Characterization of dietary and herbal sourced natural compounds that modulate SEL1L-HRD1 ERAD activity and alleviate protein misfolding in the ER

Yang, Jifeng; Zhi, Yaping; Wen, Shiyi; Pan, Xuya; Wang, Heting; He, Xianghui; Lü, Yan; Zhu, Yanhua; Chen, Yanming; Shi, Guojun

doi:10.1016/j.jnutbio.2022.109178

Cited by 3 publications

(1 citation statement)

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“…Mice overexpressing SYNV1 develop severe spontaneous arthropathy [46]. According to previous research, cryptochlorogenic acid (CCA) shows strong a nity with the binding pocket of SEL1L and inhibits SEL1L protein coded by SYNV1 [47].…”

Section: Lungmentioning

confidence: 99%

Intergalactic Interactions - Network Biology in Rodents from Spaceflight and Terra Firma

Hacking,

Sargin

2023

Preprint

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This study, utilizing data from the NASA Gene Lab Data Repository, investigates the impact of spaceflight on rodents, analyzing changes in lung, colorectal, and skin tissues. We examined RNA-seq data from rodents that had experienced space flight, comparing them with control groups that remained on Earth. Our focus was to better decipher the molecular alterations induced by the unique conditions of space. A comprehensive initial cohort of rodents was selected, ensuring the integrity and completeness of genomic data. We employed Proteinarium, a sophisticated multi-sample analysis tool, to explore and compare protein-protein interaction (PPI) networks between space flight-exposed and control rodents. This approach allowed us to identify significant clusters and distinct PPI networks in the space flight group, which were not present in the control group. Our results revealed that space flight leads to unique molecular changes, with certain genes becoming upregulated in response to the extraterrestrial environment. These changes were tissue-specific, indicating varied physiological responses across different organ systems. We also identified distinct gene hub targets for drug repurposing, which could be evaluated in future studies. The present study contributes to a deeper understanding of how spaceflight affects living organisms at the molecular level, providing insights that could inform future space missions and enhance our knowledge of biological systems in spaceflight environments.

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Section: Lungmentioning

confidence: 99%

Intergalactic Interactions - Network Biology in Rodents from Spaceflight and Terra Firma

Hacking,

Sargin

2023

Preprint

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HRD1 reduction promotes cholesterol-induced vascular smooth muscle cell phenotypic change via endoplasmic reticulum stress

Wang,

Ren,

et al. 2023

Mol Cell Biochem

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Aims: Phenotypic change of vascular smooth muscle cells (VSMCs) contributes a lot in obesity induced vascular pathological remodeling. The endoplasmic reticulum (ER) is critical for maintaining VSMC function, but the accumulation of misfolded proteins in the ER impairs cell function. As the major ER protein quality control responsible for clearing misfolded proteins, ER-associated degradation (ERAD) whose key member is HRD1 plays vital role in lipid metabolism, but its function in VSMC phenotypic change remains poorly understood.Main methods: The level of HRD1 expression was analyzed in aortic tissues of mice fed with a high-fat diet (HFD). The HE and EVG (VERHOEFF'S VAN GIESON) staining were used to demonstrate vascular pathological changes. Cripr and transcriptomic analysis were applied in in vitro studies to explore the cellular mechanism. Key ndings: Data showed a signi cant reduction of HRD1 in aortic tissues of mice under HFD feeding. VSMC phenotypic change and HRD1 downregulation were detected by cholesterol treatment.Transcriptomic and further analysis of HRD1-KO VSMCs showed that HRD1 de ciency increased the expression of genes related with ER stress, proliferation, and migration, but decreased the VSMC contractile-related genes. HRD1 de ciency in VSMCs also exacerbated the proliferation, migration, and ROS production induced by cholesterol, which promoted the VSMC phenotypic change process.Signi cance: Our results proved that HRD1 plays an essential role in the contractile homeostasis of VSMCs by negatively regulating ER stress. Thus, HRD1 may have the potential to be a therapeutic target in lipid metabolic disorders induced vascular remodeling caused by VSMC phenotypic change. HighlightsWe proved HRD1 KO exacerbated the proliferation, migration, and ROS production induced by cholesterol, promoted the VSMCs transfer from a contractile phenotype to a synthetic phenotype, our study provided a new target in treating the vascular pathological remodeling caused by VSMC phenotypic change.University, as well as the Animal Laboratory Administration Center and Ethics Committee of the Sun Yat-Sen University, the third a liated hospital. Male C57Bl6/J mice were purchased from the Guangdong Medical Laboratory Animal center. The persistent ID is SYSU-IACUC-2022-001869. All mice were maintained in a SPF environment with controlled humidity and temperature (22 ± 2°C) under a 12 h:12 h light/dark cycle and received water and a chow diet (CD) ad libitum. At 2 months of age, the mice were divided to receive CD (3.86 kcal/g), or HFD (a very high fat, 60% calories from fat; 5.55 kcal/g diet) for 4 months. Manipulations of Cultured VSMCsHuman primary VSMCs were purchased from Guangzhou BIOSPECIES Company (batch number 20220704), shown in Table SI, cultured in DMEM containing 10% fetal bovine serum and antibiotics (1% ER: endoplasmic reticulum VSMC: vascular smooth muscle cell ERAD: endoplasmic reticulum-associated degradation UPR: unfolded protein response

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Cholesterol-induced HRD1 reduction accelerates vascular smooth muscle cell senescence via stimulation of endoplasmic reticulum stress-induced reactive oxygen species

Wang,

Niu

et al. 2024

Journal of Molecular and Cellular Cardiology

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Characterization of dietary and herbal sourced natural compounds that modulate SEL1L-HRD1 ERAD activity and alleviate protein misfolding in the ER

Cited by 3 publications

References 50 publications

Intergalactic Interactions - Network Biology in Rodents from Spaceflight and Terra Firma

Intergalactic Interactions - Network Biology in Rodents from Spaceflight and Terra Firma

HRD1 reduction promotes cholesterol-induced vascular smooth muscle cell phenotypic change via endoplasmic reticulum stress

Cholesterol-induced HRD1 reduction accelerates vascular smooth muscle cell senescence via stimulation of endoplasmic reticulum stress-induced reactive oxygen species

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