All-trans-Retinoic Acid Induces Integrin-Independent B-Cell Adhesion to ADAM Disintegrin Domains

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• 作者：Lance C. Bridges ; Joshuah D. Lingo ; Rachel A. Grandon ; Melissa D. Kelley
• 刊名：Biochemistry
• 出版年：2008
• 出版时间：April 15, 2008
• 年：2008
• 卷：47
• 期：15
• 页码：4544 - 4551
• 全文大小：541K
• 年卷期：v.47,no.15(April 15, 2008)
• ISSN：1520-4995

文摘

Cell adhesion is an integral aspect of immunity facilitating extravasation of immune cells during homing and activation. All-trans-Retinoic acid (t-RA) regulates leukocyte differentiation, proliferation, and transmigration. However, the role of t-RA in immune cell adhesion is poorly defined. In this study, we evaluated the impact of t-RA and its metabolism on B and T cell adhesion. Specifically, we address the impact of t-RA on the adhesive properties of the human mature B and T cell lines RPMI 8866, Daudi and Jurkats. The effect of t-RA exposure on cell adhesion to vascular cell adhesion molecule-1 (VCAM-1), a well-established integrin counter receptor involved in immunity, and to nonconventional ADAM integrin ligands was assessed. We show for the first time that t-RA potently induces B cell adhesion in an integrin-independent manner to both VCAM-1 and select ADAM disintegrin domains. Using retinoid extraction and reverse-phase HPLC analysis, we identify the retinoid that is functionally responsible for this augmented adhesion. We also provide evidence that this novel t-RA adhesive response is not prototypical of lymphocytes since both Daudi and Jurkats do not alter their adhesive properties upon t-RA treatment. Further, the t-RA metabolic profiles between these lineages is distinct with 9-cis-retinoic acid being exclusively detected in Jurkat media. This study is the first to demonstrate that t-RA directly induces B cell adhesion in an integrin-independent manner and is not contingent upon t-RA metabolism.