Kegg Pathway: Cell adhesion molecules (CAMs)

Toxicol In Vitro. 2009 Nov 4;
Xue Y, Liu X, Sun J

Polyurethane (PU) and polytetrafluoroethylene (PTFE) are two commonly used blood-contacting biomaterials. In the present study, we used a noncontact coculture model to evaluate the thrombosis-causing potential of monocyte-mediated PU and PTFE. We used human endothelial Cells from umbilical cord (HUVECs) and human monocytes (THP1 Cells). The THP1 Cells were directly exposed to PU/PTFE, and the resultant Cell-free supernatants were harvested for stimulating HUVECs. The treated HUVECs constituted the test group. HUVECs treated with supernatants of LPS-stimulated THP1 Cells were used as the positive controls. To investigate the effects of the supernatant treatment on HUVECs, we measured the expression of the leukocyte-endothelial-Cell adhesion molecules (CAMs) CD54 (ICAM-1), CD106 (VCAM-1), and CD62E (E-selectin) and evaluated the release of tissue factor (TF). The results demonstrated that both PU and PTFE induced the expressions of CD62E and TF. These activation effects were accompanied by activation of the NF-kappaB transcription factor. To further investigate the monocyte-derived soluble factors that might contribute to these effects, we evaluated the effects of the PU/PTFE stimulation on the expression of reactive oxygen species (ROS), TNF-alpha, IL-1beta, and IL-6 in monocyte monocultures. In comparison with the results for the negative control, both PU and PTFE significantly induced ROS release after 0.5h, while the expressions of TNF-alpha, IL-1beta, and IL-6 were variably increased after 24h. Our results suggest that the biomaterial induces monocytic activation and subsequently causes the release of soluble factors, which contribute to the inflammatory activation in HUVECs.

J Agric Food Chem. 2009 Oct 14; 57(19): 8852-9
Chen CH, Song TY, Liang YC, Hu ML

Acteoside, an active phenylethanoid glycoside of many medicinal plants and bitter tea, displays anti-inflammatory properties in vitro. However, it is unclear whether acteoside and similar compounds may inhibit the expression of Cell adhesion molecules (CAMs), which plays a role in the pathogenesis of atherosclerosis and inflammation. Here, we found that acteoside, isoacteoside, and 6-O-acetylacteoside inhibited IL-1beta-activated expression of interCellular CAM-1 (ICAM-1) and vascular CAM-1 (VCAM-1) in human umbilical vein endothelial Cells (HUVECs); the inhibitory potency was as follows: 6-O-acetylacteoside > acteoside > isoacteoside. Acteoside and 6-O-acetylacteoside also dose-dependently inhibited VCAM-1 gene promoter activity in IL-1beta-activated HUVECs. The inhibition of acteoside and 6-O-acetylacteoside on IL-1beta-activated expression of CAMs was manifested by decreased phosphorylation of extraCellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). These results indicate that acteoside and 6-O-acetylacteoside may exert anti-inflammatory activities in vascular endothelium by inhibiting the expression of CAMs, primarily through decreased phosphorylation of ERK and JNK.

Biol Pharm Bull. 2009 Sep; 32(9): 1565-70
Wang XC, Feng J, Huang F, Fan YS, Wang YY, Cao LY, Wen CP

The present study was performed to evaluate the potential protective effects of Shikonin extracted from Zicao on lupus nephritis (LN) using NZB/W F1 mice. Oral administration of Shikonin (24, 40 mg/kg body weight/d) or vehicle was applied to sixty female NZB/W F1 mice of 28-week-old with LN. Treatment with Shikonin for 14 weeks suppressed proteinuria dose-dependently with the mean proteinuria of 274.0 mg/dl and 160.3 mg/dl for low-dose and high-dose Shikonin groups, respectively, compared to 499.2 mg/dl for the vehicle. Also, Shikonin was observed to reduce circulating adhesion molecules significantly and down-regulate interCellular adhesion molecule-1 (ICAM-1) and vascular Cell adhesion molecule-1 (VCAM-1) mRNA expression in kidney. However, anti-double stranded (ds)DNA antibody in mice with low or high Shikonin dose administration both exhibited no significant elevation, differing from vehicle group. Kidney histological examination showed that renal glomerular lesions were alleviated after Shikonin application. These results suggest that Shikonin has therapeutic effects on LN in NZB/W F1 mice, to which inhibition of anti-dsDNA may be potential contribution, and its part mechanism is related to suppression of mRNA expression of Cell adhesion molecules (CAMs) in the kidney.

