RETREG1-mediated ER-phagy activation induced by glucose deprivation alleviates nucleus pulposus cell damage via ER stress pathway

Luo, Rongjin; Liang, Huaizhen; Zhang, Weifeng; Li, Gaocai; Zhao, Kangcheng; Hua, Wenbin; Song, Yu; Yang, Cao

doi:10.3724/abbs.2022024

Cited by 6 publications

(8 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, there is a reduced delivery of ER proteins to lysosomes for degradation in mouse embryonic fibroblasts (Forrester et al, 2019). Interestingly, overexpression of FAM134B results in enhanced cell death in HeLa cells, with cell death increasing from 15% to 29% (Liao et al, 2019) which is not observed in other HEK293/A549 cell lines (Hill, Mellick and Sykes unpublished data), (Fregno et al, 2018; Jiang et al, 2020), nor in U2OS (Bhaskara et al, 2019; Forrester et al, 2019; Khaminets et al, 2015), HCT116 (Liang et al, 2018), or nucleus pulposus cells (Luo, Li, et al, 2022; Luo, Liang, et al, 2022).…”

Section: Membrane‐associated Receptorsmentioning

confidence: 89%

“…Overexpression of FAM134B results in increased fragmentation of the ER and enhanced ER‐phagy, as measured by increased degradation of ER‐resident proteins such as SEC61B or autophagy marker p62 (Bhaskara et al, 2019; Fregno et al, 2018; Jiang et al, 2020; Khaminets et al, 2015; Liang et al, 2018; Liao et al, 2019; Luo, Li, et al, 2022; Luo, Liang, et al, 2022). Conversely, decreasing FAM134B expression leads to expansion of the ER in knockdown experiments (Jiang et al, 2020; Khaminets et al, 2015; Kohno et al, 2019; Kurth et al, 2009; Lennemann & Coyne, 2017; Luo, Liang, et al, 2022; Reggio et al, 2021) and this expansion is also evident in FAM134B knockout mouse embryonic fibroblasts (Chiramel et al, 2016; Reggio et al, 2021). Furthermore, there is a reduced delivery of ER proteins to lysosomes for degradation in mouse embryonic fibroblasts (Forrester et al, 2019).…”

Section: Membrane‐associated Receptorsmentioning

confidence: 99%

“…Interestingly, transcription of the other ER‐phagy receptors was unaffected, suggesting alternative transcriptional control that may be stress dependent (Cinque et al, 2020). Glucose deprivation increased the protein expression of FAM134B and its colocalization with LC3, which when considered along with the decreased protein expression of p62, suggests enhanced FAM134B‐mediated ER‐phagy in glucose‐deprived nucleus pulposus cells (Luo, Liang, et al, 2022). In M14 cancer cells, FAM134B expression was inversely proportional to Sec23a, which is a COPII protein involved in transport from the ER to the Golgi.…”

Section: Membrane‐associated Receptorsmentioning

confidence: 99%

See 2 more Smart Citations

ER‐phagy in neurodegeneration

Hill

Sykes

Mellick

2023

J of Neuroscience Research

View full text Add to dashboard Cite

There are many cellular mechanisms implicated in the initiation and progression of neurodegenerative disorders. However, age and the accumulation of unwanted cellular products are a common theme underlying many neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and Niemann–Pick type C. Autophagy has been studied extensively in these diseases and various genetic risk factors have implicated disruption in autophagy homoeostasis as a major pathogenic mechanism. Autophagy is essential in the maintenance of neuronal homeostasis, as their postmitotic nature makes them particularly susceptible to the damage caused by accumulation of defective or misfolded proteins, disease‐prone aggregates, and damaged organelles. Recently, autophagy of the endoplasmic reticulum (ER‐phagy) has been identified as a novel cellular mechanism for regulating ER morphology and response to cellular stress. As neurodegenerative diseases are generally precipitated by cellular stressors such as protein accumulation and environmental toxin exposure the role of ER‐phagy has begun to be investigated. In this review we discuss the current research in ER‐phagy and its involvement in neurodegenerative diseases.

show abstract

Section: Membrane‐associated Receptorsmentioning

confidence: 89%

Section: Membrane‐associated Receptorsmentioning

confidence: 99%

Section: Membrane‐associated Receptorsmentioning

confidence: 99%

See 1 more Smart Citation

ER‐phagy in neurodegeneration

Hill

Sykes

Mellick

2023

J of Neuroscience Research

View full text Add to dashboard Cite

show abstract

“…It has been described that hyperosmotic stress (as the IVD microenvironment) results in abnormally swollen melanosomes by disturbing vesicle trafficking (Bin et al, 2014). In turn, ER stress modulation by ER‐phagy, is an adaptive mechanism to stress, namely to glucose deprivation in the IVD (Luo et al, 2022). By exploring the differentially expressed proteins between young and old NP cells, we identified several age‐related components which were significantly upregulated in old NP cells.…”

