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Inhibition of protein kinase C beta II attenuates local hyperglycemia‐induced leukocyte‐endothelial interactions
Author(s) -
Chen Qian,
Iames Edward,
Torino Daniel,
Perkins KerryAnne,
Rueter Brian,
Prince Catherine,
Young Lindon Howard
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.590.12
Subject(s) - intraperitoneal injection , intravital microscopy , protein kinase c , endocrinology , medicine , in vivo , venule , diabetes mellitus , oxidative stress , beta (programming language) , chemistry , inflammation , pharmacology , kinase , endothelium , biology , microcirculation , biochemistry , microbiology and biotechnology , computer science , programming language
Hyperglycemia is causally related to the vascular complications of diabetes. This patho‐physiological process may be mediated by the activation of protein kinase C (PKC) beta II resulting in an increased oxidative stress and inflammatory response. However, the role of a PKC beta II inhibitor regulating hyperglycemia‐induced endothelial‐leukocyte interactions has not been evaluated in vivo in real‐time. The effect of PKC beta II peptide inhibitor on leukocyte‐endothelial interactions in rat mesenteric postcapillary venule circulation was determined by using intravital microscopy. We found that intraperitoneal injection of 25 mM D‐glucose (2.5 ml, n=6) caused intraperitoneal hyperglycemia and exhibited significantly higher leukocyte rolling, adherence, and transmigration compared to control rats which were intraperitoneal injection of saline (2.5 ml, n=4, P<0.05). By contrast, intraperitoneal injection of D‐glucose with 10 mM PKC beta II inhibitor (12.5 μl, n=3/25.0 μl, n=6) induced the similar intraperitoneal hyperglycemia, but showed significantly less leukocyte‐endothelial interactions compared to D‐glucose injection (P<0.05). In summary, the PKC beta II inhibitor attenuates local hyperglycemia‐induced leukocyte‐endothelial interactions, which may be related to the attenuation of oxidative stress in blood. This study was supported by Center for Chronic Disorders of Aging at PCOM.