Sa1689 Microtubule Based Motility of Autophagic and Lysosomal Compartments In Vitro: Vesicles With LC3 on Their Surface Show Greater Motility Than Those That Contain Lamp1

Abstract

Background and aim: Angiotensin 2, an important byproduct of renin angiotensin system can lead to increased extracellular matrix formation and fibrosis via enhanced TGF β-1 production in many organ systems including liver. Angiotensin converting enzyme (ACE) coding gen polymorphisms can lead to different degree of ACE expressions and hence, various angiotensin 2 tissue levels. ACE gen polymorphisms have been reported as ACE I/ D. Especially, ACE gen D homozygotic patients produce more tissue levels of ACE and this may be a potential hazard for many organ systems. We aimed to investigate if there is any role of ACE I/D gen polymorphism in the degree of liver fibrosis due to various etiologies. Methods: We enrolled 411 patients with a histopathological diagnosis of liver fibrosis. There were 240 patients with the diagnosis of mild and moderate fibrosis (Ishak's stage; 1-3) and the rest, 171 patients had advanced liver fibrosis (Ishak's stage; 4-6). Polymerase chain reaction was used to determine the type of ACE I/D gen polymorphisms. We also studied serum ACE levels with enzymatic kinetic testing method on spectrometry. Results: There were 208 male and 203 female subjects with a mean age of 51.1±13.5 years, (range; 1880 years). Within the mild and moderate liver fibrosis group, the etiologies were chronic viral hepatitis B in 131, chronic viral hepatitis C in 59, non-alcoholic steatohepatitis in 46, autoimmune hepatitis in 1 and primary biliary cirrhosis in 3 patients. Within the advanced liver fibrosis group, the etiologies were chronic viral hepatitis B in 71, chronic viral hepatitis C in 61, non-alcoholic steatohepatitis in 24, alcoholic liver disease in 11 and autoimmune hepatitis in 4 patients. On statistical analysis, there was no difference between the two groups with regard to ACE genotypes. Moreover, we could not find any significant difference between the groups regarding serum levels of angiotensin converting enzyme. Conclusion: The ACE I/D gen polymorphism do not seem to contribute as a significant risk factor for advanced liver fibrosis.