Division of Molecular Genetics, Institute of Human Genetics, University of Tübingen, Wilhelmstraße, Germany.
Cell Mol Life Sci. 2011 Aug;68(16):2739-49. doi: 10.1007/s00018-010-0586-1. Epub 2010 Nov 15.
Tff3 peptide exerts important functions in cytoprotection and restitution of the gastrointestinal (GI) tract epithelia. Moreover, its presence in the rodent inner ear and involvement in the hearing process was demonstrated recently. However, its role in the auditory system still remains elusive. Our previous results showed a deterioration of hearing with age in Tff3-deficient animals.
Present detailed analysis of auditory brain stem response (ABR) measurements and immunohistochemical study of selected functional proteins indicated a normal function and phenotype of the cochlea in Tff3 mutants. However, a microarray-based screening of tissue derived from the auditory central nervous system revealed an alteration of securin (Pttg1) and serpina3n expression between wild-type and Tff3 knock-out animals. This was confirmed by qRT-PCR, immunostaining and western blots.
We found highly down-regulated Pttg1 and up-regulated serpina3n expression as a consequence of genetically deleting Tff3 in mice, indicating a potential role of these factors during the development of presbyacusis.
Tff3 肽在胃肠道（GI）上皮的细胞保护和修复中发挥重要作用。此外，最近已经证明其存在于啮齿动物内耳中，并参与听力过程。然而，其在听觉系统中的作用仍然难以捉摸。我们之前的结果表明，Tff3 缺陷动物的听力随年龄增长而恶化。
目前对听觉脑干反应（ABR）测量的详细分析和对选定功能蛋白的免疫组织化学研究表明，Tff3 突变体的耳蜗功能和表型正常。然而，基于微阵列的对来自听觉中枢神经系统的组织的筛选显示，在野生型和 Tff3 敲除动物之间 securin（Pttg1）和 serpina3n 的表达发生改变。这通过 qRT-PCR、免疫染色和 Western blot 得到了证实。
我们发现由于在小鼠中基因删除 Tff3，Pttg1 的表达高度下调，而 serpina3n 的表达上调，表明这些因素在老年聋的发展过程中可能具有潜在作用。