Cell Biochem Funct. 2009 Oct; 27(7): 496-8
Hashimoto T, Maekawa S, Miyata S

IgLON Cell adhesion molecules (CAMs) belonging to the immunoglobulin superfamily comprise of LAMP, neurotrimin (Ntm), OBCAM, and Kilon. In the present study, we performed the single and double transfection of IgLON gene constructs into hippocampal neurons in vitro and evaluated synaptic number. The quantitative analysis showed that the single over-expression of LAMP or OBCAM increased synaptic number, while the over-expression of Kilon reduced synaptic number and Ntm had no effects. The double over-expression of Kilon-Ntm, Kilon-OBCAM, LAMP-Ntm, and Ntm-OBCAM decreased synaptic number and that of Kilon-LAMP and LAMP-OBCAM had no effect. These results suggest that IgLON CAMs participate in regulating synapse formation in hippocampal neurons.

Neuron Glia Biol. 2008 Aug; 4(3): 197-209
Dityatev A, Bukalo O, Schachner M

Adhesive and repellent molecular cues guide migrating Cells and growing neurites during development. They also contribute to synaptic function, learning and memory in adulthood. Here, we review the roles of Cell adhesion molecules of the immunoglobulin superfamily (Ig-CAMs) and semaphorins (some of which also contain Ig-like domains) in regulation of synaptic transmission and plasticity. Interestingly, among the seven studied Ig-CAMs, the neuronal Cell adhesion molecule proved to be important for all tested forms of hippocampal plasticity, while its associated unusual glycan polysialic acid is necessary and sufficient part for synaptic plasticity only at CA3-CA1 synapses. In contrast, Thy-1 and L1 specifically regulate long-term potentiation (LTP) at synapses formed by entorhinal axons in the dentate gyrus and cornu ammonis, respectively. Contactin-1 is important for long-term depression but not for LTP at CA3-CA1 synapses. Analysis of CHL1-deficient mice illustrates that at intermediate stages of development a deficit in a Cell adhesion molecule is compensated but appears as impaired LTP during early and late postnatal development. The emerging mechanisms by which adhesive Ig-CAMs contribute to synaptic plasticity involve regulation of activities of NMDA receptors and L-type Ca2+ channels, signaling via mitogen-activated protein kinase p38, changes in GABAergic inhibition and motility of synaptic elements. Regarding repellent molecules, available data for semaphorins demonstrate their activity-dependent regulation in normal and pathological conditions, synaptic localization of their receptors and their potential to elevate or inhibit synaptic transmission either directly or indirectly.

Surg Neurol. 2009 Aug 5;
Chaichana KL, Pradilla G, Huang J, Tamargo RJ

BACKGROUND: Delayed vasospasm is the leading cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (aSAH). This phenomenon was first described more than 50 years ago, but only recently has the role of inflammation in this condition become better understood. METHODS: The literature was reviewed for studies on delayed vasospasm and inflammation. RESULTS: There is increasing evidence that inflammation and, more specifically, leukocyte-endothelial Cell interactions play a critical role in the pathogenesis of vasospasm after aSAH, as well as in other conditions including meningitis and traumatic brain injury. Although earlier clinical observations and indirect experimental evidence suggested an association between inflammation and chronic vasospasm, recently direct molecular evidence demonstrates the central role of leukocyte-endothelial Cell interactions in the development of chronic vasospasm. This evidence shows in both clinical and experimental studies that Cell adhesion molecules (CAMs) are up-regulated in the perivasospasm period. Moreover, the use of monoclonal antibodies against these CAMs, as well as drugs that decrease the expression of CAMs, decreases vasospasm in experimental studies. It also appears that certain individuals are genetically predisposed to a severe inflammatory response after aSAH based on their haptoglobin genotype, which in turn predisposes them to develop clinically symptomatic vasospasm. CONCLUSION: Based on this evidence, leukocyte-endothelial Cell interactions appear to be the root cause of chronic vasospasm. This hypothesis predicts many surprising features of vasospasm and explains apparently unrelated phenomena observed in aSAH patients. Therapies aimed at preventing inflammation may prevent and/or reverse arterial narrowing in patients with aSAH and result in improved outcomes.

