Other Publications (1)
Articles by Ming H. Lye in JoVE
Органотипической культуры взрослых сетчатки кролика Ming H. Lye1, Tatjana C. Jakobs1, Richard H. Masland1, Amane Koizumi1 1Havard Medical School, MGH - Massachusetts General Hospital В этой статье показано вскрытие и инкубации сетчатки кролика и частица-опосредованного переноса генов плазмид кодирования GFP или различных субклеточных маркеров в ганглиозных клеток сетчатки.
Other articles by Ming H. Lye on PubMed
Eosinophils Adhere to Vascular Cell Adhesion Molecule-1 Via Podosomes American Journal of Respiratory Cell and Molecular Biology. Oct, 2004 | Pubmed ID: 15220135 Vascular cell adhesion molecule (VCAM)-1 supports specific eosinophil adhesion via alpha4beta1 integrin. We tested the hypothesis that adhesive contacts formed by eosinophils on VCAM-1 are different from focal adhesions formed by adherent fibroblasts. Eosinophils adherent on VCAM-1 formed punctate adhesions that fit the criteria for podosomes, highly dynamic structures found in adherent transformed fibroblasts, osteoclasts, and macrophages. The structures contained beta1 integrin subunit, phosphotyrosine-containing proteins, punctate filamentous actin, and gelsolin, a podosome marker. In contrast, nontransformed fibroblasts on VCAM-1 formed peripheral focal adhesions that were positive for alpha4, beta1, phosphotyrosine, vinculin, talin, and paxillin; negative for gelsolin; and associated with microfilaments. Phorbol myristate acetate or tumor necrosis factor-alpha and interleukin-5 stimulated podosome formation in adherent eosinophils. Because podosomes in tumor cells are associated with extracellular matrix degradation, we analyzed the VCAM-1 layer. VCAM-1 was lost under adherent eosinophils but not under adherent fibroblasts. This loss was inhibited by the metalloproteinase inhibitor ortho-phenanthroline and correlated with expression and podosome localization of a membrane-tethered metalloproteinase, a disintegrin and metalloproteinase domain 8. Podosome-mediated VCAM-1 clearance may be a mechanism to regulate eosinophil arrest and extravasation in allergic conditions such as asthma.