Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats

Rancan, Mario; Otto, Viviane I.; Hans, Volkmar; Gerlach, Irene; Jork, R.; Trentz, O; Kossmann, Thomas; Morganti-Kossmann, Maria Cristina

doi:10.1002/1097-4547(20010301)63:5<438::aid-jnr1039>3.0.co;2-p

Cited by 74 publications

(14 citation statements)

References 54 publications

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“…9,78 Some of these chemokines attract peripheral macrophages to the brain to transdifferentiate into microglia and further participate in cytokine release. 77,79 In normal reactions to a single mild TBI, over time microglia eventually enter a reparative phase composed of phagocytic activity to repair any debris and damaged cells, and ultimately return to their resting state. 8 With repeated brain injury, microglia may enter a constitutively activated state and become neurodestructive, which may translate into risk for chronic traumatic encephalopathy.…”

Section: The Role Of Neuroinflammationmentioning

confidence: 99%

An overview of the basic science of concussion and subconcussion: where we are and where we are going

Dashnaw

Petraglia

Bailes

2012

FOC

116

118

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There has been a growing interest in the diagnosis and management of mild traumatic brain injury (TBI), or concussion. Repetitive concussion and subconcussion have been linked to a spectrum of neurological sequelae, including postconcussion syndrome, chronic traumatic encephalopathy, mild cognitive impairment, and dementia pugilistica. A more common risk than chronic traumatic encephalopathy is the season-ending or career-ending effects of concussion or its mismanagement. To effectively prevent and treat the sequelae of concussion, it will be important to understand the basic processes involved. Reviewed in this paper are the forces behind the primary phase of injury in mild TBI, as well as the immediate and delayed cellular events responsible for the secondary phase of injury leading to neuronal dysfunction and possible cell death. Advanced neuroimaging sequences have recently been developed that have the potential to increase the sensitivity of standard MRI to detect both structural and functional abnormalities associated with concussion, and have provided further insight into the potential underlying pathophysiology. Also discussed are the potential long-term effects of repetitive mild TBI, particularly chronic traumatic encephalopathy. Much of the data regarding this syndrome is limited to postmortem analyses, and at present there is no animal model of chronic traumatic encephalopathy described in the literature. As this arena of TBI research continues to evolve, it will be imperative to appropriately model concussive and even subconcussive injuries in an attempt to understand, prevent, and treat the associated chronic neurodegenerative sequelae.

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Section: The Role Of Neuroinflammationmentioning

confidence: 99%

An overview of the basic science of concussion and subconcussion: where we are and where we are going

Dashnaw

Petraglia

Bailes

2012

FOC

116

118

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“…ICAM-1 expression and sICAM-1 release are strongly increased in response to inflammatory stimuli and injury (2)(3)(4)(5)(6)(7). After severe traumatic brain injury, the number of ICAM-1-positive brain vessels as well as the concentration of sICAM-1 in cerebrospinal fluid (CSF) are strongly increased (8,9). The increased sICAM-1 concentration in CSF may result from leakage from serum through a dysfunctional blood-brain barrier, because sICAM-1 levels are up to 100-fold higher in serum than in CSF of patients with severe traumatic brain injury (6).…”

Section: Intercellular Adhesion Molecule-1 (Icam-1)mentioning

confidence: 99%

Sialylated Complex-type N-Glycans Enhance the Signaling Activity of Soluble Intercellular Adhesion Molecule-1 in Mouse Astrocytes

