A protein deficiency is associated with liver regeneration
May 11, 2016 Source: China Biotechnology Network
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];Scientists at the Children's Medical Center Research Institute (CRI) at the University of Texas Southwestern Medical Center recently discovered that shutting down a particular protein-coding gene can boost mammalian liver regeneration.
Dr. HaoZhu, assistant professor of CRI, said: "This study provides guidance for new treatments for liver damage and chronic liver disease." The findings were published this week in the journal CellStemCell.
The lizards' tails and starfish tentacles have amazing regenerative capabilities, but mammals partially lose the ability to regenerate body tissues. The liver is a human solid organ with regenerative capacity. A healthy liver can regenerate 70% of tissue after damage.
However, when the liver suffers from repetitive damage (chemical poisoning or chronic disease), it loses its ability to regenerate. If you suffer multiple injuries, cirrhosis and scar tissue will appear, which will greatly increase the risk of liver cancer. Professor Zhu's laboratory has studied two kinds of regeneration, one is the cell to repair the proliferation of organs, and the other is the proliferation of cells that are out of control when cancer occurs.
According to the National Cancer Institute (NCI), liver cancer mortality was the highest among all common cancers between 2003 and 2012. In addition to cirrhosis, risk factors for liver cancer include hepatitis C virus (HCV), liver damage caused by alcohol, chronic liver disease, or a small number of genetic disorders.
Professor Zhu studied mice lacking the Arid1a gene, which is associated with some human cancers. Zhu said: "Arid1a gene will produce mutations in some cancers, including liver cancer, pancreatic cancer, breast cancer, lung cancer, etc. Not all cancers will be mutated. There are about 10% to 20% of cancers. This genetic mutation occurs, which causes the gene to be shut down."
Based on this connection, the researchers hypothesized that mice lacking the Arid1a gene would develop liver damage and eventually lead to liver cancer. What surprised them was that there was no liver damage. In fact, the livers of these mice regenerate faster and function better.
Professor Zhu said: "These livers can resist liver damage and recover better. This result provides us with a new way of thinking. Through this research we have discovered the new function of this gene."
By observation, the liver of mice without the Arid1a gene is healthier. Blood tests have shown that their liver function is also better. When the researchers deleted the Arid1a gene from mice that suffered from liver damage, they found that the liver tissue of the mice recovered faster and the degree of fibrosis of the liver against chemical damage was also reduced. In addition, other tissues (such as injured skin) are also recovering better.
There are currently no drugs that can mimic the absence of this protein, and researchers are using the Texas Cancer Prevention and Research Institute (CPRIT) to develop the drug.
Professor Zhu said: "We need to identify small molecules that can mimic the function of this gene. The ideal drug should be able to prevent cancer while repairing the liver. This is good news for patients. This gene and the protein it expresses. The lack of can accelerate the regeneration of damaged liver tissue, the principle is to reorganize the gene arrangement, so the cells can more easily and repeatedly switch to a more regenerative state. This study is an organ without risk of cancer. Tissue regeneration offers new ideas, but a lot of testing is needed to determine how all types of liver cancer risk are being altered.
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