Literature DB >> 15977176

JAM-A expression during embryonic development.

James J Parris1, Vesselina G Cooke, William C Skarnes, Melinda K Duncan, Ulhas P Naik.   

Abstract

Cell adhesion molecules of the immunoglobulin superfamily play an important role in embryonic development. We have shown recently that JAM-A, a member of this family expressed at endothelial and epithelial tight junctions, is involved in platelet activation, leukocyte transmigration, and angiogenesis. Here, we determine the expression pattern of the JAM-A gene during embryogenesis using transgenic mice expressing lacZ under the control of the endogenous JAM-A promoter. Histochemical staining for beta-galactosidase in heterozygous mouse embryos was first seen in the inner cell mass and trophectoderm of the blastocyst. By 8.5 days post coitum (dpc), JAM-A gene activity was detected in the endoderm and part of the surface ectoderm. At 9.5 dpc, JAM-A expression began to localize to certain organ systems, most notably the developing inner ear and early vasculature. Localization of JAM-A to embryonic vasculature was confirmed by double-staining with antibodies against JAM-A and platelet endothelial cell adhesion molecule-1, a known endothelial cell marker. As organogenesis progressed, high levels of JAM-A expression continued in the epithelial component of the inner ear as well as the epithelium of the developing skin, olfactory system, lungs, and kidneys. In addition, JAM-A gene activity was found in the developing liver, choroid plexuses, and gut tubes. Immunofluorescent staining with a JAM-A antibody was performed to confirm that expression of the JAM-A-beta-galactosidase fusion protein accurately represented endogenous JAM-A protein. Thus, JAM-A is prominently expressed in embryonic vasculature and the epithelial components of several organ systems and may have an important role in their development. (c) 2005 Wiley-Liss, Inc.

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Year:  2005        PMID: 15977176     DOI: 10.1002/dvdy.20481

Source DB:  PubMed          Journal:  Dev Dyn        ISSN: 1058-8388            Impact factor:   3.780


  7 in total

1.  JAM-A protects from thrombosis by suppressing integrin αIIbβ3-dependent outside-in signaling in platelets.

Authors:  Meghna U Naik; Timothy J Stalker; Lawrence F Brass; Ulhas P Naik
Journal:  Blood       Date:  2012-01-23       Impact factor: 22.113

2.  The sorting behaviour of olfactory and vomeronasal axons during regeneration.

Authors:  Fatemeh Chehrehasa; James St John; Brian Key
Journal:  J Mol Histol       Date:  2006-03-03       Impact factor: 2.611

3.  Effects of JAM-A deficiency or blocking antibodies on neutrophil migration and lung injury in a murine model of ALI.

Authors:  Sowmya P Lakshmi; Aravind T Reddy; Meghna U Naik; Ulhas P Naik; Raju C Reddy
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2012-08-17       Impact factor: 5.464

Review 4.  Structural determinants of Junctional Adhesion Molecule A (JAM-A) function and mechanisms of intracellular signaling.

Authors:  Eric A Severson; Charles A Parkos
Journal:  Curr Opin Cell Biol       Date:  2009-07-14       Impact factor: 8.382

5.  Junctional adhesion molecule-A suppresses platelet integrin αIIbβ3 signaling by recruiting Csk to the integrin-c-Src complex.

Authors:  Meghna U Naik; Jeffrey L Caplan; Ulhas P Naik
Journal:  Blood       Date:  2013-12-03       Impact factor: 22.113

Review 6.  Junctional Adhesion Molecules: Potential Proteins in Atherosclerosis.

Authors:  Junqi Wang; Xiaoping Chen
Journal:  Front Cardiovasc Med       Date:  2022-07-07

7.  Non-invasive Embryo Assessment: Altered Individual Protein Profile in Spent Culture Media from Embryos Transferred at Day 5.

Authors:  Alexander Freis; Sabine Roesner; Anne Marshall; Julia Rehnitz; Kyra von Horn; Edison Capp; Jens Erik Dietrich; Thomas Strowitzki; Ariane Germeyer
Journal:  Reprod Sci       Date:  2020-11-05       Impact factor: 3.060

  7 in total

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