Biol Pharm Bull. 2009 Aug; 32(8): 1371-7
Moon MK, Lee YJ, Kim JS, Kang DG, Lee HS

Recruitment of specific leukocyte subpopulations at the site of inflammation requires a series of Cell adhesion molecules (CAMs)-mediated interactions. The major CAMs, viz., intraCellular adhesion molecule-1 (ICAM-1), vascular Cell adhesion molecule-1 (VCAM-1), and E-selectin are expressed on endothelium in response to various cytokines. Caffeic acid (CA), a natural phenolic compound from herbs and other sources, has been shown to prevent cardiovascular diseases. We investigated the effect of CA on the expression of CAMs by human umbilical vein endothelial Cells (HUVECs) stimulated with tumor necrosis factor (TNF-alpha). adhesion of monocytes to CA-treated HUVECs was evaluated by co-culture experiments using 2,7-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethylester (BCECF-AM) labeling of U937 Cells. The expression of adhesion and chemoattractant molecules was evaluated by Western blot and reverse transcription-polymerase chain reaction (RT-PCR), respectively. CA significantly inhibited the TNF-alpha-induced increase in U937 monocyte adhesion to HUVECs as well as decreased the protein and mRNA expression levels of CAMs on HUVECs. CA also inhibited the mRNA expression of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8). The involvement of nuclear factor (NF)-kappaB in the transcriptional control of CAMs protein was assessed by degradation of inhibitory (I)kappaB and nuclear translocation of NF-kappaB using Western blotting and immunofluorescence staining. CA attenuated TNF-alpha-induced IkappaB degradation and NF-kappaB translocation from cytosol to the nucleus. In conclusion, TNF-alpha-induced NF-kappaB-DNA complex formation was inhibited by CA. CA reduced TNF-alpha-induced endothelial adhesiveness to HUVECs by inhibiting transcription factor activation, and CAMs expression suggesting its potential role in atherosclerosis diseases.

Toxicol Appl Pharmacol. 2009 Oct 15; 240(2): 299-305
Eum SY, Andras I, Hennig B, Toborek M

Exposure to persistent organic pollutants, such as polychlorinated biphenyls (PCBs), can lead to chronic inflammation and the development of vascular diseases. Because Cell adhesion molecules (CAMs) of the cerebrovascular endothelium regulate infiltration of inflammatory Cells into the brain, we have explored the molecular mechanisms by which ortho-substituted polychlorinated biphenyls (PCBs), such as PCB153, can upregulate CAMs in brain endothelial Cells. Exposure to PCB153 increased expression of interCellular adhesion molecule-1 (ICAM-1) and vascular Cell adhesion molecule-1 (VCAM-1), as well as elevated adhesion of leukocytes to brain endothelial Cells. These effects were impeded by inhibitors of EGFR, JAKs, or Src activity. In addition, pharmacological inhibition of NADPH oxidase or disruption of lipid rafts by cholesterol depleting agents blocked PCB153-induced phosphorylation of JAK and Src kinases and upregulation of CAMs. In contrast, silencing of caveolin-1 by siRNA interference did not affect upregulation of ICAM-1 and VCAM-1 in brain endothelial Cells stimulated by PCB153. Results of the present study indicate that lipid raft-dependent NADPH oxidase/JAK/EGFR signaling mechanisms regulate the expression of CAMs in brain endothelial Cells and adhesion of leukocytes to endothelial monolayers. Due to its role in leukocyte infiltration, induction of CAMs may contribute to PCB-induced cerebrovascular disorders and neurotoxic effects in the CNS.

