2016年7月12日星期二

New findings on WNT10B gene mutations help to achieve precise treatment of congenital oligodontia

Wenzhou Medical College in China recently announced that the Genome Institute of Medicine school of this school united with Peking University School of Stomatology, Zhengzhou University School of Stomatology, Beijing Anzhen Hospital, Chinese Academy of Sciences Beijing Institute of Life Sciences, American National Institutes of Maxillofacial and Oral to first discovered that WNT10B gene mutations can lead to congenital or hereditary oligodontia. The study was recently published online in the journal Human Genetics, which is a sub-Journal of the American journal Cell. The journal also published some other studies about recombinant human proteins.

The morbidity of congenital hypodontia is 1.6% -9.6%. Oligodontia means hypodontia of six or more teeth, and it is the more serious disorders of tooth agenesis. It may be associated with abnormal development of other ectodermal body tissues, which seriously affects masticatory function and maxillofacial development in patients. It is one of the most difficult clinical oral diseases.

Currently, research on the pathogenic mechanism of oligodontia is still incomplete. The research team used technologies including the technology of recombinant protein and exome sequencing technology - namely detection of the relevant part of the whole genome encodes proteins - to conduct molecular genetic analysis on more than 150 cases of patients with oligodontia. They found that about 5% of patients showed WNT10B gene mutations, which is related to oligodontia especially lateral incisors and premolars missing, including patients with autosomal dominant inheritance and sporadic oligodontia. On this basis, the researchers explained the possible mechanisms of Wnt/beta-catenin signaling pathway the WNT10B genes involve in tooth development and oligodontia. The study found that the mutations which impact WNT10B gene function damaged the regulative ability of Wnt / beta-catenin signaling pathway to downstream TCF transcription factors, significantly reducing the ability of Wnt pathway inducing teeth embryonic stem cells to differentiate into vascular endothelial cells.

It is reported that the research results expand the gene mutation spectrum of human congenital oligodontia, providing a new basis for clinical diagnosis of congenital oligodontia, improving the pathogenesis of the disease and ultimately achieving precise treatment. Flarebio also offers recombinant CDH4 of good quality.

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