N. Harroun1, G. S. De Silva1, J. Kornbluth3, L. A. Sanchez1, M. A. Zayed1,2 1Washington University In St. Louis,Division Of Vascular Surgery,Saint Louis, MO, USA 2Veterans Affairs St. Louis Health Care System,Division Of Vascular Surgery,Saint Louis, MO, USA 3Saint Louis University School Of Medicine,Department Of Pathology,Saint Louis, MO, USA
Introduction:
Atherosclerosis is prevalent in western society. Understanding the processes of atherogenesis remain an area of intense investigation. Fatty acid synthesis and tissue inflammation have been demonstrated to influence atherogenesis and atheroprogression. Fatty Acid Synthase (FAS) is a central enzyme responsible for de novo synthesis of long chain saturated fatty acids. Natural Killer Lytic-Associated Molecule (NKLAM) is an important inflammatory mediator that can alter cellular viability. We hypothesize that FAS and NKLAM are important molecular mediators of disease progression and are therefore differentially expression in variably diseased segments of carotid arterial plaque
Methods:
Using an IRB-approved, prospectively maintained vascular tissue biobank, we analyzed eight carotid endarterectomy plaque samples from patients undergoing carotid endarterectomy (CEA). CEA plaque was partitioned into maximally (Max) and minimally (Min) diseased segments. Protein lysates were obtained for both Max and Min diseased segments and Western blot analysis was used to evaluate FAS and NKLAM protein expression levels. Values are reported as a mean SEM and as ratios of protein expression to a loading control (Caveolin). Wilcoxon paired-match rank test was performed to determine any significant differences, with p < 0.05 considered significant.
Results:
Max diseased carotid segments demonstrated higher FAS expression compared to Min diseased segments (0.230.07 vs 0.05 0.02, respectively; p =0.04). Interestingly, NKLAM expression was visibly lower in Max diseased segments, though this value was not statistically significant.
Conclusion:
We have preliminarily observed significant differential expression of FAS and NKLAM, which are important disease mediators in Max and Min diseased carotid plaque segments. These findings suggest that different plaque regions may be affected by different biological processes that can influence disease progression.
