Pharmacological Targeting of ICAM-1 Signaling in Brain Endothelial Cells: Potential for Treating Neuroinflammation

Turowski, Patric; Adamson, Peter; Greenwood, John

doi:10.1007/s10571-004-1380-0

Cited by 72 publications

(68 citation statements)

References 107 publications

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“…Several lines of evidence support that ICAM1-mediated direct cell contact has a major impact on a wide range of biological responses including cell differentiation (Gortz et al 2004, Long et al 1995, Olsen et al 1988, Saho et al 2003, Tanaka et al 1995. It has been shown that ICAM1 plays an important role in direct cell-to-cell contact-mediated signals via mitogen-activated protein kinase (MAPK) pathway including p38, extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) 1/2/3 (Cernuda-Morollon and Ridley 2006, Turowski et al 2005), which could subsequently stimulate osteoblast differentiation of stem/progenitor cells. Fu et al (2009) further suggested that ICAM1 and p38 MAPK also significantly influence the migration of stem cells to their target sites, such as PDL tissue and alveolar bone.…”

Section: Discussionmentioning

confidence: 99%

Highly osteogenic PDL stem cell clones specifically express elevated levels of ICAM1, ITGB1 and TERT

Sununliganon

Singhatanadgit

2011

Cytotechnology

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Cells derived from the periodontal ligament (PDL) have previously been reported to have stem cell-like characteristics (PDL stem cells; PDLSCs) and play an important part in bone engineering, including that of alveolar bone. However, these populations have been heterogeneous, and thus far no specific marker has yet been established from adult human stem cells derived from PDL tissue. We have previously isolated highly purified single cellderived PDLSC clones and delineated their phenotypic and functional characteristics. In this report, we further obtained three homogeneous and distinct PDLSC clones demonstrating low, moderate and high mineralized matrix forming ability-namely PC12, PC4 and PC3, respectively, and the expression of mesenchymal stem cell pathway-specific genes in these clones was investigated. PCR array revealed that the expression of intercellular adhesion molecule 1 (ICAM1), integrin beta 1 (ITGB1) and telomerase reverse transcriptase (TERT) was associated with highly osteogenic PDLSC clones, as determined by the expression of key osteoblastic markers and their ability to form alizarin red S positive mineralized matrix in vitro. The present results suggest that these three mesenchymal stem cell-associated markers could potentially be used to isolate PDLSCs with high osteogenic capability for engineering new bone.

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Section: Discussionmentioning

confidence: 99%

Highly osteogenic PDL stem cell clones specifically express elevated levels of ICAM1, ITGB1 and TERT

Sununliganon

Singhatanadgit

2011

Cytotechnology

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“…Aging-associated BBB modifications are due, at least in part, to a significant age-dependent reduction in the number of lamininpositive [20] and collagen-type-IV-containing vessels [33], and reduced capillary density [34]. In addition, in several pathological conditions of the CNS, associated inflammation alters BBB morphology and function, inducing adherence of leukocytes to the vasculature, and penetration into the CNS [11,35,36].…”

Section: Aged-induced Changes In Neutrophil Densitymentioning

confidence: 99%

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Campuzano¹,

Castillo-Ruiz²,

Acarín³

et al. 2011

Experimental Gerontology

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Brain aging is associated to several morphological and functional alterations that influence the evolution and outcome of CNS damage. Acute brain injury such as an excitotoxic insult induces initial tissue damage followed by associated inflammation and oxidative stress, partly attributed to neutrophil recruitment and the expression of oxidative enzymes such as myeloperoxidase (MPO), among others. However, to date, very few studies have focused on how age can influence neutrophil infiltration after acute brain damage. Therefore, to evaluate the age-dependent pattern of neutrophil cell infiltration following an excitotoxic injury, intrastriatal injection of Nmethyl-D-aspartate was performed in young and aged male Wistar rats. Animals were sacrificed at different times between 12 hours post-lesion (hpl) to 14 days post-lesion (dpl). Cryostat sections were processed for myeloperoxidase (MPO) immunohistochemistry, and double labeling for either neuronal cells (NeuN), astrocytes (GFAP), perivascular macrophages (ED-2), or microglia/macrophages (tomato lectin histochemistry). Our observations showed that MPO+ cells were observed in the injured striatum from 12 hpl (when maximum values were found) until 7 dpl, when cell density was strongly diminished. However, at all survival times analyzed, the overall density of MPO+ cells was lower in the aged versus the adult injured striatum. MPO+ cells were mainly identified as neutrophils (especially at 12 hpl and 1 dpl), but it should be noted that MPO+ neurons and microglia/macrophages were also found. MPO+ neurons were most commonly observed at 12 hpl and reduced in the aged. MPO+ microglia/macrophages were the main population expressing MPO from 3 dpl, when density was also reduced in aged subjects.These results point to neutrophil infiltration as another important factor contributing to the different response of the adult and aged brain to damage, highlighting the need of using aged animals for the study of acute agerelated brain insults.

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“…The endothelial intercellular adhesion molecule-1 (ICAM-1, CD54), an immunoglobulin surface receptor, has been shown to induce changes in the endothelial cytoskeleton, transcription and interendothelial junctions, factors which may modulate endothelial disposition to infiltrating leukocytes (Turowski et al, 2005). Using CIP, Huber et al (2006) showed an increase in ICAM mRNA and protein expression at the BBB.…”

Section: Introductionmentioning

confidence: 99%

Nociceptive inhibition prevents inflammatory pain induced changes in the blood–brain barrier

et al. 2008

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Previous studies by our group have shown that peripheral inflammatory insult, using the λ-carrageenan inflammatory pain (CIP) model, induced alterations in the molecular and functional properties of the blood-brain barrier (BBB). The question remained whether these changes were mediated via an inflammatory and/or neuronal mechanism. In this study, we investigated the involvement of neuronal input from pain activity on alterations in BBB integrity by peripheral inhibition of nociceptive input. A perineural injection of 0.75% bupivacaine into the right hind leg prior to CIP was used for peripheral nerve block. Upon nerve block, there was a significant decrease in thermal allodynia induced by CIP, but no effect on edema formation 1 h post CIP. BBB permeability was increased 1 h post CIP treatment as determined by in situ brain perfusion of [ 14 C] sucrose; bupivacaine nerve block of CIP caused an attenuation of [ 14 C] sucrose permeability, back to saline control levels. Paralleling the changes in [ 14 C] sucrose permeability, we also report increased expression of three tight junction (TJ) proteins, zonula occluden-1 (ZO-1), occludin and claudin-5 with CIP. Upon bupivacaine nerve block, changes in expression were prevented. These data show that the λ-carrageenan induced changes in [ 14 C] sucrose permeability and protein expression of ZO-1, occludin and claudin-5 are prevented with inhibition of nociceptive input. Therefore, we suggest that nociceptive signaling is in part responsible for the alteration in BBB integrity under CIP.

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Pharmacological Targeting of ICAM-1 Signaling in Brain Endothelial Cells: Potential for Treating Neuroinflammation

Cited by 72 publications

References 107 publications

Highly osteogenic PDL stem cell clones specifically express elevated levels of ICAM1, ITGB1 and TERT

Highly osteogenic PDL stem cell clones specifically express elevated levels of ICAM1, ITGB1 and TERT

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Nociceptive inhibition prevents inflammatory pain induced changes in the blood–brain barrier

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