Diabetes alters vascular mechanotransduction data: Pressure-induced regulation of Nf-kapa-B p65 and translational associated signaling in the rat inferior vena cava.

Diabetic patients have a high rate of vein graft failure due to attrition or vessel occlusion that cause recurrent ischemic events or vein graft. Veins grafted into a high-pressure arterial environment must undergo vascular remodeling to better handle the altered hemodynamics and intravascular increased pressure. Multiple cellular and molecular events are purported to be associated with vascular remodeling of veins. Understanding the effect diabetes has on vascular mechano-transductive response is critical to decreasing graft failure rates. This article represents data regarding a study published in Cardiovascular Diabetology [1] and Open Journal of Endocrine and Metabolic Diseases [2] with the purpose of evaluating the effect of pressurization on rat inferior venae cavae (IVC). Here we provide the information about the method and processing of raw data related to our prior publish work and Data in Brief articles [3], [4]. The data contained in this article evaluates the contribution of NF-kB signaling and associated proteins. IVC from lean and obese animals were exposed to a 30 min of perfusion at 120 mm Hg pressure and evaluated for changes in expression and (IkB-alpha, NF-kB p50, NF-kB p105, NF-kB p65, Traf2, caspase 12), phosphorylation of (IkB-alpha (ser 32), Fox01 (ser 256), and Fox04 (ser 193)) proteins thought to be involved in the regulation of vascular mechanotransduction.