New Findings from Kyushu University in the Area of Tissue Engineering Described (Suppression of Autophagy During Liver Regeneration Impairs Energy Charge and Hepatocyte Senescence in Mice)
By a News Reporter-Staff News Editor at Energy Weekly News -- Current study results on Biomedicine and Biomedical Engineering have been published. According to news originating from Fukuoka, Japan, by VerticalNews correspondents, research stated, "Autophagy is a homeostatic mechanism that regulates protein and organelle turnover and uses the amino acids from degraded proteins to produce adenosine 5'-triphosphate (ATP). We investigated the activity of autophagy-associated pathways in liver regeneration after partial hepatectomy (PHx) in liver-specific autophagy-related gene 5 (Atg5) knockout (KO) mice."
Our news journalists obtained a quote from the research from Kyushu University, "Liver regeneration was severely impaired by 70% PHx, with a reduction in postoperative mitosis, but a compensating increase in hepatocyte size. PHx induced intracellular adenosine triphosphate and beta-oxidation reduction as well as injured cellular mitochondria. Furthermore, PHx in Atg5 KO mice enhanced hepatic accumulation of p62 and ubiquitinated proteins. These results indicated that reorganization of intracellular proteins and organelles during autophagy was impaired in the regenerating liver of these mice. Up-regulation of p21 was associated with hepatocyte senescence, senescence-associated beta-galactosidase expression, irreversible growth arrest, and secretion of senescence-associated molecules, including interleukin (IL)-6 and IL-8."
According to the news editors, the research concluded: "These findings indicate that autophagy plays a critical role in liver regeneration and in the preservation of cellular quality, preventing hepatocytes from becoming fully senescent and hypertrophic."
For more information on this research see: Suppression of Autophagy During Liver Regeneration Impairs Energy Charge and Hepatocyte Senescence in Mice. Hepatology, 2014;60(1):290-300. Hepatology can be contacted at: Wiley-Blackwell, 111 River St, Hoboken 07030-5774, NJ, USA. (Wiley-Blackwell - www.wiley.com/; Hepatology - onlinelibrary.wiley.com/journal/10.1002/(ISSN)1527-3350)
The news correspondents report that additional information may be obtained from T. Toshima, Kyushu University, Div Pathophysiol & Expt Pathol, Dept. of Pathol, Grad Sch Med Sci, Fukuoka 8128582, Japan. Additional authors for this research include K. Shirabe, T. Fukuhara, T. Ikegami, T. Yoshizumi, Y. Soejima, T. Ikeda, S. Okano and Y. Maehara.
Keywords for this news article include: Fukuoka, Japan, Asia, Bioengineering, Biomedical Engineering, Biomedicine, Biomedicine and Biomedical Engineering, Gastroenterology, Hepatocytes, Hepatology, Liver Regeneration
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