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Articles by C Wong
Total Records ( 2 ) for C Wong
  M. P Kuligowski , R. Y. Q Kwan , C Lo , C Wong , W. G James , D Bourges , J. D Ooi , L. D Abeynaike , P Hall , A. R Kitching and M. J. Hickey

Patients with antineutrophil cytoplasmic antibodies (ANCAs) frequently develop severe vasculitis and glomerulonephritis. Although ANCAs, particularly antimyeloperoxidase (anti-MPO), have been shown to promote leukocyte adhesion in postcapillary venules, their ability to promote adhesion in the glomerular vasculature is less clear. We used intravital microscopy to examine glomerular leukocyte adhesion induced by anti-MPO. In mice pretreated with LPS, 50 µg anti-MPO induced LFA-1–dependent adhesion in glomeruli. In concert with this finding, in mice pretreated with LPS, more than 80% of circulating neutrophils bound anti-MPO within 5 minutes of intravenous administration. However, even in the absence of LPS, more than 40% of circulating neutrophils bound anti-MPO in vivo, a response not seen in MPO–/– mice. In addition, a higher dose of anti-MPO (200 µg) induced robust glomerular leukocyte adhesion in the absence of LPS. The latter response was β2-integrin independent, instead requiring the 4-integrin, which was up-regulated on neutrophils in response to anti-MPO. These data indicate that anti-MPO antibodies bind to circulating neutrophils, and can induce glomerular leukocyte adhesion via multiple pathways. Lower doses induce adhesion only after an infection-related stimulus, whereas higher doses are capable of inducing responses in the absence of an additional inflammatory stimulus, via alternative adhesion mechanisms.

  V Chesnokova , C Wong , S Zonis , A Gruszka , K Wawrowsky , S. G Ren , A BenShlomo and R. Yu

Pituitary tumor transforming gene (PTTG) encodes a securin protein critical in regulating chromosome separation. PTTG-null (PTTG–/–) mice exhibit pancreatic β-cell hypoplasia and insulinopenic diabetes. We tested whether PTTG deletion causes β-cell senescence, resulting in diminished β-cell mass. We examined β-cell mass, proliferation, apoptosis, neogenesis, cell size, and senescence in PTTG–/– and WT mice from embryo to young adulthood before diabetes is evident. The roles of cyclin-dependent kinase inhibitors and DNA damage in the pathogenesis of diabetes in PTTG–/– mice were also addressed. Relative β-cell mass in PTTG–/– mice began to decrease at 2–3 wk, whereas β-cell proliferation rate was initially normal but decreased in PTTG–/– mice beginning at 2 months. Apoptosis was also much more evident in PTTG–/– mice. At 1 month, β-cell neogenesis was robust in wild-type mice but was absent in PTTG–/– mice. In addition, the size of β-cells became larger and macronuclei were prominent in PTTG–/– animals. Senescence-associated β-galactosidase was also active in PTTG–/– β-cells at 1 month. Cyclin-dependent kinase inhibitor p21 was progressively up-regulated in PTTG–/– islets, and p21 deletion partially rescued PTTG–/– mice from development of diabetes. mRNA array showed that DNA damage-associated genes were activated in PTTG–/– islets. We conclude that β-cell apoptosis and senescence contribute to the diminished β-cell mass in PTTG–/– mice, likely secondary to DNA damage. Our results also suggest that ductal progenitor β-cells are exhausted by excessive neogenesis induced by apoptosis in PTTG–/– mice.

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