Diabetes patients have poor healing ability after fracture? Scientists find important causes and treatments
January 17, 2017 Source: Bio Valley
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)];According to a recent study by Stanford University School of Medicine, a protein that stimulates bone cell activity can restore a fractured diabetic mouse better. The researchers observed a decrease in bone stem cell activity in diabetic mouse models and bone tissue samples from diabetic patients, and this protein was able to counteract the decline in stem cell activity. They hope that this discovery will facilitate the development of new methods to help diabetics recover better from fractures.
The relevant research results were published in the international academic journal Science Translational Medicine.
Hundreds of millions of people around the world are suffering from diabetes, and this number is increasing year by year. In addition to the risk of postprandial blood glucose fluctuations, diabetes can cause many other symptoms, including soft tissue damage and fracture healing. The precise molecular mechanisms involved are not fully understood.
In a previous study, researchers have found a group of bone cells in the bone tissue of mice that form all the components of the skeletal system. By removing these adult stem cells, the ability of the mouse to heal after fracture is severely damaged.
In this study, the researchers used a mouse model of type 2 diabetes, which began to develop symptoms of diabetes at about 4 weeks of age, but before the onset of diabetes, the efficiency of fracture healing in mice was essentially absent from wild-type mice. difference. In contrast, the bone density of mice after diabetes was significantly lower than that of the control group, and the healing ability was significantly worse after bone injury. The researchers compared the number of bone stem cells after seven days of fracture and found the bone cells of diabetic mice. The number was significantly less than that of the control mice.
The researchers ruled out a systematic cause of a decrease in the number of stem cells through a series of experiments and confirmed that the stem cells themselves have normal functions. Subsequently, they analyzed the microenvironment of stem cells and found that the level of signaling proteins called hedgehog in diabetic mice is significantly lower. This family of proteins plays important roles in many biological processes, including embryonic development and tissue regeneration.
The researchers hypothesized that blocking the hedgehog signaling pathway could also damage the bone healing ability of non-diabetic mice, and the experimental results also confirmed this hypothesis, and the addition of hedgehog signaling protein to the localized fracture of diabetic mice can restore mice. The ability to heal bone.
Finally, the researchers examined the expression of some important proteins in the hedgehog signaling pathway in bone tissue samples from diabetic patients and non-diabetic patients. It was found that the analysis results of human tissues were in full compliance with the phenomena observed in the mouse model.
These results suggest that direct targeting of some molecules in the hedgehog signaling pathway of bone cells may contribute to healing after bone injury, but more research is needed before conversion to clinical applications.
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