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Articles by C. C Chang
Total Records ( 2 ) for C. C Chang
  J. H Liu , C. C Chang , S. M Wang , C. Y Chou , Y. F Yang , Y. L Liu , H. H Lin and C. C. Huang

Peripheral arterial disease (PAD) is associated with significant morbidity and mortality and is an important marker of systemic atherosclerosis. However, little is known about the associated risk factors for PAD in patients on maintenance hemodialysis (HD). We collected the basic data and possible risk factors associated with PAD for 277 patients on maintenance HD. Furthermore, we measured ankle-brachial blood pressure index (ABI) in these patients. PAD was defined as an ABI value less than 0.90. The prevalence of PAD in our HD center was 22.8% (61/268). Advanced age (P = 0.006), longer history of HD (P < 0.001), diabetes (P = 0.002) and presence of PAD symptoms (P < 0.001) were independent predictors of PAD. PAD patients with diabetes had shorter history of HD (P = 0.001). 2-vessel PAD had higher serum cholesterol in HD patients (≥ 200 vs < 200 mg/dL; Odds ratio, 12.12, 95% confidence interval, 2.199-67.79; P < 0.004).

  Y. M Sue , C. P Chung , H Lin , Y Chou , C. Y Jen , H. F Li , C. C Chang and S. H. Juan

We previously showed that an increase in the peroxisome proliferator-activated receptor- (PPAR), together with subsequent induction of inducible nitric oxide synthase (iNOS) by beraprost (BPS), inhibits aortic smooth muscle cell proliferation. Herein, we delineated the mechanisms of the antiproliferative effects of BPS through the induction of p21/p27. BPS concentration dependently induced the p21/p27 promoter- and consensus cAMP-responsive element (CRE)-driven luciferase activities, which were significantly suppressed by blocking PPAR activation. Surprisingly, other than altering the CRE-binding protein (CREB), BPS-mediated PPAR activation increased nuclear localization of the CREB-binding protein (CBP), a coactivator, which was further confirmed by chromatin immunoprecipitation. Furthermore, novel functional PPAR-responsive elements (PPREs) next to CREs in the rat p21/p27 promoter regions were identified, where PPAR interacted with CREB through CBP recruitment. BPS-mediated suppression of restenosis in mice with angioplasty was associated with p21/p27 induction. Herein, we demonstrate for the first time that BPS-mediated PPAR activation enhances transcriptional activation of p21/p27 by increasing CBP nuclear translocation, which contributes to the vasoprotective action of BPS.

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