Cell adhesion molecule 1 (CADM1) is ubiquitously present in the endothelium and smooth muscle cells of the human macro- and micro-vasculature

Tatsumi, Kanayo; Taatjes, Douglas J.; Wadsworth, Marilyn P.; Bouchard, Beth A.; Bovill, Edwin G.

doi:10.1007/s00418-012-1024-2

Cited by 9 publications

(9 citation statements)

References 14 publications

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“…The cell adhesion molecule CADM1 (NECL2), C-type lectin, CLEC9A (which recognizes damaged cells), and the chemokine receptor XCR1 are expressed on human and mouse cDC1 ( 19 , 22 , 64 – 66 ). However, CADM1 expression is not restricted to leukocytes and CLEC9A is also expressed on murine DC precursors ( 67 , 68 ). Although cDC1 is the only leukocyte expressing XCR1, a commercial antibody against it is currently unavailable.…”

Section: DC Monocyte and Macrophage Subsets In Mice And Humansmentioning

confidence: 99%

Human and Mouse Mononuclear Phagocyte Networks: A Tale of Two Species?

2015

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Dendritic cells (DCs), monocytes, and macrophages are a heterogeneous population of mononuclear phagocytes that are involved in antigen processing and presentation to initiate and regulate immune responses to pathogens, vaccines, tumor, and tolerance to self. In addition to their afferent sentinel function, DCs and macrophages are also critical as effectors and coordinators of inflammation and homeostasis in peripheral tissues. Harnessing DCs and macrophages for therapeutic purposes has major implications for infectious disease, vaccination, transplantation, tolerance induction, inflammation, and cancer immunotherapy. There has been a paradigm shift in our understanding of the developmental origin and function of the cellular constituents of the mononuclear phagocyte system. Significant progress has been made in tandem in both human and mouse mononuclear phagocyte biology. This progress has been accelerated by comparative biology analysis between mouse and human, which has proved to be an exceptionally fruitful strategy to harmonize findings across species. Such analyses have provided unexpected insights and facilitated productive reciprocal and iterative processes to inform our understanding of human and mouse mononuclear phagocytes. In this review, we discuss the strategies, power, and utility of comparative biology approaches to integrate recent advances in human and mouse mononuclear phagocyte biology and its potential to drive forward clinical translation of this knowledge. We also present a functional framework on the parallel organization of human and mouse mononuclear phagocyte networks.

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Section: DC Monocyte and Macrophage Subsets In Mice And Humansmentioning

confidence: 99%

Human and Mouse Mononuclear Phagocyte Networks: A Tale of Two Species?

2015

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“…There exists an extensive body of literature describing CADM1 as a tumor suppressor protein, but only two studies that describe “CADM1” and its role in the vascular system . Hasstedt et al was the follow‐up on a human linkage study that had the goal of identifying single nucleotide polymorphisms (SNPs) in genes of the Kindred Vermont II family .…”

Section: Discussionmentioning

confidence: 99%

“…Cell Adhesion Molecule 1 is a protein that has been found to be strongly expressed in neurons, [71][72][73][74][75] spermatogenic cells, [52,[76][77][78] immune cells, [79][80][81][82][83][84][85][86][87] and endothelial cells [88,89]. Functionally, CADM1 has been shown to participate in homophilic binding, and paradoxically, tumor suppression.…”