Hum Mol Genet. 2009 Oct 15; 18(20): 3822-31
Nagaraj K, Kristiansen LV, Skrzynski A, Castiella C, Garcia-Alonso L, Hortsch M

L1-Cell adhesion molecule (L1-CAM) belongs to a functionally conserved group of neural Cell adhesion molecules that are implicated in many aspects of nervous system development. In many neuronal Cells the adhesive function of L1-type CAMs induces Cellular signaling processes that involves the activation of neuronal tyrosine protein kinases and among other functions regulates axonal growth and guidance. Mutations in the human L1-CAM gene are responsible for a complex neurodevelopmental condition, generally referred to as L1 syndrome. Several pathogenic L1-CAM mutations have been identified in humans that cause L1 syndrome in affected individuals without affecting the level of L1-CAM-mediated homophilic Cell adhesion when tested in vitro. In this study, an analysis of two different pathogenic human L1-CAM molecules indicates that although both induce normal L1-CAM-mediated Cell aggregation, they are defective in stimulating human epidermal growth factor receptor tyrosine kinase activity in vitro and are unable to rescue L1 loss-of-function conditions in a Drosophila transgenic model in vivo. These results indicate that the L1 syndrome-associated phenotype might involve the disruption of L1-CAM's functions at different levels. Either by reducing or abolishing L1-CAM protein expression, by interfering with L1-CAM's Cell surface expression, by reducing L1-CAM's adhesive ability or by impeding further downstream adhesion-dependent signaling processes.

J Am Acad Dermatol. 2009 Aug; 61(2): 263-70
López-Lerma I, Estrach MT

BACKGROUND: Cell adhesion molecules (CAMs) play a pivotal role in cutaneous localization of T Cells. Tissue-selective localization of T lymphocytes to the skin is crucial for immune surveillance and in the pathogenesis of skin disorders. OBJECTIVE: To detect the profile of soluble CAMs in patients with cutaneous T-Cell lymphoma (CTCL), we investigated the levels of interCellular adhesion molecule-1 (ICAM-1, soluble ICAM-1 [sICAM-1]); interCellular adhesion molecule-3 (sICAM-3); vascular Cell adhesion molecule-1 (sVCAM-1); and E-selectin (sE-selectin) in sera from patients with T-Cell-mediated skin diseases. METHODS: Serum levels of the 4 CAMs were measured by enzyme-linked immunosorbent assay in 42 participants including 11 patients with early stages of CTCL; 7 with advanced stages of CTCL including Sézary syndrome; 12 with inflammatory skin diseases (psoriasis and atopic dermatitis); 8 with skin diseases that may evolve into CTCL; and healthy individuals. Levels were correlated with biological parameters known as prognostic factors in non-Hodgkin lymphomas. RESULTS: In patients with CTCL, significantly increased levels of sICAM-1 and sICAM-3 were found when compared with healthy individuals and patients with inflammatory dermatosis. Soluble E-selectin and sVCAM-1 levels were not increased. There were significant positive correlations between sICAM-1 and sICAM-3 levels and each of them with beta2-microglobulin levels. LIMITATIONS: Limited number of patients was a limitation. CONCLUSION: There is a distinct profile of soluble CAMs in patients with CTCL. However, future studies with a larger group of patients are needed to confirm these findings. We propose that high sICAM-1 and sICAM-3 levels have important implications in the context of immune response and immune surveillance in these patients.

Neurosci Lett. 2009 Oct 25; 462(3): 272-5
McEwen DP, Chen C, Meadows LS, Lopez-Santiago L, Isom LL

Voltage-gated Na(+) channel (VGSC) beta1 and beta2 subunits are multifunctional, serving as both channel modulators and Cell adhesion molecules (CAMs). The purpose of this study was to determine whether VGSC beta3 subunits function as CAMs. The beta3 extraCellular domain is highly homologous to beta1, suggesting that beta3 may also be a functional CAM. We investigated the trans homophilic Cell adhesive properties of beta3, its association with the beta1-interacting CAM contactin, as well as its ability to interact with the cytoskeletal protein ankyrin. Our results demonstrate that, unlike beta1, beta3 does not participate in trans homophilic Cell-Cell adhesion or associate with contactin. Further, beta3 does not associate with ankyrin(G) in a heterologous system. Previous studies have shown that beta3 interacts with the CAM neurofascin-186 but not with VGSC beta1. Taken together, these findings suggest that, although beta1 and beta3 exhibit similar channel modulatory properties in heterologous systems, these subunits differ with regard to their homophilic and heterophilic CAM binding profiles.

