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Elevated mitochondrial gene expression during rat liver regeneration after portal vein ligation

โœ Scribed by Yasuhiro Shimizu; Dr Hiroshi Suzuki; Yuji Nimura; Shigemi Onoue; Masato Nagino; Masashi Tanaka; Takayuki Ozawa


Publisher
John Wiley and Sons
Year
1995
Tongue
English
Weight
859 KB
Volume
22
Category
Article
ISSN
0270-9139

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โœฆ Synopsis


We explored the molecular basis of mitochondrial energy production during rat liver regeneration after portal vein ligation. Ligation of the left branch of the portal vein induces an increase in the weight of the nonligated lobe, counterbalancing the reduced weight of the ligated lobe. Using this model, we investigated changes in mitochondrial DNA-binding proteins, mitochondrial DNA, and mitochondrial messenger RNA (mRNA) in rat hepatocytes of the nonligated lobes. The amount of mitochondrial DNA-binding protein increased maximally (200% to 300% of the preoperative level) at 12 hours after the operation, before an increase (390%) in mitochondrial DNA content at 24 hours, and parallel to an increase (24w0) in mitochondrial mRNA levels at 12 hours. These results suggest that the energy supply for liver regeneration is achieved through enhancement of mitochondrial DNA replication as well as transcription, in which the mitochondrial DNA-binding proteins probably play regulatory roles. We also found that in the nonligated lobes, mR.NA levels of hepatocyte growth factor increased to a detectable level only 12 hours after the operation. These molecular biochemical data help explain why preoperative portal vein embolization, which is a modification of portal vein branch ligation, is an effective method to prevent posthepatectomy liver failure. (HEPATOLOGY Recently, extensive liver resection has been performed to treat carcinomas of the hepatic hilus, intrahepatic cholangiocarcinoma, and advanced carcinoma of the gallbladder, which often involve the hepatic hi-1995; 221222-1229.


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Expression of multidrug resistance genes
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We analyzed expression of multidrug resistance (mdr) genes in rat liver during regeneration after partial hepatectomy or carbon tetrachloride-induced necrosis. In situ hybridization revealed that in the normal liver the cellular distribution of mdr transcripts and protein is restricted to hepatocyte