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Henipaviruses
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Olivier Escaffre, Viktoriya Borisevich, Barry Rockx
In addition, NiV-M can productively infect porcine peripheral blood monocytes, CD+6CD+8T lymphocytes, and NK cells. Infection of T cells expressing CD6, a strong ligand for the activated leukocyte cell adhesion molecule (ALCAM) which is highly expressed on the microvascular endothelial cells of the blood–air and the blood–brain barriers (BBBs), may explain the preferential tropism of NiV-M for small blood vessels of the lung and brain.67 Interestingly, human lymphocytes and monocytes are not permissive for NiV-M. Despite the absence of infection, lymphocytes could efficiently bind NiV-M and transfer infection to endothelial and Vero cells.68 In hamsters, such NiV-loaded mononuclear leukocytes transfer lethal NiV infection into naive animals, demonstrating efficient virus transinfection in vivo.
The S100A7/8/9 Proteins: Novel Biomarker and Therapeutic Targets for Solid Tumor Stroma
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Sanjay Mishra, Dinesh Ahirwar, Mohd W. Nasser, Ramesh K. Ganju
In melanoma patients, immune-based antibody drug ipilimumab treatment response has been shown to be positively associated with increase in eosinophil count and negatively associated with elevated amounts of MDSC and monocytes as compared with basal levels and with responding patients. It was also observed that ipilimumab treatment in non-responders resulted in elevated serum concentrations of S100A8/A9 and HMGB1 that attract and activate MDSCs [88]. In another study, S100A8 levels were found to be associated with clinical response rate in acute myeloblastic leukemia (AML). Knockdown of S100A8 increases autophagy and chemotherapy-induced cytotoxicity in AML cells. In addition, S100A8 directly regulates autophagy protein Beclin 1 and dissociates Beclin1-Bcl-2 complex [89, 90]. In search for novel S100 protein receptors, by using affinity isolation-mass spectrometry, cell surface glycoprotein EMMPRIN/BASIGIN (CD147/BSG) was identified as specific receptor to S100A9, which does not bind to S100A8. It was found that besides RAGE, S100A9 interacts with EMMPRIN to activate TNF receptor-associated factor TRAF2 and induce cytokines and metalloproteases expression [91]. Immunohistochemistry analysis revealed that EMMPRIN was expressed at the edge of melanoma lesion and adjacent epidermis and co-localize with S100A9 [91]. Similarly, ALCAM and MCAM molecules were identified as novel receptors for S100A8/A9 and induce melanoma progression by activating ROS production and NF-κB activation [92]. ß-1,3-galactosyl-O-glycosyl-glycoprotein ß-1,6-N-acetylglucosaminyltransferase 3 (GCNT3) has been shown to be overexpressed in metastatic melanomas. Molecular inhibition of GCNT3 resulted in reduced migration and invasion of melanoma cells, mediated by loss of S100A8/A9 signaling [93].
CircMED12L Protects Against Hydrogen Peroxide-induced Apoptotic and Oxidative Injury in Human Lens Epithelial Cells by miR-34a-5p/ALCAM axis
Published in Current Eye Research, 2022
Baohua Wu, Yan Sun, Jingmei Hou
Based on the ceRNA hypothesis,19,20 the localization of circMED12L was then investigated. This study confirmed that circMED12L was localized in the cytoplasm of HLECs. Thus, the potential network of circMED12L was forecasted, and we identified the circMED12L/miR-34a-5p/ALCAM axis in HLECs. MiRNAs are a kind of small noncoding RNAs of ∼23 nucleotides that are powerful modulators in complex processes.35 MiRNAs have been found to be differentially expressed in ARC patients, and play significant effects on the pathophysiology of ARC process by affecting the antioxidant function and apoptosis of HLECs.36–38 In this work, we found that miR-34a-5p could promote apoptosis and oxidative damage in HLECs, which was consistent with previous findings.22,23 Moreover, we also investigated that miR-34a-5p overexpression reversed the antioxidant and anti-apoptotic effects of circMED12L on HLECs under H2O2 treatment. ALCAM is a glycoprotein involved in the activation of T-cells, neutrophils trans-endothelial migration, hematopoiesis, inflammation and tumor propagation and invasiveness via heterophilic and homophilic interactions.39 In our work, a decreased ALCAM in ARC was observed; then, we proved that ALCAM deficiency could abate the suppressing influences of miR-34a-5p inhibitor on HLEC oxidant damage and apoptosis.