Ophthalmic Res. 2009; 42(2): 106-11
Carreras FJ, Porcel D, Alaminos M, Garzón I

PURPOSE: This paper aims to study the anterior surface of the optic nerve in relation to its ability to support a source of stress acting from the vitreous cavity. The interCellular junctions of the lining astrocytes mediated by Cellular adhesion molecules (CAMs) may be the main targets for ionic stress. METHODS: The optic nerve of the domestic pig was prepared for light, confocal laser and transmission electron microscopy. Immunostaining was performed for antibodies against glial fibrillary acidic protein, neural cadherin (N-cadherin) and neural CAM (N-CAM). RESULTS: Only 1 type of interCellular junction was found among the bordering astrocytes, which was characterized as a zonula adherens. Unions between lining Cells showed a positive immunogold effect and immunofluorescence against N-cadherin in the zonula adherens and membrane apposition. N-CAM was also present in areas of nonjunctional Cellular adhesion. CONCLUSION: The stability of interCellular junctions of the nerve-vitreous boundary is sensitive to altered concentrations of Ca(2+). Since aqueous humor has half the Ca(2+) concentration of plasma, any contact of aqueous humor with the optic nerve head can interfere with the ionic concentration of calcium in the extraCellular spaces. This mechanism may contribute to age-related changes and some types of glaucoma.

Am J Physiol Gastrointest Liver Physiol. 2009 Aug; 297(2): G259-68
Binion DG, Heidemann J, Li MS, Nelson VM, Otterson MF, Rafiee P

Endothelial activation and surface expression of Cell adhesion molecules (CAMs) is critical for binding and recruitment of circulating leukocytes in tissues during the inflammatory response. Endothelial CAM expression plays a critical role in the intestinal microvasculature in inflammatory bowel disease (IBD), as blockade of leukocyte alpha4-integrin binding by gut endothelial CAM ligands has therapeutic benefit in IBD. Mechanisms underlying expression of vascular Cell adhesion molecule (VCAM)-1, a ligand for alpha4-integrin in primary cultures of human intestinal microvascular endothelial Cells (HIMEC) has not been defined. We investigated the effect of curcumin, phosphatidylinositol 3-kinase (PI 3-kinase)/protein kinase B (Akt), and mitogen-activated protein kinase (MAPK) inhibitors on VCAM-1 expression and function in HIMEC. CAM expression was assessed and HIMEC-leukocyte adhesion was visualized under static and flow conditions. Western blotting and in vitro kinase assays were used to assess Akt and MAPK activation. Nuclear factor-kappaB (NF-kappaB) activation and nuclear translocation of its p65 subunit were determined. Tumor necrosis factor (TNF)-alpha/lipopolysaccharide (LPS)-induced VCAM-1 expression in HIMEC was suppressed by Akt small-interfering RNA, curcumin, and inhibitors of NF-kappaB (SN-50), p38 MAPK (SB-203580) and PI 3-kinase/Akt (LY-294002). VCAM-1 induction was partially suppressed by p44/42 MAPK (PD-098059) but unaffected by c-Jun NH2-terminal kinase (SP-600125) inhibition. Curcumin inhibited Akt/MAPK/NF-kappaB activity and prevented nuclear translocation of the p65 NF-kappaB subunit following TNF-alpha/LPS. At physiological shear stress, curcumin attenuated leukocyte adhesion to TNF-alpha/LPS-activated HIMEC monolayers. In conclusion, curcumin inhibited the expression of VCAM-1 in HIMECs through blockade of Akt, p38 MAPK, and NF-kappaB. Curcumin may represent a novel therapeutic agent targeting endothelial activation in IBD.

