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首页> 外文期刊>Cell and Tissue Research >Malformation of stria vascularis in the developing inner ear of the German waltzing guinea pig
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Malformation of stria vascularis in the developing inner ear of the German waltzing guinea pig

机译：德国华尔兹豚鼠发育中的内耳中的血管纹畸形

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摘要

Auditory function and cochlear morphology have previously been described in the postnatal German waltzing guinea pig, a strain with recessive deafness. In the present study, cochlear histopathology was further investigated in the inner ear of the developing German waltzing guinea pig (gw/gw). The lumen of the cochlear duct diminished progressively from embryonic day (E) 35 to E45 and was absent at E50 because of the complete collapse of Reissner’s membrane onto the hearing organ. The embryonic stria vascularis, consisting of a simple epithelium, failed to transform into the complex trilaminar tissue seen in normal animals and displayed signs of degeneration. Subsequent degeneration of the sensory epithelium was observed from E50 and onwards. Defective and insufficient numbers of melanocytes were observed in the developing gw/gw stria vascularis. A gene involved in cochlear melanocyte development, Pax3, was markedly reduced in lateral wall tissue of the cochlea of both E40 and adult gw/gw individuals, whereas its expression was normal in the skin and diaphragm muscle of adult gw/gw animals. The Pax3 gene may thus be involved in the pathological process but is unlikely to be the primary mutated gene in the German waltzing guinea pig. TUNEL assay showed no signs of apoptotic cell death in the developing stria vascularis of this type of guinea pig. Thus, malformation of the stria vascularis appears to be the primary defect in the inner ear of the German waltzing guinea pig. Defective and insufficient numbers of melanocytes might migrate to the developing stria vascularis but fail to provide the proper support for the subsequent development of marginal and basal cells, thereby leading to stria vascularis malformation and dysfunction in the inner ear of the German waltzing guinea pig.
机译：听觉功能和耳蜗形态先前已在出生后的德国华尔兹豚鼠（一种隐性耳聋品系）中进行了描述。在本研究中，进一步对发育中的德国华尔兹豚鼠（gw / gw）的内耳进行了耳蜗组织病理学研究。耳蜗腔从胚胎第35天到E45逐渐减少，在E50时消失，因为Reissner膜完全塌陷到听力器官上。由简单上皮组成的胚胎血管纹未能转化为正常动物中见到的复杂的三层组织，并显示出退化的迹象。从E50开始观察到感觉上皮的随后变性。在发育中的gw / gw血管纹中观察到黑素细胞的缺陷和数量不足。在E40和成年gw / gw个体的耳蜗侧壁组织中，参与耳蜗黑素细胞发育的基因Pax3明显减少，而在成年gw / gw动物的皮肤和and肌中其表达正常。因此Pax3基因可能参与了病理过程，但不太可能成为德国华尔兹豚鼠的主要突变基因。 TUNEL分析显示在这种豚鼠的正在发育的血管纹中没有凋亡细胞死亡的迹象。因此，血管纹状畸形似乎是德国华尔兹豚鼠内耳的主要缺陷。黑色素细胞的缺陷和数量不足可能会迁移到发育中的血管纹，但不能为边缘细胞和基底细胞的后续发育提供适当的支持，从而导致豚毛豚鼠内耳的血管纹畸形和功能障碍。

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