Trafficking pathway between plasma membrane and mitochondria via clathrin-mediated endocytosis

Wei, Zhongya; Su, Wenfeng; Lou, Huifang; Duan, Shumin; Chen, Gang

doi:10.1093/jmcb/mjy060

Cited by 25 publications

(21 citation statements)

References 45 publications

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“…The three classical endocytic pathways are clathrin‐mediated, caveolin‐mediated endocytosis and macropinocytosis . Recent work has indicated that all three of these pathways can mediate occludin internalization in intestinal epithelial TJ, depending on the type of stimulus.…”

Section: Discussionmentioning

confidence: 99%

Occludin endocytosis is involved in the disruption of the intestinal epithelial barrier in a mouse model of alcoholic steatohepatitis

Wang

Chi

et al. 2019

J of Digest Diseases

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Objective: We aimed to investigate the involvement of the endocytosis of occludin, a key component of tight junction (TJ), in the ethanol-induced disassembly of TJ in a model of alcoholic steatohepatitis. Methods: Wild-type mice were fed an ethanol-containing or isocaloric liquid diet for 8 weeks and then assessed for liver injury (histopathology and measurement of serum enzymes), gut permeability (in vivo lactulose/mannitol and ex vivo dye leakage assays), intestinal epithelium ultrastructure (transmission electron microscopy), and intestinal occludin localization (immunofluorescence microscopy). The human intestinal epithelial cell line Caco-2 was also analyzed in vitro for the effects of ethanol on the barrier function (transepithelial electrical resistance), occludin localization (immunofluorescence microscopy and Western blotting), and endocytosis pathways (double-labeling immunofluorescence microscopy with selective pathway inhibitors). Results: The ethanol-fed mice developed steatohepatitis and displayed intestinal barrier dysfunction, the disruption of intestinal TJ, and enhanced intestinal endocytosis of occluding compared with the control mice. In the Caco-2 monolayers, ethanol treatment decreased transepithelial electrical resistance, disrupted TJ formation, and enhanced occludin endocytosis in a dose-and time-dependent manner. These deleterious events were reversed by pretreating the Caco-2 cells with a selective pharmacological inhibitor of macropinocytosis, but not with the inhibitors of clathrin or caveolin-mediated endocytic pathways. Conclusion: Chronic ethanol exposure may increase intestinal permeability by inducing the micropinocytosis of occludin, resulting in the disruption of intestinal TJ.

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Section: Discussionmentioning

confidence: 99%

Occludin endocytosis is involved in the disruption of the intestinal epithelial barrier in a mouse model of alcoholic steatohepatitis

Wang

Chi

et al. 2019

J of Digest Diseases

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“…Even though the mitochondrial genome is only composed of 13 genes, there are over 2000 proteins that have been identified that participated in the overall functions of the mitochondria [38,39]. Past studies suggest that miRNAs of mitochondrial origin can regulate nuclear mRNA translation that alter cell phenotype [40][41][42].…”

Section: Discussionmentioning

confidence: 99%

Differential Expression Profiles of Mitogenome Associated MicroRNAs Among Colorectal Adenomatous Polyps

Wallace¹,

Aikhionbare²,

Banerjee³

et al. 2021

CRJ

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Colorectal tumors are mostly of epithelial origin and represent a wide spectrum of neoplasms. About 97% of colorectal cancer originating from benign lesions of adenomatous polyps are adenocarcinomas. Reactive oxygen species (ROS) generating from mitochondrial DNA (mtDNA) mutations and microRNAs (miRNAs) are associated with oncogene and tumor suppressor genes regulation which are known to parallel the tissue abnormalities involved with tumorigenesis such as colorectal adenoma to adenocarcinoma. However, the differential expression patterns of mitochondrial associated microRNAs (referred as MitomiRs) among colorectal adenomatous polyps progression is yet to be determined. Thus, the aim of this study was to determine the differential expressions profiles of MitomiRs (miR-24, miR-181, miR-210, miR-21 and miR378) in patients with colorectal adenomatous polyps tissues in correlation with clinicopathological tumor architectures of tubular, tubulovillous, villous adenomas and adenocarcinomas. Isolation of mitochondria RNA from colorectal adenomatous polyps, adenocarcinomas, and normal adjacent tissue samples was performed and assessed for mitochondrial associated miRNAs expression differences using quantitative reverse transcription PCR. Data from this study demonstrates that mitochondria genome expression of mitomiRNAs; miR-24, miR-181, miR-210, miR-21 and miR-378 in colorectal tissue samples varies among the adenomatous polyps. Expression of mitomiRNAs 24, 181, 210 and 378 progressively increased from the precancerous of adenomatous polyps to adenocarcinoma. In addition, miR-210 and miR-181 expression increased 3 folds in villous adenomas and greater than 3 folds increased in miR378 in adenocarcinoma (p < 0.005) when compared to tubular adenoma. Meanwhile, miR-21 increased progressively in adenoma tissues but decreased almost 2.5 folds in adenocarcinomas when compared to villous adenoma tissues (p < 0.001). These results suggest mitomiRs may regulate important mitochondrial functional pathways leading to a more favorable environment for transformation or progression of colorectal adenomatous polyps into adenocarcinomas.

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“…TNT was produced in induced pluripotent stem cells (iPSCs) by tumor necrosis factor alpha (TNF-α) and the microstructure interacted with cardiomyocytes through TNFαIP2 expression, which may promote the effective transfer of mitochondria (Zhang et al, 2016). Furthermore, when extracellular mitochondria were internalized into the cells, activation of several pathways including endocytosis (Wei et al, 2018), integrin-dependent pathways (Hayakawa et al, 2016), macro-pinocytosis (Kitani et al, 2014), TNT, or cell fusion (Spees et al, 2006;Torralba et al, 2016) have been observed. Future studies are warranted to identify the specific internalization pathway when extracellular mitochondria are either healthy or disrupted under pathophysiological conditions (Figure 1).…”

Section: Mechanisms Of Experimental Mitochondrial Transfermentioning

confidence: 99%

Extracellular Mitochondria Signals in CNS Disorders

Park

Hayakawa

2021

Front. Cell Dev. Biol.

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Mitochondria actively participate in the regulation of cell respiratory mechanisms, metabolic processes, and energy homeostasis in the central nervous system (CNS). Because of the requirement of high energy, neuronal functionality and viability are largely dependent on mitochondrial functionality. In the context of CNS disorders, disruptions of metabolic homeostasis caused by mitochondrial dysfunction lead to neuronal cell death and neuroinflammation. Therefore, restoring mitochondrial function becomes a primary therapeutic target. Recently, accumulating evidence suggests that active mitochondria are secreted into the extracellular fluid and potentially act as non-cell-autonomous signals in CNS pathophysiology. In this mini-review, we overview findings that implicate the presence of cell-free extracellular mitochondria and the critical role of intercellular mitochondrial transfer in various rodent models of CNS disorders. We also discuss isolated mitochondrial allograft as a novel therapeutic intervention for CNS disorders.

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Trafficking pathway between plasma membrane and mitochondria via clathrin-mediated endocytosis

Cited by 25 publications

References 45 publications

Occludin endocytosis is involved in the disruption of the intestinal epithelial barrier in a mouse model of alcoholic steatohepatitis

Occludin endocytosis is involved in the disruption of the intestinal epithelial barrier in a mouse model of alcoholic steatohepatitis

Differential Expression Profiles of Mitogenome Associated MicroRNAs Among Colorectal Adenomatous Polyps

Extracellular Mitochondria Signals in CNS Disorders

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