Cytokine Growth Factor Rev. 2009 Jun; 20(3): 241-9
McEwan M, Lins RJ, Munro SK, Vincent ZL, Ponnampalam AP, Mitchell MD

The establishment of human pregnancy requires the orchestration of substantial Cell differentiation and tissue remodelling processes in the context of a complex dialogue between the receptive endometrium and the implanting blastocyst, and is therefore dependent upon a complex sequence of signalling events. Cytokines play an important role in each step of implantation, modulating expression of adhesion molecules on both the fetal and maternal surfaces, regulating expression of the proteases that remodel the extra-Cellular matrix, and promoting invasion and differentiation of trophoblasts. Here we review the role of cytokines in regulating the establishment of the fetal-maternal interface, with a particular focus on regulation of the functional expression of CAMs, the ECM and of the proteinases that modulate their function.

Cell Adh Migr. 2009 Jul-Sep; 3(3): 275-7
Siesser PF, Maness PF

Fast growing malignant cancers represent a major therapeutic challenge. Basic cancer research has concentrated efforts to determine the mechanisms underlying cancer initiation and progression and reveal candidate targets for future therapeutic treatment of cancer patients. With known roles in fundamental processes required for proper development and function of the nervous system, L1-CAMs have been recently identified as key players in cancer biology. In particular L1 has been implicated in cancer invasiveness and metastasis, and has been pursued as a powerful prognostic factor, indicating poor outcome for patients. Interestingly, L1 has been shown to be important for the survival of cancer stem Cells, which are thought to be the source of cancer recurrence. The newly recognized roles for L1CAMs in cancer prompt a search for alternative therapeutic approaches. Despite the promising advances in cancer basic research, a better understanding of the molecular mechanisms dictating L1-mediated signaling is needed for the development of effective therapeutic treatment for cancer patients.

Semin Cancer Biol. 2009 May 29;
Francavilla C, Maddaluno L, Cavallaro U

Cell adhesion molecules (CAMs) are Cell surface glycoproteins that mediate the physical interactions between adjacent Cells and between Cells and the surrounding extraCellular matrix. CAMs belong to different protein families, depending on their structural and functional properties. Furthermore, the expression of certain CAMs under physiological conditions is restricted to specific Cell types. Besides playing a key homeostatic role in maintaining the architecture of quiescent tissues, CAMs have also to adapt to the microenvironmental changes that occur during certain physiological and pathological processes. This is best exemplified by cancer vascularization, where the expression and function of vascular CAMs are dynamically regulated in response to tissue alterations induced by tumor growth as well as by changes in the surrounding stroma. This enables endothelial Cells (ECs) to leave the quiescent state and re-enter the angiogenic cascade. The latter is a multistep process carried out by different types of specialized ECs. This review describes the actual or supposed function of the various CAM subsets in the sequential series of events that underlie vascular changes during tumor angiogenesis. Notably, elucidating the mechanism of action of endothelial CAMs in cancer vasculature is expected to open new therapeutic avenues aimed at interfering with tumor growth and dissemination.

Lab Chip. 2009 May 21; 9(10): 1395-402
Lovchik RD, Bianco F, Matteoli M, Delamarche E

We present a method for depositing Cells in a sealed microfluidic device. The device consists of a poly(dimethylsiloxane) (PDMS) microfluidic network (MFN) sealed with a Si chip. The Si chip has vias and ports that are connected to high-precision motorized pumps. The surfaces of the PDMS MFN are homogeneously coated with fibronectin Cell adhesion molecules (CAMs). Flow velocity boundaries are created between vicinal microfluidic structures to prevent or permit deposition of Cells in specific regions of the MFN. In narrow flow paths, Cells experience a wall shear stress from the fast-moving liquid that overcomes the initial adhesion of the Cells with CAMs. Conversely, Cells can adhere to CAMs in larger flow paths such as Cell chambers inside which the velocity of the liquid and the shear stress are reduced. Interactively changing pumping rates makes the critical velocity (the velocity at which Cells deposit in the chamber but not elsewhere) easy to find. The transparent PDMS MFN allows both real-time visualization of the deposition process and Cellular assays. We illustrate this method using N9 mouse microglia Cells. In one experiment, approximately 75 microglia are deposited per min in a approximately 0.5 microL chamber. The deposited Cells remain viable, as assessed from staining and biofunctional assays. This method is simple, reliable, fast, and flexible, and therefore is an attractive technique for depositing Cells in microfluidic systems for numerous applications.