Otto

Schürpf

Folkers

et al. 2004

Journal of Biological Chemistry

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Intercellular adhesion molecule-1 (ICAM-1) occurs as both a membrane and a soluble, secreted glycoprotein (sICAM-1). ICAM-1 on endothelial cells mediates leukocyte adhesion by binding to leukocyte function associated antigen-1 (LFA-1) and macrophage antigen-1 (Mac-1). Recombinant mouse sICAM-1 induces the production of macrophage inflammatory protein-2 (MIP-2) in mouse astrocytes by a novel LFA-1-and Mac-1-independent mechanism. Here we showed that N-glycan structures of sI-CAM-1 influence its ability to induce MIP-2 production. sICAM-1 expressed in Chinese hamster ovary (CHO) cells was a more potent inducer of MIP-2 production than sI-CAM-1 expressed in HEK 293 cells, suggesting that posttranslational modification of sICAM-1 could influence its signaling activity. To explore the roles of glycosylation in sICAM-1 activity, we expressed sICAM-1 in mutant CHO cell lines differing in glycosylation, including Lec2, Lec8, and Lec1 as well as in CHO cells cultured in the presence of the ␣-mannosidase-I inhibitor kifunensine. Signaling activity of sICAM-1 lacking sialic acid was reduced 3-fold compared with sICAM-1 from CHO cells. The activity of sICAM-1 lacking both sialic acid and galactose was reduced 12-fold, whereas the activity of sICAM-1 carrying only high mannose-type N-glycans was reduced 12-26-fold. sICAM-1 glycoforms carrying truncated glycans retained full ability to bind to LFA-1 on leukocytes. Thus, sialylated and galactosylated complex-type N-glycans strongly enhanced the ability of sICAM-1 to induce MIP-2 production in astrocytes but did not alter its binding to LFA-1 on leukocytes. Glycosylation could therefore serve as a means to regulate specifically the signaling function of sICAM-1 in vivo.

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“…Thus, the inhibitory effect of berberine may improve DAI-induced learning and memory deficits in rats. Monocytes, macrophages, endothelial cells and contractile fiber cells express MCP-1 (18,19). The major biological effects of MCP-1 are the chemotaxis of monocytes and that it can act on lymphocytes and basophilic granulocytes, while it has no biological effect on neutrophil granulocytes.…”

Section: Discussionmentioning

confidence: 99%

“…The major biological effects of MCP-1 are the chemotaxis of monocytes and that it can act on lymphocytes and basophilic granulocytes, while it has no biological effect on neutrophil granulocytes. MCP-1 receptor is a member of the g-protein coupled receptor super-family (18). Following the combination of MCP-1 and its targeted specific receptor, the receptor of MCP-1 is activated, thus activating the phosphoinositide 3-kinase pathway through g-protein coupling on the cytomembrane (20).…”

Section: Discussionmentioning

confidence: 99%

“…Meanwhile, MCP-1 activation may trigger the release of calcium ion in cytoplasm and induce the activation of protein kinase C. Subsequent to DAI, injured cerebral tissues produce various inflammatory chemokine factors. One of these factors is MCP-1, which is a major inflammatory chemokine factor that induces strong chemotaxis to monocytes/macrophages (18). Monocytes/macrophages gather in inflammatory response regions and participate in the occurrence and progression of inflammatory response in DAI.…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury

Wang

Chen

et al. 2017

Exp Ther Med

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Abstract. The aim of the present study was to assess the neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury (DAI). DAI rats were orally gavaged with berberine at a dose of 200 mg/kg of body weight for 4 weeks. Behavioral tests were used to analyze the neuroprotective effect of berberine against DAI-induced learning and memory deficits. In the present study, treatment with berberine significantly protected against DAI-induced inhibition of learning and memory in rats. Notably, berberine significantly suppressed the levels of tumor necrosis factor, interleukin-1β and monocyte chemoattractant protein-1, as well as reduced the protein expression levels of nuclear factor-κB, Bcl-2-associated X protein and cytochrome c in DAI rats. In addition, berberine significantly suppressed the protein expression of p38 mitogen-activated protein kinase, activating transcription factor 2 and vascular endothelial growth factor in DAI rats. These results suggested that berberine exhibited a neuroprotective effect against learning and memory deficits in severe DAI through the suppression of inflammation, angiogenesis and apoptosis in a rat model.

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Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats

Cited by 74 publications

References 54 publications

An overview of the basic science of concussion and subconcussion: where we are and where we are going

An overview of the basic science of concussion and subconcussion: where we are and where we are going

Sialylated Complex-type N-Glycans Enhance the Signaling Activity of Soluble Intercellular Adhesion Molecule-1 in Mouse Astrocytes

Neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury

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