scholarly journals A Preliminary Investigation on Plasma Cell Adhesion Molecules Levels by Protein Microarray Technology in Major Depressive Disorder

2021 ◽  
Vol 12 ◽  
Author(s):  
Wanying Liu ◽  
Yanqun Zheng ◽  
Fuxu Zhang ◽  
Mo Zhu ◽  
Qian Guo ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Cell Adhesion ◽  
Depressive Disorder ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecules ◽  
Cell Adhesion Molecule ◽  
Protein Microarray ◽  
Diagnostic Value ◽  
Microarray Technology ◽  
Major Depressive

Objectives: Major depressive disorder (MDD) is a serious mental disorder, and there is a great difficulty to diagnose and treat. Hitherto, relatively few studies have explored the correlation between the levels of plasma cell adhesion molecules and MDD.Methods: Thirty outpatients with acute episodes of MDD in Shanghai Mental Health Center and 34 healthy volunteers from the community were recruited as subjects. Protein microarray technology was applied to compared the differences in plasma levels of 17 kinds of adhesion molecular proteins between the two groups. Meanwhile, the diagnostic value of different proteins in depression was discussed by using the receiver operating characteristic curve.Results: The levels of Carcinoembryonic Antigen Related Cell Adhesion Molecule-1(CEACAM-1) and Neural Cell Adhesion Molecule (NrCAM) in MDD patients were significantly higher than those in healthy controls (P < 0.05). The area under ROC curve of CEACAM-1 combined with NrCAM was 0.723, with the sensitivity 0.800 and the specificity 0.676.Conclusion: The plasma levels of CEACAM-1 and NrCAM were significantly up-regulated in MDD, and their combined application was of potential diagnostic value, deserving to expand the sample size for further verification.

scholarly journals The Diagnostic Value of Serum L1CAM in Patients With Colorectal Cancer

2020 ◽  
Vol 19 ◽  
pp. 153303382092097
Author(s):  
Ling-Yu Chu ◽  
Dong-Ming Guo ◽  
Jun-Tian Chen ◽  
Wang-Kai Fang ◽  
Jian-Jun Xie ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Adhesion ◽  
Confidence Interval ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Operating Characteristic ◽  
Early Stage ◽  
Diagnostic Value ◽  
L1 Cell Adhesion Molecule ◽  
Normal Controls

Objective: Colorectal cancer is one of the most important malignant cancer in the world with high incidence and mortality. Some studies have found that the expression of low serum L1 cell adhesion molecule is associated with poor prognosis in some malignancies. It is suggested that L1 cell adhesion molecule is a candidate serum marker for certain tumors. However, the relationship between serum L1 cell adhesion molecule and colorectal cancer, especially about the diagnostic value, is rarely reported. Therefore, this study aimed to evaluate the diagnostic potential of serum L1 cell adhesion molecule in patients with colorectal cancer. Methods: Enzyme-linked immunosorbent assay was carried out to detect L1 cell adhesion molecule level in sera of 229 patients with colorectal cancer and 145 normal controls. Receiver operating characteristic curves were employed to calculate the accuracy of diagnosis. Results: The levels of serum L1 cell adhesion molecule in the colorectal cancer group were significantly lower than that in normal controls ( P < .05). In the normal group, the area under the receiver operating characteristic curve (area under the curve) of all colorectal cancer was 0.781 (95% confidence interval: 0.734-0.828) and early-stage colorectal cancer was 0.764 (95% confidence interval: 0.705-0.823). With optimized cutoff of 17.760 ng/mL, L1 cell adhesion molecule showed certain diagnostic value with specificity of 90.3% and sensitivities of 43.2% and 36.2% in colorectal cancer and early-stage colorectal cancer, respectively. Clinical data analysis showed that the levels of L1 cell adhesion molecule were significantly correlated with gender ( P < .05) and early and late stages ( P < .05). Furthermore, when compared with carcinoembryonic antigen, serum L1 cell adhesion molecule had significantly improved diagnostic accuracy for both colorectal cancer and early-stage colorectal cancer. Conclusions: Our study demonstrated that serum L1 cell adhesion molecule might be served as a potential biomarker for the diagnosis of colorectal cancer.

MAdCAM mediates lymphocyte-endothelial cell adhesion in a murine model of chronic colitis

2001 ◽  
Vol 281 (5) ◽  
pp. G1309-G1315 ◽  
Author(s):  
Takeharu Shigematsu ◽  
Robert D. Specian ◽  
Robert E. Wolf ◽  
Matthew B. Grisham ◽  
D. Neil Granger
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
T Lymphocytes ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecules ◽  
Cell Adhesion Molecule ◽  
Scid Mice ◽  
Endothelial Cell Adhesion Molecules ◽  
Cell Adhesion Molecule 1 ◽  
Endothelial Cell Adhesion

