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Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
TNFα is an inflammatory cytokine whose antagonists are currently being successfully used in psoriasis, PsA, RA, and so forth. It was originally named TNF or lymphotoxin based on experiments in the late 1960s and early 1970s, when this factor was found to induce necrosis of fibrosarcoma cells. However, this factor is a general apoptotic signal to many cells unless rescued by some growth factor or other rescue mechanisms. It is one of the acute phase reactants circulating in blood that goes up during inflammatory conditions. Commonly, it is produced in response to danger signals or alarmins by activated macrophages or dendritic cells, although it can be produced by many other cell types, such as Th1 cells, NK cells, neutrophils, mast cells, keratinocytes, and endothelial cells. Structurally, it is a homotrimer that is formed in a membrane-bound state shed from the membrane by TNFα-converting enzyme (TACE), a “secretase.” Originally, TACE was ADAM17, but now the action is known to be possible by ADAM9, 17, and 19 and MMP7 and 17. TNFα is the prototype member of a large superfamily of cytokines that cause receptor-mediated cell death.
ADAM12 abrogation alters immune cell infiltration and improves response to checkpoint blockade therapy in the T11 murine model of triple-negative breast cancer
Published in OncoImmunology, 2023
Guanpeng Wang, Yeni Romero, Indhujah Thevarajan, Anna Zolkiewska
Using data mining approaches, we then examined whether our results linking the loss of ADAM12 to anti-tumor responses and ICB susceptibility in the T11 mouse model may be applicable to human TNBC patients. First, expression profiling of different immune cell populations by RNA-Seq suggests that ADAM12 is expressed at very low levels in immune cells (Figure 8a, data retrieved at http://www.immgen.org). In contrast, most other catalytically active ADAMs, except for ADAM9, are expressed at high levels in various types of immune cells (Figure 8a). This means that ADAM12 expression values obtained during mRNA profiling of bulk tumors should predominantly reflect ADAM12 expression in cancer cells, with a minimal contribution from tumor-infiltrating immune cells.
Circ_0005714/miR-223-3p/ADAM9 regulatory axis affects proliferation, migration, invasion, and angiopoiesis in trophoblast cells
Published in Autoimmunity, 2022
ADAM9 3′UTR sequence was observed to have the binding sites for miR-223-3p after the analysis by starbase (http://starbase.sysu.edu.cn) (Figure 5(A)). Then, the binding between miR-223-3p and ADAM9 3′UTR was validated by the luciferase signal reduction of WT-ADAM9-3′UTR and miR-223-3p mimic co-transfection in HTR-8/SVneo and JEG-3 cells (Figure 5(B,C)). RT-qPCR and western blot suggested that ADAM9 was highly expressed in PE tissues contrasted to normal tissues (Figure 5(D,E)). ADAM9 protein level was successfully knocked down by si-ADAM9, in comparison with si-NC group (Figure 5(F)). The inhibitory efficiency of miR-223-3p inhibitor was also significant in HTR-8/SVneo and JEG-3 cells (Figure 5(G)). Inhibition of miR-223-3p promoted the protein expression of ADAM9, which was subsequently eliminated by transfection of si-ADAM9 (Figure 5(H)). Overall, miR-223-3p could directly regulate the ADAM9 level by targeting the 3′UTR.
The relationship between cholesterol level and Alzheimer’s disease-associated APP proteolysis/Aβ metabolism
Published in Nutritional Neuroscience, 2019
Chaoqun Wang, Yikai Shou, Jie Pan, Yue Du, Cuiqing Liu, Huanhuan Wang
APP α-secretase is thought to be a membrane-bound zinc metalloproteinase composed of disintegrin and metalloprotease (ADAM) family members, such as ADAM9, ADAM10, ADAM19, and tumour necrosis factor-converting enzyme (TACE)/ADAM17.62–64 ADAM10 is the dominant form of α-secretase in neurons.65 Under conditions of normal intracellular cholesterol levels, APP is predominantly cleaved by α-secretase but not BACE1,58 producing a C83 fragment and sAPPα, which is neurotrophic and neuroprotective.66–68 The C83 fragment can be cleaved by PS1 and produces the p3 peptide, which mainly contains Aβ17-40 and Aβ17-42. Unlike Aβ, the p3 peptide lacks 16 amino acids and does not easily form oligomers that produce a neurotoxic effect.69 Therefore, the higher the level of α-secretase in neurons, the greater is the chance that AD development could be postponed.