Nadal C
Institut Curie, Orsay, France.
Cell Tissue Kinet. 1987 May;20(3):331-41. doi: 10.1111/j.1365-2184.1987.tb01315.x.
The activity of a glycopeptide prepared from rat serum by treatment with trypsin and ultrafiltration was investigated in several in vivo proliferation systems. In baby rat hepatocytes synchronized by a subcutaneous injection of casein solution it caused a G1-S block, stopping cells at the end of the G1 phase and sending them back to the G0 phase. The glycopeptide also caused a G1-S block in young adult rats during the first semi-synchronized wave of proliferation that followed partial hepatectomy. Inhibition of hepatocyte proliferation by the glycopeptide was suppressed by blood proteins from normal rats but not from acute phase rats. Alpha 1-acid glycoprotein, an acute phase protein, increased this inhibition and reversed the antagonistic effect of normal blood proteins. In normal baby rats a G1-S block of non-synchronously proliferating hepatocytes was produced in two situations in which the antagonistic effect of normal blood proteins was eliminated: after treatment of the glycopeptide with leucine-aminopeptidase, and after mixing it with alpha 1-acid glycoprotein. The glycopeptide did not inhibit cell proliferation in kidney, submaxillary gland, or tongue epithelium. It seems to be the active component of a system that inhibits the proliferation of hepatocytes, probably by reducing their sensitivity to various mitogenic stimuli.
通过用胰蛋白酶处理和超滤从大鼠血清中制备的一种糖肽的活性，在几种体内增殖系统中进行了研究。在通过皮下注射酪蛋白溶液同步化的新生大鼠肝细胞中，它导致了G1-S阻滞，使细胞在G1期结束时停止，并将它们送回G0期。在部分肝切除术后随后的第一个半同步增殖波期间，该糖肽在年轻成年大鼠中也引起了G1-S阻滞。该糖肽对肝细胞增殖的抑制作用被正常大鼠的血液蛋白所抑制，但急性期大鼠的血液蛋白则不能。急性期蛋白α1-酸性糖蛋白增强了这种抑制作用，并逆转了正常血液蛋白的拮抗作用。在正常新生大鼠中，在两种消除了正常血液蛋白拮抗作用的情况下，非同步增殖的肝细胞出现了G1-S阻滞：在用亮氨酸氨肽酶处理糖肽后，以及将其与α1-酸性糖蛋白混合后。该糖肽不抑制肾脏、颌下腺或舌上皮细胞的增殖。它似乎是一个抑制肝细胞增殖系统的活性成分，可能是通过降低肝细胞对各种促有丝分裂刺激的敏感性来实现的。