Previous studies have revealed that the expression of several endothelial cell adhesion molecules [e.g., intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and mucosal addressin cell adhesion molecule 1 (MAdCAM-1)] is dramatically elevated in the chronically inflamed colonic vasculature of severe combined immunodeficient (SCID) mice reconstituted with congenic CD4+, CD45RBhigh T lymphocytes. The objective of this study was to define the contribution of different endothelial cell adhesion molecules to the lymphocyte-endothelial cell (L/E) adhesion observed in the colonic microvasculature in this experimental model of inflammatory bowel disease. Fluorescently labeled T lymphocytes, isolated from spleens of normal BALB/C mice, were injected intravenously into SCID mice that had been reconstituted with CD4+, CD45RBhigh T lymphocytes either before (3 wk after reconstitution) or after (7 wk postreconstitution) the onset of clinical signs of colitis (i.e., diarrhea, loss of body wt). Intravital fluorescence microscopy was used to quantify L/E adhesion in different-sized venules of the colonic submucosa during the development of colitis. L/E adhesion was noted in some segments of the vasculature in precolitic SCID mice (3 wk after reconstitution) but not in similar-sized vessels of control (wild type and SCID) mice. L/E adhesion was observed in a greater proportion of venules and occurred with greater intensity in the mucosa of colitic mice (7 wk postreconstitution). Pretreatment with a blocking monoclonal antibody against MAdCAM-1, but not ICAM-1 or VCAM-1, significantly and profoundly reduced L/E adhesion in colitic mice. Immunohistochemical staining also revealed the localization of T cells on colonic endothelial cells expressing MAdCAM-1. These findings indicate that MAdCAM-1 is largely responsible for recruiting T lymphocytes into inflamed colonic tissue.

scholarly journals Migration inhibitory factor up-regulates vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 via Src, PI3 kinase, and NFκB

Blood ◽  
2006 ◽  
Vol 107 (6) ◽  
pp. 2252-2261 ◽  
Author(s):  
M. Asif Amin ◽  
Christian S. Haas ◽  
Kui Zhu ◽  
Pamela J. Mansfield ◽  
Michael J. Kim ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecules ◽  
Cell Adhesion Molecule ◽  
Intercellular Adhesion Molecule ◽  
Dependent Manner ◽  
Vascular Cell Adhesion ◽  
Intercellular Adhesion Molecule 1 ◽  
Cell Adhesion Molecule 1

AbstractCell adhesion molecules are critical in monocyte (MN) recruitment in immune-mediated and hematologic diseases. We investigated the novel role of recombinant human migration inhibitory factor (rhMIF) in up-regulating vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) and their signaling pathways in human MNs. rhMIF-induced expression of VCAM-1 and ICAM-1 was significantly higher compared with nonstimulated MNs. rhMIF induced MN VCAM-1 and ICAM-1 expression in a concentration-dependent manner (P < .05). Antisense oligodeoxynucleotides (ODNs) and inhibitors of Src, PI3K, p38, and NFκB significantly reduced rhMIF-induced MN VCAM-1 and ICAM-1 expression (P < .05). However, Erk1/2 and Jak2 were not involved. Silencing RNA directed against MIF, and inhibitors of Src, PI3K, NFκB, anti–VCAM-1, and anti–ICAM-1 significantly inhibited rhMIF-induced adhesion of HL-60 cells to human dermal microvascular endothelial cells (HMVECs) or an endothelial cell line, HMEC-1, in cell adhesion assays, suggesting the functional significance of MIF-induced adhesion molecules (P < .05). rhMIF also activated MN phospho-Src, -Akt, and -NFκB in a time-dependent manner. rhMIF induced VCAM-1 and ICAM-1 up-regulation in 12 hours via Src, PI3K, and NFκB as shown by Western blotting and immunofluorescence. MIF and MIF-dependent signaling pathways may be a potential target for treating diseases characterized by up-regulation of cell adhesion molecules.

scholarly journals Cell Adhesion Molecules—Update

1997 ◽  
Vol 34 (1) ◽  
pp. 61-73 ◽  
Author(s):  
C. S. Elangbam ◽  
C. W. Qualls ◽  
R. R. Dahlgren
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecules ◽  
Cell Adhesion Molecule ◽  
Immunoglobulin Superfamily ◽  
Specific Cell ◽  
Leukocyte Function ◽  
Cell Adhesion Molecule 1 ◽  
Integrin Family

Cell adhesion molecules are glycoproteins expressed on the cell surface and play an important role in inflammatory as well as neoplastic diseases. There are four main groups: the integrin family, the immunoglobulin superfamily, selectins, and cadherins. The integrin family has eight subfamilies, designated as β1, through β8. The most widely studied subfamilies are β1 (CD29, very late activation [VLA] members), β2 (leukocyte integrins such as CDlla/CD18, CDllb/CD18, CDllc/CD18, and αdβ2), β3 (CD61, eytoadhesions), and β7 (α4β7 and αEβ7). The immunoglobulin superfamily includes leukocyte function antigen-2 (LFA-2 or CD2), leukocyte function antigen-3 (LFA-3 or CD58), intercellular adhesion molecules (ICAMs), vascular adhesion molecule-1 (VCAM-1), platelet-endothelial cell adhesion molecule-1 (PE-CAM-1), and mucosal addressin cell adhesion molecule-1 (MAdCAM-1). The selectin family includes E-selectin (CD62E), P-selectin (CD62P), and L-selectin (CD62L). Cadherins are major cell-cell adhesion molecules and include epithelial (E), placental (P), and neural (N) subclasses. The binding sites (ligands/receptors) are different for each of these cell adhesion molecules (e.g., ICAM binds to CD11/CD18; VCAM-1 binds to VLA-4). The specific cell adhesion molecules and their ligands that may be involved in pathologic conditions and potential therapeutie strategies by modulating the expression of these molecules will be discussed.

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