Endoplasmic reticulum composition and form: Proteins in and out

Sun, Sha; Tang, Xiao Song; Guo, Yusong; Hu, Junjie

doi:10.1016/j.ceb.2021.01.008

Cited by 21 publications

(14 citation statements)

References 56 publications

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“…In addition, prominent vacuoles were observed in GCs, which indicated an inhibited synthesis of MUC2 ( Figure 4C ). Exocrine protein was synthesized, maturated and secreted in the endoplasmic reticulum (ER) membrane ( 36 ). When the homeostasis of the internal environment is disturbed by the excessive lipid, proteins destined for secretion cannot be adequately assembled and then ER stress is induced ( 37 ).…”

Section: Resultsmentioning

confidence: 99%

The Mechanism of Lipopolysaccharide Escaping the Intestinal Barrier in Megalobrama amblycephala Fed a High-Fat Diet

et al. 2022

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With the popularity of western food characterized by excessive fat and sugars, obesity has currently been a public health issue. Low-grade chronic inflammation accompanied by obesity increases the risk of multiple epidemics such as diabetes, cancer and cardiovascular diseases. Here, we show that feeding Megalobrama amblycephala with a high-fat diet (HFD) drives obesity-related chronic inflammation and the penetration of lipopolysaccharide (LPS). Interference with antibiotics inhibits the produce of LPS and this alleviates the sustained release of pro-inflammatory factors induced by HFD. LPS penetration is attributed to weakened intestinal mucus barrier after high-fat exposure. Mechanically, the consumption of HFD inhibits the secretion of mucin 2 (MUC2) due to the induction of endoplasmic reticulum stress mediated by the inositol-requiring enzyme 1 (IRE1) /X box-binding protein 1 (XBP1) pathway in goblet cells. Furthermore, excessive lipid exacerbates the leakage of LPS across the intestinal epithelial cell barrier via the transcellular pathway. Mechanically, lipid increases the internalization of LPS in intestinal epithelial cells depending on the activation of fatty acid translocase (FAT/CD36). These results demonstrate that HFD causes the penetration of LPS due to the weakened intestinal mucosal barrier and the assistance of CD36.

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Section: Resultsmentioning

confidence: 99%

The Mechanism of Lipopolysaccharide Escaping the Intestinal Barrier in Megalobrama amblycephala Fed a High-Fat Diet

et al. 2022

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“…The smooth ER is mainly involved in the synthesis of sugars and lipids. It can not only supply lipids to itself but also transport synthesized lipids to other organelles, such as lysosomes and mitochondria, to maintain their membranous structure [ 94 ].The function of the rough ER is to synthesize proteins and transport them to other compartments within the cell or out of the cell [ 95 ]. The function of ER protein-folding machinery is impaired under oxidative stress condition, leading to the accumulation of misfolded proteins in the ER lumen, this condition is referred to as ERS [ 96 ].…”

Section: The Damage and Repair Of Organelles In Tecs During Akimentioning

confidence: 99%

The pathological role of damaged organelles in renal tubular epithelial cells in the progression of acute kidney injury

Liu

Luo

et al. 2022

Cell Death Discov.

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Acute kidney injury (AKI) is a common clinical condition associated with high morbidity and mortality. The pathogenesis of AKI has not been fully elucidated, with a lack of effective treatment. Renal tubular epithelial cells (TECs) play an important role in AKI, and their damage and repair largely determine the progression and prognosis of AKI. In recent decades, it has been found that the mitochondria, endoplasmic reticulum (ER), lysosomes, and other organelles in TECs are damaged to varying degrees in AKI, and that they can influence each other through various signaling mechanisms that affect the recovery of TECs. However, the association between these multifaceted signaling platforms, particularly between mitochondria and lysosomes during AKI remains unclear. This review summarizes the specific pathophysiological mechanisms of the main TECs organelles in the context of AKI, particularly the potential interactions among them, in order to provide insights into possible novel treatment strategies.

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Section: Cellular Organelles and Proteins Involved In Hev Translation And Replicationmentioning

confidence: 99%

“…The ER is a membranous system that mediates the biosynthesis of membrane and secreted proteins, as well as lipids such as fatty acids, sphingolipids, phospholipids, and cholesterol [ 58 , 59 ]. The synthesis of approximately one-third of all cellular proteins is governed in this organelle [ 58 ]. As obligate parasites that solely rely on host machineries to thrive and produce progeny virions, almost all viruses usurp the endogenous functions of numerous ER-resident channels, chaperones, and enzymes throughout the whole viral life cycle [ 60 , 61 , 62 , 63 ].…”

Section: Cellular Organelles and Proteins Involved In Hev Translation And Replicationmentioning

confidence: 99%

Cellular Organelles Involved in Hepatitis E Virus Infection

2021

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Hepatitis E virus (HEV), a major cause of acute hepatitis worldwide, infects approximately 20 million individuals annually. HEV can infect a wide range of mammalian and avian species, and cause frequent zoonotic spillover, increasingly raising public health concerns. To establish a successful infection, HEV needs to usurp host machineries to accomplish its life cycle from initial attachment to egress. However, relatively little is known about the HEV life cycle, especially the functional role(s) of cellular organelles and their associated proteins at different stages of HEV infection. Here, we summarize current knowledge regarding the relation of HEV with the different cell organelles during HEV infection. Furthermore, we discuss the underlying mechanisms by which HEV infection is precisely regulated in infected cells and the modification of host cell organelles and their associated proteins upon HEV infection.

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Endoplasmic reticulum composition and form: Proteins in and out

Cited by 21 publications

References 56 publications

The Mechanism of Lipopolysaccharide Escaping the Intestinal Barrier in Megalobrama amblycephala Fed a High-Fat Diet

The Mechanism of Lipopolysaccharide Escaping the Intestinal Barrier in Megalobrama amblycephala Fed a High-Fat Diet

The pathological role of damaged organelles in renal tubular epithelial cells in the progression of acute kidney injury

Cellular Organelles Involved in Hepatitis E Virus Infection

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