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Start Over Author "Guo, Sheng" Topic apoptosis Journal cell biology international
3 results on '"Guo, Sheng"'

1. MicroRNA‐16‐5p exacerbates sepsis by upregulating aerobic glycolysis via SIRT3‐SDHA axis

Author

Yue‐Xian He, Bo‐Lun Huang, Yi‐Yu Yang, Wen‐Xiu Song, Yong‐Bo Fan, Li‐Mei Zhang, and Guo‐Sheng Liu

Subjects
Lipopolysaccharides, Electron Transport Complex II, Succinates, Apoptosis, Cell Biology, General Medicine, MicroRNAs, Sirtuin 3, Sepsis, Leukocytes, Mononuclear, Lactates, Humans, HMGB1 Protein, Glycolysis
Abstract

Sepsis is a life-threatening condition, and treatment for sepsis in clinic is often not available, partially due to insufficient understanding of the pathogenesis of sepsis. Extensive study to elucidate the pathogenesis is required to improve the clinical management and outcome of sepsis. In this study, we investigated the pathogenesis of sepsis using peripheral blood mononuclear cells (PBMCs) from septic patients and studied the underlying mechanism of miR-16-5p on aerobic glycolysis in lipopolysaccharide (LPS)-treated THP1 and Raw264.7 cells. The levels of RNA and protein were determined by real-time quantitative PCR and immunoblotting assay, respectively. The production of high mobility group box 1 (HMGB1) was measured by enzyme-linked immunosorbent assay. The levels of succinate and lactate were determined using colorimetric kits. The extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were measured by extracellular flux analyzer. The results showed that the expression of miR-16-5p was elevated, while sirtuin 3 (SIRT3) was decreased in PBMCs from septic patients and LPS-treated cells, along with accumulation of acetylated succinate dehydrogenase complex, subunit A. Concomitantly, an increase in HMGB1, succinate, lactate, as well as ECAR and a decrease in OCR were observed. Knockdown of miR-16-5p upregulated SIRT3 expression, facilitated SDHA deacetylation, and attenuated sepsis-related aerobic glycolysis. Further study identified that SIRT3 is targeted by miR-16-5p, and overexpression of SIRT3 rescued LPS-induced responses via deacetylation of SDHA. Our findings revealed a novel miR-16-5p-regulated SIRT3-SDHA axis in sepsis and provided novel insights for sepsis treatment.

Published
2022

2. Fluvoxamine prompts the antitumor immune effect via inhibiting the PD‐L1 expression on mice‐burdened colon tumor.

Author

Wei, Pengkun, Jia, Huijie, Li, Ruipeng, Zhang, Congli, Guo, Shuoshuo, Wei, Sujiao, Sun, Ke, Cheng, Sichang, Cui, Tongquan, Huang, Juan, Guo, Sheng, Guo, Jing, Yang, Zishan, Zhong, Jiateng, Lu, Chengbiao, Feng, Zhiwei, and Zhao, Tiesuo

Subjects
COLON tumors, PROGRAMMED cell death 1 receptors, PROGRAMMED death-ligand 1, APOPTOSIS, MATRIX metalloproteinases, ALIMENTARY canal, T cells
Abstract

A colon tumor, one of the digestive tract malignant tumors, is harmful to human health. A potential new treatment still deserves attention. The development of a new drug needs more resources, including time and expense. Therefore, the old drug with new targets has become a current research hotspot. Fluvoxamine, as an antidepressant, could play an effect on inhibiting 5‐hydroxytryptamine reuptake. In the present research, the antitumor effects and possible mechanisms of fluvoxamine are validated. The results showed that fluvoxamine significantly suppressed the migration and proliferation of tumor cells, and increased the apoptosis in vitro. Additionally, fluvoxamine significantly delays tumor development, and prompts the apoptosis in tumor tissues of mice‐burdened colon tumors in vivo. The tumor suppression might be related with that fluvoxamine inhibits the expression of phosphorylated signal transducer and activator of transcription 3, matrix metalloproteinase 2, and cleaved‐caspase 3. Importantly, fluvoxamine significantly reduces the expression level of programmed cell death ligand 1. This could be a possible reason that treatment with fluvoxamine drives the infiltration of T lymphocytes and M1‐type macrophages in tumor tissues. Taken together, this research suggests that fluvoxamine might be a promising drug to treat colon cancer by inhibiting the proliferation and migration, inducing apoptosis, and even increasing the immune response of antitumor. [ABSTRACT FROM AUTHOR]

Published
2023
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3. Efficient cardiomyocyte differentiation of embryonic stem cells by bone morphogenetic protein-2 combined with visceral endoderm-like cells

Author

Jiang Hong, Shen Hui, Zeng Bin, Yang Bo, Zhu-Chen Gang, Lin-Guo Sheng, and Cai Jun

Subjects
Cellular differentiation, Population, Bone Morphogenetic Protein 2, Apoptosis, Mice, Microscopy, Electron, Transmission, Transforming Growth Factor beta, medicine, Animals, Myocyte, Myocytes, Cardiac, education, Cells, Cultured, Embryonic Stem Cells, Embryonic Induction, education.field_of_study, biology, Reverse Transcriptase Polymerase Chain Reaction, Endoderm, Cell Differentiation, Cell Biology, General Medicine, Transforming growth factor beta, Embryonic stem cell, Coculture Techniques, Cell biology, Viscera, medicine.anatomical_structure, Cell culture, Bone Morphogenetic Proteins, biology.protein
Abstract

As the signals required for cardiomyocyte differentiation and functional regulation are complex and only partly understood, the mechanisms prompting the differentiation and specification of pluripotential embryonic stem (ES) cells into cardiomyocytes remain unclear. We hypothesized that a combined technology system, cocultured with a visceral endoderm (VE) - like cell line, END-2, and added cytokine BMP-2, would induce high percentage conversion of murine ES-D3 cell line into cardiomyocytes, and derived cardiomyocytes in this system would exhibit more mature characteristics. It was observed that 92% (P

Published
2006

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