Soluble ICAM-1 in CSF Coincides with the Extent of Cerebral Damage in Patients with Severe Traumatic Brain Injury

Pleines, Ulrike E.; Stover, John; Kossmann, Thomas; Trentz, O; Morganti-Kossmann, Maria Cristina

doi:10.1089/neu.1998.15.399

Cited by 88 publications

(48 citation statements)

References 58 publications

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“…Our preclinical studies have further confirmed that baseline CVR positively correlated with plasma levels of VEGF, VEGF-C, and P-selectin. Our results are consistent with other investigators' reports that elevated levels of IL-8 and sICAM-1 in the CSF may correlate with blood-brain barrier (BBB) dysfunction after TBI; sICAM-1 and TNF-α can induce macrophage inflammatory protein MIP-2 in astrocytes and microvascular endothelial cells; sICAM-1, selectins, and vWF were proposed as biomarkers of vascular endothelial damage and dysfunction [5,[11][12][13]; TBI upregulated VEGF, Flt-1, and Flk-1 [14].…”

Section: Discussionsupporting

confidence: 92%

“…TVI is a common finding in TBI. For example, angiopoietins (Ang) are hallmarks of vascular injury [3]; serum SAA, which has been found to increase after abusive head trauma not evident from neuroimaging, is a potential biomarker for mild TBI [4]; levels of TNF and sICAM-1 in the cerebrospinal fluid (CSF) are increased after severe TBI [5]. Exercise improves recovery after ischemic brain injury by inducing the expression of Ang-1 and Tie-2, indicating their protective potentials for vascular integrity [6].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Biomarkers of Vascular Integrity in Traumatic Brain Injury and Correlation with Cerebrovascular Reactivity

Gong¹,

Amyot²,

Qu³

et al. 2017

Biomark J

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Biomarkers of Vascular Integrity in Traumatic Brain Injury and Correlation with Cerebrovascular Reactivity

Gong¹,

Amyot²,

Qu³

et al. 2017

Biomark J

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“…It appears that the degree of BBB compromise correlates with serum ICAM levels after TBI. 66 Monocyte chemo-attractant protein-1 is important for the recruitment of monocytes into the brain. Using rodent TBI models, it has been reported that expression of monocyte chemo-attractant protein-1 is enhanced in the brain by 4-h post-injury.…”

Section: Chemokinesmentioning

confidence: 99%

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

et al. 2010

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“…Under normal conditions, ICAM-1 is expressed at low levels on vascular endothelium, lymphocytes, and macrophages. 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).…”

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.

show abstract

Soluble ICAM-1 in CSF Coincides with the Extent of Cerebral Damage in Patients with Severe Traumatic Brain Injury

Cited by 88 publications

References 58 publications

Biomarkers of Vascular Integrity in Traumatic Brain Injury and Correlation with Cerebrovascular Reactivity

Biomarkers of Vascular Integrity in Traumatic Brain Injury and Correlation with Cerebrovascular Reactivity

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

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

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