Over-expression of integrin β3 can partially overcome the defect of integrin β3 signaling in transglutaminase 2 null macrophages |
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Authors: | Be ta T th, Zsolt Sarang, Gy rgy Vereb, Ailiang Zhang, Sakae Tanaka, Gerry Melino, L szl F sü s,Zsuzsa Szondy |
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Affiliation: | Beáta Tóth, Zsolt Sarang, György Vereb, Ailiang Zhang, Sakae Tanaka, Gerry Melino, László Fésüs,Zsuzsa Szondy, |
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Abstract: | Transglutaminase 2 (TG2) is a protein crosslinking enzyme with many additional biological functions. We have previously shown that in TG2−/− mice the in vivo clearance of apoptotic cells is defective leading to autoimmunity. TG2 contributes to the formation of phagocytic portals by binding to both integrin β3, a known phagocytic receptor, and its bridging molecule, MFG-E8. In TG2 null macrophages integrin β3 cannot accumulate around the apoptotic cells and its signaling is impaired. In the present study we describe a subline of TG2 null mice, in which a compensatory increase in integrin β3 expression, which resulted alone in a high receptor concentration around the apoptotic cells without the requirement for accumulation, partially corrected the defect in integrin β3 signaling. Our data provide a proof for the concept that the function of TG2 is to stabilize accumulated integrin β3 concentration in the phagocytic cup. |
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Keywords: | Macrophages Apoptotic cells Transglutaminase 2 Integrin signaling |
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