Section: Discussionmentioning

confidence: 99%

Alterations of bovine nucleus pulposus cells with aging

et al. 2023

View full text Add to dashboard Cite

Aging is one of the major etiological factors driving intervertebral disc (IVD) degeneration, the main cause of low back pain. The nucleus pulposus (NP) includes a heterogeneous cell population, which is still poorly characterized. Here, we aimed to uncover main alterations in NP cells with aging. For that, bovine coccygeal discs from young (12 months) and old (10–16 years old) animals were dissected and primary NP cells were isolated. Gene expression and proteomics of fresh NP cells were performed. NP cells were labelled with propidium iodide and analysed by flow cytometry for the expression of CD29, CD44, CD45, CD146, GD2, Tie2, CD34 and Stro‐1. Morphological cell features were also dissected by imaging flow cytometry. Elder NP cells (up‐regulated bIL‐6 and bMMP1 gene expression) presented lower percentages of CD29+, CD44+, CD45+ and Tie2+ cells compared with young NP cells (upregulated bIL‐8, bCOL2A1 and bACAN gene expression), while GD2, CD146, Stro‐1 and CD34 expression were maintained with age. NP cellulome showed an upregulation of proteins related to endoplasmic reticulum (ER) and melanosome independently of age, whereas proteins upregulated in elder NP cells were also associated with glycosylation and disulfide bonds. Flow cytometry analysis of NP cells disclosed the existence of 4 subpopulations with distinct auto‐fluorescence and size with different dynamics along aging. Regarding cell morphology, aging increases NP cell area, diameter and vesicles. These results contribute to a better understanding of NP cells aging and highlighting potential anti‐aging targets that can help to mitigate age‐related disc disease.

show abstract

“…The Ubi-HBx-SV40-Neomycin plasmid, which carries inserts encoding HBx, was cloned into the vector CV084 which is a consequence of optimization derived from commercial vector pfu-GW (GeneChem, China). To generate stable HBx-overexpression cell lines (LO2-HBx, Huh-7-HBx), LV-HBx (GeneChem, China) were constructed and used for corresponding cells by lentivirus-mediated transfection [39,40]. For two weeks prior to the ensuing studies, stable transfections were chosen and treated with G418 (GeneChem, China).…”

Section: Transient Transfection Generation Of Stable Cell Lines and R...mentioning

confidence: 99%

HBx promotes tumorigenicity through RRM2-mediated autophagy in hepatocellular carcinoma

wang,

yaqun,

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

HBV infection can exacerbate liver disease progression through multiple mechanisms, eventually leading to hepatocellular carcinoma (HCC). HBV-encoded oncogene X protein (HBx), a key regulatory protein of HBV infection, serves as a positive regulator of hepatocarcinogenesis. Ribonucleotide-diphosphate reductase M2 subunit (RRM2), which is indispensable for DNA replication and repair, has been shown overexpressed in a range of malignancies. Our previous studies clarified that RRM2 expression is highly elevated in HCC, particularly in HBV-related HCC. Given the robust RRM2 expression is strongly associated with poor survival rate of the patients with HCC, while the specific functions and underlying mechanisms of RRM2 in HBV-related HCC remain elusive; the present study was performed to elucidate whether HBx increases RRM2 expression, and whether RRM2 engages in interaction with HBx in vivo and in vitro. Autophagy is a crucial step in the oncogenic process of HBx, while autophagy inhibition attenuates HBx-initiated proliferation response. We further demonstrated that RRM2 interference lowered HBx-induced autophagy, inhibited the production of autophagic vesicles and lysosomes, and caused G1/S blockage, thereby inhibiting HBx-stimulated hepatocellular carcinogenesis. Our findings indicate that RRM2 may play a tumor-promoting role in HBV-associated HCC by modulating autophagy, suggesting that RRM2 may be a potential therapeutic target for HCC.

show abstract

RETREG1-mediated ER-phagy activation induced by glucose deprivation alleviates nucleus pulposus cell damage via ER stress pathway

Cited by 6 publications

References 54 publications

ER‐phagy in neurodegeneration

ER‐phagy in neurodegeneration

Alterations of bovine nucleus pulposus cells with aging

HBx promotes tumorigenicity through RRM2-mediated autophagy in hepatocellular carcinoma

Contact Info

Product

Resources

About