IF: 14.9
Promotion effect of TGF-β-Zfp423-ApoD pathway on lip sensory recovery after nerve sacrifice caused by nerve collateral compensation
文獻(xiàn)使用產(chǎn)品：大鼠載脂蛋白D(apo-D)elisa試劑盒
供應(yīng)商：遠(yuǎn)慕生物
摘要：Resection of oral ａnd maxillofacial tumors is often accompanied by the inferior alveolar nerve neurectomy, resulting in abnormal sensation in lower lip. It is generally believed that spontaneous sensory recovery in this nerve injury is difficult. However, during our follow-up, patients with inferior alveolar nerve sacrifice showed different degrees of lower lip sensory recovery. In this study, a prospective cohort study was conducted to demonstrate this phenomenon ａnd analyze the factors influencing sensory recovery. A mental nerve transection model of Thy1-YFP mice ａnd tissue clearing technique were used to explore possible mechanisms in this process. Gene silencing ａnd overexpression experiments were then conducted to detect the changes in cell morphology ａnd molecular markers. In our follow-up, 75% of patients with unilateral inferior alveolar nerve neurectomy had complete sensory recovery of the lower lip 12 months poseratively. Patients with younger age, malignant tumors, ａnd preservation of ipsilateral buccal ａnd lingual nerves had a shorter recovery time. The buccal nerve collateral sprouting compensation was observed in the lower lip tissue of Thy1-YFP mice. ApoD was demonstrated to be involved in axon growth ａnd peripheral nerve sensory recovery in the animal model. TGF-β inhibited the expression of STAT3 ａnd the transcription of ApoD in Schwann cells through Zfp423. Overall, after sacrificing the inferior alveolar nerve, the collateral compensation of the ipsilateral buccal nerve could innervate the sensation. And this process was regulated by TGF-β-Zfp423-ApoD pathway.
原創(chuàng)作者：上海遠(yuǎn)慕生物科技有限公司
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