Eur Heart J. 2009 Jun; 30(12): 1516-24
Hanusch-Enserer U, Zorn G, Wojta J, Kopp CW, Prager R, Koenig W, Schillinger M, Roden M, Huber K

AIMS: Obesity and type 2 diabetes are associated with increased cardiovascular risk and elevation of traditional and non-traditional risk markers. As bariatric surgery reduces overweight and improves metabolic derangement, we examined a cluster of established and emerging cardiovascular risk factors, such as soluble CD40 ligand (sCD40L) and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), which might improve prediction of future cardiovascular events because of their more direct involvement in plaque destabilization. METHODS AND RESULTS: Obese patients [n = 32, body mass index (BMI) 46.1 +/- 5.9 kg/m(2)] underwent clinical examinations and blood sampling for measurement of glucose and lipid parameters as well as non-traditional cardiovascular risk markers, i.e. high-sensitivity C-reactive protein, plasminogen activator inhibitor-1 (PAI-1), soluble Cellular adhesion molecules (CAM), MMP-2, MMP-9, CD40L, and Lp-PLA(2) before and after 1 year following laparoscopic adjustable gastric banding (LAGB), respectively. In patients undergoing LAGB, blood pressure (P < 0.0001) and blood glucose (P = 0.02) were significantly lowered by approximately 16% as well as triglyceride levels by approximately 29% (P = 0.002). In addition to a decrease of the inflammatory and pro-thrombotic marker PAI-1 (P = 0.001), CAMs, and MMP-9 (P = 0.004) were reduced, whereas no change was observed for plasma levels of MMP-2, sCD40L, and Lp-PLA(2) after LAGB, respectively. Individual changes in (ICAM-1) interCellular adhesion molecule-1 (DeltaICAM-1) were related to changes in insulin (Deltafasting insulin) before and after LAGB (r = 0.36 and r = 0.38; both P = 0.04). E-selectin correlated positively with changes in BMI (r = 0.38; P = 0.04 and r = 0.36; P = 0.05), while Lp-PLA(2) concentration was negatively correlated with BMI (r =-0.41; P = 0.02) after 1 year. Changes were comparable in both overweight diabetic and non-diabetic subjects. CONCLUSION: LAGB not only induced weight loss but also an improvement in the subclinical pro-inflammatory state. However, concentrations of most of the non-traditional risk factors for plaque instability, i.e. MMP-9, sCD40L, and Lp-PLA(2) remained unchanged.

Biochem J. 2009 May 1; 419(3): 519-31
Herron LR, Hill M, Davey F, Gunn-Moore FJ

The L1 family of CAMs (Cell adhesion molecules) has long aroused the interest of researchers, but primarily the extraCellular interactions of these proteins have been elucidated. More recently, attention has turned to the intraCellular signalling potentiated by transmembrane proteins and the cytoplasmic proteins with which they can interact. The present review brings up to date the current body of published knowledge for the intraCellular interactions of L1-CAM family proteins and the potential importance of these interactions for the mechanisms of L1-CAM action.

Biochem Biophys Res Commun. 2009 Apr 17; 381(4): 459-61
Xu Y, Li S

Vasculitis is becoming more common worldwide, but there is no effective therapeutic method towards this series of disease till now. InterCellular adhesion molecule (ICAM)-1 is one of an important Cell adhesion molecules (CAMs) family glycoprotein that plays pivotal role in inflammation process and participates in vasculitis. Blockade of ICAM-1 has been witnessed with its satisfactory effect on inflammatory disease treatment. Therefore, this method may be considered as a novel way towards treatment of vasculitis.