Endothelial biomarker soluble CD146 suggests that angiogenesis plays an important role in progression of fibrosis in liver disease

نویسندگان

  • Efrossini Nomikou
  • Alexandra Alexopoulou
  • Larisa Vasilieva
  • Spyridon P. Dourakis
چکیده

CD146, an element of the endothelial junctionhas been evaluated in several pathological conditions with altered endothelial function but never before in patients with liver disease. As angiogenesis and inflammation were implicated in the development of liver fibrosis, we have explored this suggestion by evaluating levels of sCD146 in a group of patients with chronic liver diseases (CLD) and in cirrhotic patients. The results indicated that there is a clear connection between sCD146 levels and the progression of liver disease. They can differentiate noncirrhotic patients with CLD from cirrhotics, supporting the usefulness of CD146 in the noninvasive diagnosis of liver cirrhosis. Furthermore, our findings provided evidence of sCD146 upregulation in decompensated compared to compensated cirrhosis and sCD146 values were clearly associated with Model for End Stage Liver Disease (MELD) score. Thus, by using an easy to perform ELISA method, we demonstrated that sCD146 can accurately distinguish advanced fibrosis and prognosticate decompensation in cirrhosis.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

CD146 is a coreceptor for VEGFR-2 in tumor angiogenesis.

CD146 is a novel endothelial biomarker and plays an essential role in angiogenesis; however, its role in the molecular mechanism underlying angiogenesis remains poorly understood. In the present study, we show that CD146 interacts directly with VEGFR-2 on endothelial cells and at the molecular level and identify the structural basis of CD146 binding to VEGFR-2. In addition, we show that CD146 i...

متن کامل

VASCULAR BIOLOGY CD146 is a coreceptor for VEGFR-2 in tumor angiogenesis

CD146 is a novel endothelial biomarker and plays an essential role in angiogenesis; however, its role in the molecular mechanism underlying angiogenesis remains poorly understood. In the present study, we show that CD146 interacts directly with VEGFR-2 on endothelial cells and at the molecular level and identify the structural basis of CD146 binding to VEGFR-2. In addition, we show that CD146 i...

متن کامل

Soluble CD146 displays angiogenic properties and promotes neovascularization in experimental hind-limb ischemia.

CD146, an endothelial molecule involved in permeability and monocyte transmigration, has recently been reported to promote vessel growth. As CD146 is also detectable as a soluble form (sCD146), we hypothesized that sCD146 could stimulate angiogenesis. Experiments of Matrigel plugs in vivo showed that sCD146 displayed chemotactic activity on endogenous endothelial cells, and exogenously injected...

متن کامل

A Review of The Role of The Microbiome on Immune Responses and Its Association With Cystic Fibrosis

In recent years, the microbiome has been recognized as a key regulator of immune responses. Evidence suggests that changes in the microbiome can lead to chronic disease and even exacerbation of the disease. Impairment of innate immunity resulting from microbial incompatibility may worsen host susceptibility to infection and exacerbate chronic lung diseases. Specific microbes play a key role in ...

متن کامل

Neovascularization and oxidative stress in the progression of non-alcoholic steatohepatitis.

Reactive oxygen species (ROS) is known to play an important role in the pathogenesis of non-alcoholic steatohepatitis (NASH); however, as we previously reported, angiogenesis also plays a pivotal role in NASH progression - the development of liver fibrosis and hepatocellular carcinoma - in rats. The aim of the current study was to elucidate the role of angiogenesis in the development of fibrosi...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2015