Section: Cadm1: An Additional Role For a Versatile Protein?mentioning

confidence: 99%

Tumor Necrosis Factor α Regulates Endothelial Progenitor Cell Migration via CADM1 and NF-kB

et al. 2016

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Shortly after the discovery of endothelial progenitor cells (EPCs) in 1997, many clinical trials were conducted using EPCs as a cellular based therapy with the goal of restoring damaged organ function by inducing growth of new blood vessels (angiogenesis). Results were disappointing, largely because the cellular and molecular mechanisms of EPC-induced angiogenesis were not clearly understood. Following injection, EPCs must migrate to the target tissue and engraft prior to induction of angiogenesis. In this study EPC migration was investigated in response to tumor necrosis factor α (TNFα), a pro-inflammatory cytokine, to test the hypothesis that organ damage observed in ischemic diseases induces an inflammatory signal that is important for EPC homing. In this study, EPC migration and incorporation were modeled in vitro using a co-culture assay where TNFα treated EPCs were tracked while migrating towards vessel-like structures. It was found that TNFα treatment of EPCs increased migration and incorporation into vessel-like structures. Using a combination of genomic and proteomic approaches, NF-kB mediated upregulation of CADM1 was identified as a mechanism of TNFα induced migration. Inhibition of NF-kB or CADM1 significantly decreased migration of EPCs in vitro suggesting a role for TNFα signaling in EPC homing during tissue repair.

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“…ZO-1 exclusively localizes to tight junctions and directly binds to CADM1 at the post synaptic density protein (PSD95), drosophila disc large tumor suppressor (Dlg), and zonula occludens-1 protein (ZO-1), PDZ-binding motif) and F-actin at the C-terminal EYFI sequence (Fukuhara et al, 2003). CADM1, which belongs to the cell adhesion molecule in the immunoglobulin superfamily members, was involved in the construction of the cytoskeleton and maintaining the stability of cell adhesion (Tatsumi, Taatjes, Wadsworth, Bouchard, & Bovill, 2012). In blood vessels, the typical symptoms of Se deficiency are tight junction destruction, oxidative damage, and endothelial dysfunction.…”

Section: Introductionmentioning

confidence: 99%

MiR‐128‐1‐5p regulates tight junction induced by selenium deficiency via targeting cell adhesion molecule 1 in broilers vein endothelial cells

Pan

Liu

et al. 2018

Journal Cellular Physiology

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Vein endothelial cells (VECs) constitute an important barrier for macromolecules and circulating cells from the blood to the tissues, stabilizing the colloid osmotic pressure of the blood, regulating the vascular tone, and rapidly changing the intercellular connection, and maintaining normal physiological function. Tight junction has been discovered as an important structural basis of intercellular connection and may play a key role in intercellular connection injuries or vascular diseases and selenium (Se) deficiency symptoms. Hence, we replicated the Se-deficient broilers model and detected the specific microRNA in response to Se-deficient vein by using quantitative real time-PCR (qRT-PCR) analysis. Also, we selected miR-128-1-5p based on differential expression in vein tissue and confirmed its target gene cell adhesion molecule 1 (CADM1) by the dual luciferase reporter assay and qRT-PCR in VECs. We made the ectopic miR-128-1-5p expression for the purpose of validating its function on tight junction. The result showed that miR-128-1-5p and CADM1 were involved in the ZO-1-mediated tight junction, increased paracellular permeability, and arrested cell cycle. We presumed that miR-128-1-5p and Se deficiency might trigger tight junction. Interestingly, miR-128-1-5p inhibitor and fasudil in part hinder the destruction of the intercellular structure caused by Se deficiency. The miR-128-1-5p/CADM1/tight junction axis provides a new avenue toward understanding the mechanism of Se deficiency, revealing a novel regulation model of tight junction injury in vascular diseases.

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Cell adhesion molecule 1 (CADM1) is ubiquitously present in the endothelium and smooth muscle cells of the human macro- and micro-vasculature

Cited by 9 publications

References 14 publications

Human and Mouse Mononuclear Phagocyte Networks: A Tale of Two Species?

Human and Mouse Mononuclear Phagocyte Networks: A Tale of Two Species?

Tumor Necrosis Factor α Regulates Endothelial Progenitor Cell Migration via CADM1 and NF-kB

MiR‐128‐1‐5p regulates tight junction induced by selenium deficiency via targeting cell adhesion molecule 1 in broilers vein endothelial cells

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