Singh Ashok K, Pancholi Nishit, Patel Jilpa, Litbarg Natalia O, Gudehithlu Krishnamurthy P, Sethupathi Perianna, Kraus Mark, Dunea George, Arruda Jose Al
Department of Medicine, Stroger Hospital of Cook County, 637 South Wood St, Durand Bldg 2nd Floor, Chicago IL 60612, United States.
World J Gastroenterol. 2009 Mar 7;15(9):1057-64. doi: 10.3748/wjg.15.1057.
To investigate the mechanism of liver regeneration induced by fusing the omentum to a small traumatic injury created in the liver. We studied three groups of rats. In one group the rats were omentectomized; in another group the omentum was left in situ and was not activated, and in the third group the omentum was activated by polydextran particles.
We pre-activated the omentum by injecting polydextran particles and then made a small wedge wound in the rat liver to allow the omentum to fuse to the wound. We monitored the regeneration of the liver by determining the ratio of liver weight/body weight, by histological evaluation (including immune staining for cytokeratin-19, an oval cell marker), and by testing for developmental gene activation using reverse transcription polymerase chain reaction (RT-PCR).
There was no liver regeneration in the omentectomized rats, nor was there significant regeneration when the omentum was not activated, even though in this instance the omentum had fused with the liver. In contrast, the liver in the rats with the activated omentum expanded to a size 50% greater than the original, and there was histologically an interlying tissue between the wounded liver and the activated omentum in which bile ducts, containing cytokeratin-19 positive oval cells, extended from the wound edge. In this interlying tissue, oval cells were abundant and appeared to proliferate to form new liver tissue. In rats pre-treated with drugs that inhibited hepatocyte growth, liver proliferation was ongoing, indicating that regeneration of the liver was the result of oval cell expansion.
Activated omentum facilitates liver regeneration following injury by a mechanism that depends largely on oval cell proliferation.
研究将大网膜与肝脏小创伤处融合诱导肝再生的机制。我们研究了三组大鼠。一组大鼠进行了大网膜切除术；另一组大鼠的大网膜保留原位且未被激活，第三组大鼠的大网膜通过聚右旋糖酐颗粒激活。
我们通过注射聚右旋糖酐颗粒预先激活大网膜，然后在大鼠肝脏上制造一个小楔形伤口，使大网膜与伤口融合。我们通过测定肝重/体重比、组织学评估（包括对细胞角蛋白-19进行免疫染色，细胞角蛋白-19是一种卵圆细胞标志物）以及使用逆转录聚合酶链反应（RT-PCR）检测发育基因激活来监测肝脏再生情况。
进行了大网膜切除术的大鼠没有肝再生，当大网膜未被激活时也没有明显的再生，即使在这种情况下大网膜已与肝脏融合。相比之下，大网膜被激活的大鼠肝脏体积扩大到比原来大50%，并且在组织学上，受伤肝脏与被激活的大网膜之间有一层中间组织，其中含有细胞角蛋白-19阳性卵圆细胞的胆管从伤口边缘延伸。在这层中间组织中，卵圆细胞丰富，似乎增殖形成了新的肝组织。在用抑制肝细胞生长的药物预处理的大鼠中，肝脏增殖仍在进行，这表明肝脏再生是卵圆细胞扩张的结果。
激活的大网膜通过一种很大程度上依赖卵圆细胞增殖的机制促进损伤后肝脏的再生。