Analytical validation of urine ALCAM ELISA as a test for lupus nephritis
Published in Expert Review of Molecular Diagnostics, 2023
Rongwei Lei, Nga Thai, Yaxi Li, Michelle Petri, Chandra Mohan
Activated leukocyte cell adhesion molecule (ALCAM), also known as CD166, belongs to the immunoglobulin superfamily and is widely expressed on both endothelial, epithelial, and myeloid cells. ALCAM binds to T-cell transmembrane glycoprotein CD6 and is involved in cell adhesion and migration. Increased expression of ALCAM has been observed in renal tissue from MRL/LPR lupus-like glomerulonephritis mice [17]. Urinary ALCAM (uALCAM) is emerging as a promising marker for continued research and monitoring of SLE disease activity. In several proteomic screens and targeted studies [18–24], uALCAM outperformed several (~1000) competing candidates in discriminating active LN from other controls (active non-renal, inactive SLE, and healthy controls) [25–30]; the discriminatory power of uALCAM had been validated in ~ 1000 subjects across five independent (multi-national) cohorts in four ethnicities [28]; by Bayesian analysis, uALCAM exhibited the most dominant effect on disease status than other biomarker levels [25]; uALCAM showed a positive correlation with renal domains of systemic lupus erythematosus disease activity index (SLEDAI) in all ethnic groups examined [25–28]; uALCAM was predictive of proliferative LN by histology and high renal pathology activity index [26]; baseline uALCAM was predictive of poor outcome 10 years later in patients with LN [27]; uALCAM tracks with disease activity over time, thus reflecting patient response to induction therapy in LN [26]; uALCAM is equally diagnostic and predictive of active disease in children with LN [24]. Thus, as a disease biomarker, uALCAM meets or outperforms current diagnostic metrics used for monitoring SLE/LN.
Upregulation of miR-630 Induced by Oxidative Damage Resists Cell Migration Through Targeting ALCAM in Human Lens Epithelium Cells
Published in Current Eye Research, 2020
Lin Mei, Hong Yan, Song Wang, Chenjun Guo, Xiaoliang Zheng, Bo Yan, Jing Zhao, Angang Yang
As a member of a subfamily of immunoglobulin receptors, ALCAM is a cell adhesion molecule containing Ig-like domain in their extracellular regions and contribute to a range of signaling programs involved in cell adhesion and migration.23,24 It has been now implicated in several adhesive and migratory procedures including leukocyte homing, axonal guidance, and inflammatory responses, also it is a predictor of tumor progression due to its promotion of cancer metastasis.24–29 To investigate the consequences caused by increased level of miR-630 and the following downregulation of ALCAM after oxidative stimulation in HLECs, we performed transwell migration assay and scratching test, discovering that cell migration ability was significantly decreased by upregulation of miR-630. Similar but less obvious phenomenon was also investigated when ALCAM was solely inhibited, revealing that upregulation of miR-630 may lead to decreased migration ability in HLECs by targeting on some mRNAs of genes related to cell adhesion, among which ALCAM is included but not the only one. Moreover, elevated cell migration was observed in HLECs treated by H2O2, but the promotion could be partly repressed by the transfection of miR-630. The previous result of gene profiling assay showed that the expression levels of many signaling pathways related to cell migration and adhesion were altered by oxidative stimulation, but their influences on cell migration were different. The cell migration tests showed that the general effect of these alterations was enhancing cell migration of HLECs even with some resistances like the upregulation of miR-630 and the repression of ALCAM. Still, further study is needed for the downstream signaling pathway inhibited by miR-630 to resist cell migration induced by oxidative stimulation.