The Kölliker's organ is a transient epithelial structure during cochlea development that gradually degenerates and disappears at postnatal 12-14 days (P12-14). While apoptosis has been shown to play an essential role in the degeneration of the Kölliker's organ, the role of another programmed cell death, autophagy, remains unclear. In our study, autophagy markers including microtubule associated protein light chain 3-II (LC3-II), sequestosome 1 (SQSTM1/p62) and Beclin1 were detected in the supporting cells of the Kölliker's organ through immunohistochemistry staining. In addition, Western blot and real-time PCR revealed a gradually decreased expression of LC3-II and an increased expression of p62 during early postnatal development. Compared to apoptosis markers that peaks between P7 and P10, autophagy flux peaked earlier at P1 and decreased from P1 to P14. By transmission electron microscopy, we observed representative autophagosome and autolysosome that packaged various organelles in the supporting cells of the Kölliker's organ. During the degeneration, these organelles were digested via autophagy well ahead of the cellular apoptosis. These results suggest that autophagy plays an important role in transition and degeneration of the Kölliker's organ prior to apoptosis during the early postnatal development.

中文翻译：

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自噬在老鼠耳蜗发育中柯氏角器官退化过程中先于细胞凋亡。

Kölliker器官是耳蜗发育过程中的瞬时上皮结构，在出生后12-14天逐渐退化并消失（P12-14）。虽然已经显示出凋亡在柯立克氏器官的退化中起着至关重要的作用，但尚不清楚另一个程序性细胞死亡的作用，即自噬。在我们的研究中，通过免疫组织化学染色在柯氏器官的支持细胞中检测到自噬标记物，包括微管相关蛋白轻链3-II（LC3-II），螯合体1（SQSTM1 / p62）和Beclin1。此外，Western印迹和实时PCR显示，在出生后早期，LC3-II的表达逐渐降低，而p62的表达增加。与峰值在P7和P10之间的凋亡标记相比，自噬通量最早在P1达到峰值，然后从P1降至P14。通过透射电子显微镜，我们观察到了代表性的自噬体和溶酶体，它们将各种细胞器包装在科勒克氏器官的支持细胞中。在变性期间，这些细胞器在细胞凋亡之前通过自噬被消化。这些结果表明自噬在出生后早期的细胞凋亡之前在柯立克氏器官的转变和变性中起重要作用。