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Requirement of α4β1 and α5β1 Integrin Expression in Bone-Marrow Derived Progenitor Cells in Preventing Endotoxin-Induced Lung Vascular Injury and Edema in Mice
Kishore K. Wary *, Stephen M Vogel, Sean Garrean, Yidan D. Zhao, Asrar B. Malik
Department of Pharmacology and Center for Lung and Vascular Biology, The University of Illinois, Chicago, IL 60612
The goal of this study was to determine the role of integrin-mediated adhesion of bone marrow derived progenitor cells (BMPCs) as a requirement for the endothelial barrier protection in a lung injury model. C57BL mice were used as the source for BMPCs, which were characterized as CD34+ and Flk1+ as well as expression of a repertoire of integrins. We used a mouse model of bacterial lipopolysaccharide (LPS)-induced lung vascular injury and edema formation to test the effects of BMPC integrin expression in preventing endothelial barrier injury. Adhesion of BMPCs to purified extracellular matrix proteins induced Fak phosphorylation and formation of branching point structures in a 4 and 5 integrin-dependent manner. BMPCs expressing red fluorescent protein (RFP) were administered via the retro-orbital venous route in mice treated intraperitonially (i.p.) with LPS [7.5 mg/kg body weight (BW). We observed increased retention of RFP-labeled Flk1+ and CD34+ BMPCs for up to 8 wk in mice injured with LPS. BMPC transplantation increased survival by 50% (at 72 to 96 hr after LPS) and reduced lung vascular injury and extravascular water content induced by LPS. However, blocking with anti-4 or anti-5 integrin antibody, or shRNA mediated silencing of 4 or 5 integrins in donor BMPCs failed to prevent the vascular injury or edema formation and mortality. Thus, 4 and 5 integrin-dependent adhesion of BMPCs in lung tissue plays a critical role in preventing lung vascular injury and increasing survival in a mouse model of LPS-induced acute lung injury.
Requirement of α4β1 and α5β1 Integrin Expression in Bone-Marrow Derived Progenitor Cells in Preventing Endotoxin-Induced Lung Vascular Injury and Edema in Mice
Kishore K. Wary *, Stephen M Vogel, Sean Garrean, Yidan D. Zhao, Asrar B. Malik
Department of Pharmacology and Center for Lung and Vascular Biology, The University of Illinois, Chicago, IL 60612
The goal of this study was to determine the role of integrin-mediated adhesion of bone marrow derived progenitor cells (BMPCs) as a requirement for the endothelial barrier protection in a lung injury model. C57BL mice were used as the source for BMPCs, which were characterized as CD34+ and Flk1+ as well as expression of a repertoire of integrins. We used a mouse model of bacterial lipopolysaccharide (LPS)-induced lung vascular injury and edema formation to test the effects of BMPC integrin expression in preventing endothelial barrier injury. Adhesion of BMPCs to purified extracellular matrix proteins induced Fak phosphorylation and formation of branching point structures in a 4 and 5 integrin-dependent manner. BMPCs expressing red fluorescent protein (RFP) were administered via the retro-orbital venous route in mice treated intraperitonially (i.p.) with LPS [7.5 mg/kg body weight (BW). We observed increased retention of RFP-labeled Flk1+ and CD34+ BMPCs for up to 8 wk in mice injured with LPS. BMPC transplantation increased survival by 50% (at 72 to 96 hr after LPS) and reduced lung vascular injury and extravascular water content induced by LPS. However, blocking with anti-4 or anti-5 integrin antibody, or shRNA mediated silencing of 4 or 5 integrins in donor BMPCs failed to prevent the vascular injury or edema formation and mortality. Thus, 4 and 5 integrin-dependent adhesion of BMPCs in lung tissue plays a critical role in preventing lung vascular injury and increasing survival in a mouse model of LPS-induced acute lung injury.
