Chultemsuren Mungunchimeg, Lee Su-Youn, Jee Mi Jin, Park Kwon Moo, Han Ki-Hwan
Department of Anatomy, Ewha Womans University College of Medicine, Room 503, 5th Floor, 25, Magokdong-ro 2-gil, Gangseo-gu, Seoul 07804, Republic of Korea.
Nanoimaging Lab, Ewha Womans University College of Medicine, Room B234, Basement 2nd Floor, 25, Magokdong-ro 2-gil, Gangseo-gu, Seoul 07804, Republic of Korea.
Microsc Microanal. 2025 May 9;31(3). doi: 10.1093/mam/ozaf042.
Primary cilia on renal tubular cells are critical for kidney function. This study investigated how acute kidney injury affects cilia length, specifically focusing on their shortening during ischemia-reperfusion injury. Using Sprague-Dawley rats, renal pedicles were clamped for 30 min followed by six hours of reperfusion. Kidney tissues were analyzed using confocal laser scanning microscopy and scanning electron microscopy. Acetylated α-tubulin and specific markers such as aquaporin 1 and H + -ATPase were used to identify proximal tubules and collecting ducts. Under normal conditions, renal tubular cells exhibited long primary cilia. Following injury, significant shortening of primary cilia was observed in both proximal tubules and collecting ducts. Intermingled microvilli in proximal tubules complicated ultrastructural observation. However, the collecting duct exhibited distinct responses. While intercalated cells detached into the lumen, principal cells remained attached to the basal lamina. Electron microscopy confirmed the shortening of cilia in principal cells, often accompanied by bulging regions of varying sizes, observed at either the tip or middle, and appearing as single or multiple structures. These findings demonstrate that acute ischaemic injury induces ciliary fragmentation in collecting duct principal cells. The observed bulging in cilia undergoing shortening may indicate potential mechanisms underlying ciliary fragmentation.
肾小管细胞上的初级纤毛对肾功能至关重要。本研究调查了急性肾损伤如何影响纤毛长度，特别关注其在缺血再灌注损伤期间的缩短情况。使用Sprague-Dawley大鼠，夹闭肾蒂30分钟，然后再灌注6小时。使用共聚焦激光扫描显微镜和扫描电子显微镜分析肾脏组织。使用乙酰化α-微管蛋白和水通道蛋白1及H + -ATP酶等特异性标志物来识别近端小管和集合管。在正常条件下，肾小管细胞呈现出长的初级纤毛。损伤后，在近端小管和集合管中均观察到初级纤毛显著缩短。近端小管中交织的微绒毛使超微结构观察变得复杂。然而，集合管表现出不同的反应。闰细胞脱入管腔，而主细胞仍附着于基膜。电子显微镜证实主细胞中纤毛缩短，通常伴有尖端或中间大小不一的凸起区域，呈单个或多个结构出现。这些发现表明急性缺血性损伤可诱导集合管主细胞中的纤毛断裂。观察到缩短的纤毛出现凸起可能表明纤毛断裂的潜在机制。
