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Pei-Ling Chiu, A., Wang, F.L., Lal, N., Wang, Y., Zhang, D.H., Hussein, B., Wan, A. Vlodavsky, I. and Rodrigues, B. (2014) Endothelial Cells Respond to Hyperglycemia by Increasing the LPL Transporter GPIHBP1. American Journal of Physiology—Endocrinology and Metabolism, 306, E1274-E1283. http://dx.doi.org/10.1152/ajpendo.00007.2014

has been cited by the following article:

• TITLE: Hyperglycemia Induced Changes in Vascular AKT3 May Inhibit Pressure-Induced Apoptosis in the Rat Inferior Venae Cavae

  AUTHORS: Kevin M. Rice, Ravi Kumar Arvapalli, Eric R. Blough

  KEYWORDS: Diabetes, Zucker Rat, Inferior Venae Cavae, AKT3

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.5 No.4, April 23, 2015

  ABSTRACT: Background: Vein graft failure after bypass surgery is greatly increase in patients with diabetes mellitus. The cellular mechanisms underlying the cause of this failure are largely unexplored. Protein kinase B/AKT is a mechanically sensitive regulator of cellular growth and apoptosis. Herein we examine whether diabetes affects the regulation of AKT in response to increased venous loading. Methods: Inferior venae cavae (IVC) from the non-diabetic lean (LNZ) and the diabetic obesesyndrome X Zucker(OSXZ) rats were isolated and incubated ex vivo under basal or pressurized conditions (120 mmHg). Protein expression, basal activation and the ability of increased pressure to activate AKT3 and apoptosis-related signaling were evaluated by immunoblot analysis. Results: Compared to that seen in the non-diabetic lean animals, increased venous pressure in the OSXZ rats was not characterized by increases in APAF-1 concentration, XIAP proteolysis, AIF cleavage, or Bad phosphorylation. This evidence of decreased apoptotic signaling was associated with increased basal p-AKT3 levels (+136% ± 13% P