia displayed distinct reactions of microglia and macrophages

Cited by 25 publications

References 25 publications

Development and Treatments of Inflammatory Cells and Cytokines in Spinal Cord Ischemia-Reperfusion Injury

Development and Treatments of Inflammatory Cells and Cytokines in Spinal Cord Ischemia-Reperfusion Injury

Role of HMGB1 translocation to neuronal nucleus in rat model with septic brain injury

Expression of MCP‐1 and fractalkine on endothelial cells and astrocytes may contribute to the invasion and migration of brain macrophages in ischemic rat brain lesions

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