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Structure of the enterocyte transcytosis compartments during lipid absorption.
Histochemistry and Cell Biology ( IF 2.1 ) Pub Date : 2020-03-11 , DOI: 10.1007/s00418-020-01851-3
Irina S Sesorova 1 , Natalia R Karelina 2 , Tatiana E Kazakova 1 , Seetharaman Parashuraman 3 , Maria A Zdorikova 1 , Ivan D Dimov 4 , Elena V Seliverstova 5 , Galina V Beznoussenko 4 , Alexander A Mironov 4
Affiliation  

In spite of tremendous progress in deciphering the molecular mechanisms involved in intracellular transport in cell culture and in the test tube, many aspects of this process in situ remain unclear. Here, we examined lipid transcytosis in enterocytes in adult rats. Apical clathrin-coated buds and the ER exit sites were not found. After starvation, the Golgi complex was in a non-transporting state and contained many vesicles, but no intercisternal connections and typical the cis-most and the trans-most cisternae. Following the addition of the lipids in the form of chyme, pre-chylomicrons (pre-ChMs) were initially found in the tubules of the smooth SER attached to the basolateral plasmalemma below the belt composed of adhesive junctions (AJ) and always connected with other cisternae. However, the ER exit sites were still absent. Pre-ChMs moved into the cis-most cisterna and were concentrated in cisternal distensions at the trans-side of the Golgi complex. This induced attachment of the cis-most and the trans-most cisternae to the Golgi complex. Post-Golgi carriers fused with the basolateral plasmalemma and delivered ChMs outside. Overloading of enterocytes with lipids resulted in an accumulation of lipid droplets, an increase of the diameter of ChMs, and shift of the Golgi complex to the transporting state with the formation of intercisternal connections, attachment of the cis-most and the trans-most cisternae and disappearance of vesicles. These data are discussed from the functional point of view. In spite of tremendous progress in deciphering the molecular mechanisms involved in intracellular transport in cell culture and in the test tube, many aspects of this process in situ remain unclear. Here, we examined lipid transcytosis in enterocytes in adult rats. Apical clathrin-coated buds and the ER exit sites were not found. After starvation, the Golgi complex was in a non-transporting state and contained many vesicles, but no intercisternal connections and typical the cis-most and the trans-most cisternae. Following the addition of the lipids in the form of chyme, pre-chylomicrons (pre-ChMs) were initially found in the tubules of the smooth SER attached to the basolateral plasmalemma below the belt composed of adhesive junctions (AJ) and always connected with other cisternae. However, the ER exit sites were still absent. Pre-ChMs moved into the cis-most cisterna and were concentrated in cisternal distensions at the trans-side of the Golgi complex. This induced attachment of the cis-most and the trans-most cisternae to the Golgi complex. Post-Golgi carriers fused with the basolateral plasmalemma and delivered ChMs outside. Overloading of enterocytes with lipids resulted in an accumulation of lipid droplets, an increase of the diameter of ChMs, and shift of the Golgi complex to the transporting state with the formation of intercisternal connections, attachment of the cis-most and the trans-most cisternae and disappearance of vesicles. These data are discussed from the functional point of view.



中文翻译:

脂质吸收过程中肠上皮细胞胞吞室的结构。

尽管在破译细胞培养和试管中细胞内转运所涉及的分子机制方面取得了巨大进展,但该过程的许多方面仍不清楚。在这里,我们检查了成年大鼠肠细胞中脂质的胞吞作用。未发现根尖包被网格蛋白的芽和内质网出口。饥饿后,高尔基复合体处于非运输状态,并包含许多囊泡,但没有脑池间连接,典型的是顺式至多数和反式-最蓄水池。在添加食糜形式的脂质后,最初在附着于由胶粘剂结合点(AJ)组成的带下方的基底外侧浆膜的光滑SER小管中发现了乳糜微粒前体(ChM)蓄水池。但是,急诊室出口站点仍然不存在。前ChMs移入最靠顺式的水箱,并集中在高尔基体的侧的脑池扩张中。这引起了顺式反式的连接-高尔基情结的大部分水箱。高尔基体后携带者融合有基底外侧质膜,并在体外递送ChM。肠细胞的脂质超载导致脂质小滴的积累,ChMs直径的增加以及高尔基复合体向运输状态的转移,形成了脑池间连接,顺式顺式反式的连接-大多数水箱和囊泡消失。从功能的角度讨论了这些数据。尽管在破译细胞培养和试管中细胞内转运所涉及的分子机制方面取得了巨大进展,但该过程的许多方面仍不清楚。在这里,我们检查了成年大鼠肠细胞中脂质的胞吞作用。未发现根尖包被网格蛋白的芽和内质网出口。饥饿后,高尔基复合体处于非运输状态,并包含许多囊泡,但没有胞间连接,典型的是顺式反式-最蓄水池。在添加食糜形式的脂质后,最初在附着于由胶粘剂结合点(AJ)组成的带下方的基底外侧浆膜的光滑SER小管中发现了乳糜微粒前体(ChM)蓄水池。但是,急诊室出口站点仍然不存在。前ChMs移入最靠顺式的水箱,并集中在高尔基体的侧的脑池扩张中。这引起了顺式反式的连接-高尔基情结的大部分水箱。高尔基体后携带者融合有基底外侧质膜,并在体外递送ChM。脂质使肠细胞超载导致脂质滴积累,ChMs直径增加,高尔基复合体转变为运输状态,并形成胞间连接,顺式反式池的附着。和囊泡的消失。从功能的角度讨论了这些数据。

更新日期:2020-03-11
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