کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2067691 | 1077905 | 2007 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Growth inhibitory actions of prothrombin on normal hepatocytes: Influence of matrix
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کلمات کلیدی
EGFDCPHCC - HCCbromo-deoxyuridine - برومو دزوویریدینBrdU - بروموداکسی اوریدینepidermal growth factor - عامل رشد اپیدرمیFibronectin - فیبرونکتینCell matrix - ماتریس سلولیWestern blot - وسترن بلاتprothrombin - پروترومبینdes-γ-carboxy prothrombin - پروترومبین دیس-γ-کاربوکسیHepatocellular carcinoma - کارسینوم هپاتوسلولار(کارسینوم سلولهای استخوانی)
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوفیزیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Most hepatomas have a defect in prothrombin carboxylation, and can secrete under-carboxylated prothrombin or des-γ-carboxy-prothrombin (DCP), the function of which is unknown. We considered that the prothrombin-DCP axis might also be involved in growth control. Hepatocytes and hepatoma cells were treated with prothrombin and DNA synthesis and cytoskeletal changes were studied. Prothrombin inhibited DNA synthesis in hepatocytes on fibronectin, but not collagen matrix. Hepatoma cell lines were not inhibited. We found that hepatoma cell matrix conferred resistance to hepatocytes. Prothrombin decreased fibronectin but not collagen amounts, but only in the presence of hepatocytes and not hepatoma cells, indicating that it has a differential action on matrix proteins. It also caused changes in cell shape and actin depolymerization. In vivo, there was a decrease in plasma prothrombin activity after a partial hepatectomy (PH), concomitant with the peak of DNA synthesis in the hepatocytes at 24 h after PH. Injection of warfarin at the time of PH, further inhibited PT activity and enhanced this 24 h peak of DNA synthesis. Furthermore, repeated injection of prothrombin lowered the peak DNA synthesis after PH. The data support the hypothesis that prothrombin can act as a hepatocyte growth inhibitor, likely at the level of fibronectin loss and result in cytoskeletal changes. Hepatomas resist this action, possibly due to their different matrix proteins. This represents a novel mechanism for growth regulation and provides a possible biological significance for the tumor marker DCP.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cell Biology International - Volume 31, Issue 9, September 2007, Pages 929-938
Journal: Cell Biology International - Volume 31, Issue 9, September 2007, Pages 929-938
نویسندگان
Brian I. Carr, Siddhartha Kar, Meifang Wang, Ziqiu Wang,