Procollagen C-Endopeptidase Enhancer 2 Secreted by Tonsil-Derived Mesenchymal Stem Cells Increases the Oxidative Burst of Promyelocytic HL-60 Cells

Yoon, Hee-Soo; Cho, Kyung‐Ah; Kim, Yu Hee; Woo, So Youn; Kim, Han Su; Kang, Jihee Lee; Ryu, Kyung‐Ha; Park, Joowon

doi:10.3390/biology11020255

Cited by 9 publications

(7 citation statements)

References 52 publications

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“…Furthermore, PCOLCE plays a key role in promoting lung metastasis of osteosarcoma [ 40 ] and participates in EMT [ 41 ]. A recent study has shown that PCOLCE2 stimulates the production of reactive oxygen species in neutrophils [ 42 ]. Moreover, a study has shown a correlation between PCOLCE2 and ferroptosis in colon adenocarcinoma [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Characterization and verification of CAF-relevant prognostic gene signature to aid therapy in bladder cancer

Zhou,

Li,

Liu

et al. 2024

Heliyon

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Section: Discussionmentioning

confidence: 99%

Characterization and verification of CAF-relevant prognostic gene signature to aid therapy in bladder cancer

Zhou,

Li,

Liu

et al. 2024

Heliyon

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“…This suggests that ACCN2 may affect the development of SHPT. Tonsil-derived mesenchymal stem cells can increase reactive oxygen species (ROS) production of neutrophils through PCOLCE2, thus enhancing host defense ( Yoon et al, 2022 ). Within living cells, mitochondria are considered relevant sources of ROS ( Willems et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of key biomarkers based on the proliferation of secondary hyperparathyroidism by bioinformatics analysis and machine learning

Shen

Shi

Wang

et al. 2023

PeerJ

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Objective Secondary hyperparathyroidism (SHPT) is a frequent complication of chronic kidney disease (CKD) associated with morbidity and mortality. This study aims to identify potential biomarkers that may be used to predict the progression of SHPT and to elucidate the molecular mechanisms of SHPT pathogenesis at the transcriptome level. Methods We analyzed differentially expressed genes (DEGs) between diffuse and nodular parathyroid hyperplasia of SHPT patients from the GSE75886 dataset, and then verified DEG levels with the GSE83421 data file of primary hyperparathyroidism (PHPT) patients. Candidate gene sets were selected by machine learning screens of differential genes and immune cell infiltration was explored with the CIBERSORT algorithm. RcisTarget was used to predict transcription factors, and Cytoscape was used to construct a lncRNA-miRNA-mRNA network to identify possible molecular mechanisms. Immunohistochemistry (IHC) staining and quantitative real-time polymerase chain reaction (qRT-PCR) were used to verify the expression of screened genes in parathyroid tissues of SHPT patients and animal models. Results A total of 614 DEGs in GSE75886 were obtained as candidate gene sets for further analysis. Five key genes (USP12, CIDEA, PCOLCE2, CAPZA1, and ACCN2) had significant expression differences between groups and were screened with the best ranking in the machine learning process. These genes were shown to be closely related to immune cell infiltration levels and play important roles in the immune microenvironment. Transcription factor ZBTB6 was identified as the master regulator, alongside multiple other transcription factors. Combined with qPCR and IHC assay of hyperplastic parathyroid tissues from SHPT patients and rats confirm differential expression of USP12, CIDEA, PCOLCE2, CAPZA1, and ACCN2, suggesting that they may play important roles in the proliferation and progression of SHPT. Conclusion USP12, CIDEA, PCOLCE2, CAPZA1, and ACCN2 have great potential both as biomarkers and as therapeutic targets in the proliferation of SHPT. These findings suggest novel potential targets and future directions for SHPT research.

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“…MTT assay was performed as described previously (Yoon et al, 2022). Briefly, primary murine hepatocytes cultured in DMEM supplemented with 0.1% BSA were treated with paracetamol (10 mM) for 24 h. Then, methylthiazolyldiphenyl‐tetrazolium bromide (MTT, Sigma; M5655) solution was added to each well with a final concentration of 0.5 mg·ml−1, and cells were incubated for 4 h. After the medium was carefully removed, DMSO was added to each well and absorbance was measured at 570 nm using a plate reader, Synergy H1M (Molecular Devices, Sunnyvale, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Mitophagy and endoplasmic reticulum‐phagy accelerated by a p62 ZZ ligand alleviates paracetamol‐induced hepatotoxicity

Yoon

Heo

Jung

et al. 2023

British J Pharmacology

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Background and Purpose Paracetamol (acetaminophen)‐induced hepatotoxicity is the leading cause of drug‐induced liver injury worldwide. Autophagy is a degradative process by which various cargoes are collected by the autophagic receptors such as p62/SQSTM1/Sequestosome‐1 for lysosomal degradation. Here, we investigated the protective role of p62‐dependent autophagy in paracetamol‐induced liver injury. Experimental Approach Paracetamol‐induced hepatotoxicity was induced by a single i.p. injection of paracetamol (500 mg·kg−1) in C57/BL6 male mice. YTK‐2205 (20 mg·kg−1), a p62 agonist targeting ZZ domain, was co‐ or post‐administered with paracetamol. Western blotting and immunocytochemistry were performed to explore the mechanism. Key Results N‐terminal arginylation of the molecular chaperone calreticulin retro‐translocated from the endoplasmic reticulum (ER) was induced in the livers undergoing paracetamol‐induced hepatotoxicity, and YTK‐2205 exhibited notable therapeutic efficacy in acute hepatotoxicity as assessed by the levels of serum alanine aminotransferase and hepatic necrosis. This efficacy was significantly attributed to accelerated degradation of ubiquitin (Ub) conjugates as well as damaged mitochondria (mitophagy) and endoplasmic reticulum (ER‐phagy). In primary murine hepatocytes treated with paracetamol, YTK‐2205 induced the co‐localization of p62+LC3+ phagophores to the sites of mitophagy and ER‐phagy. A similar activity of YTK‐2205 was observed with N‐acetyl‐p‐benzoquinone imine, a putative toxic metabolite of paracetamol in Hep3B cells. Conclusion and Implications Our results elucidated that p62‐dependent autophagy plays a key role in the removal of cytotoxic materials such as damaged mitochondria in paracetamol‐induced hepatotoxicity. Small molecule ligands to p62 may be developed into drugs to treat this pathological condition.

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Procollagen C-Endopeptidase Enhancer 2 Secreted by Tonsil-Derived Mesenchymal Stem Cells Increases the Oxidative Burst of Promyelocytic HL-60 Cells

Cited by 9 publications

References 52 publications

Characterization and verification of CAF-relevant prognostic gene signature to aid therapy in bladder cancer

Characterization and verification of CAF-relevant prognostic gene signature to aid therapy in bladder cancer

Identification of key biomarkers based on the proliferation of secondary hyperparathyroidism by bioinformatics analysis and machine learning

Mitophagy and endoplasmic reticulum‐phagy accelerated by a p62 ZZ ligand alleviates paracetamol‐induced hepatotoxicity

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