Role of YB-1 Protein in Inflammation

Rybalkina, Ekaterina Yu.; Моисеева, Н. И.

doi:10.1134/s0006297922140085

Cited by 10 publications

(5 citation statements)

References 62 publications

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“…Interestingly, the translocation of YB-1 to the nucleus was significantly increased in the APC-treated IMN model. As we well-known, under conditions of genotoxic stress, YB-1 translocates to the nucleus where activation affects immune response and apoptosis [32]. Previous study has shown that YB-1 can target the MEF2B promoter region to inhibit its expression and improve diabetic cardiomyopathy [18].…”

Section: Discussionmentioning

confidence: 99%

APC ameliorates idiopathic membranous nephropathy by affecting podocyte apoptosis through the ERK1/2/YB-1/PLA2R1 axis

Shen

Liao

et al. 2023

Mol Cell Biochem

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Idiopathic membranous nephropathy (IMN) belongs to an important pathogenic category of adult nephrotic syndrome. PLA2R1 exposure is critical for triggering the pathogenesis of PLA2R1-related IMN. However, the pathogenesis of IMN and the molecular mechanism of treatment remain to be further clarified. The expression changes of activated protein C (APC) and PLA2R1 in IMN patients were quantified by qPCR. A zymosan activated serum (ZAS)-induced IMN podocyte model was established in vitro. Podocyte apoptosis was detected via flow cytometry and caspase‑3 assay. The expression levels of APC, p-ERK1/2, ERK1/2, YB-1 and PLA2R1 were detected by western blotting. The regulation relationship between YB-1 and PLA2R1 was detected by dual fluorescent reporter system. In IMN patients, the expression level of PLA2R1 was increased, whereas the expression level of APC was decreased. When APC was added to podocytes in vitro, the phosphorylation of ERK1/2 was increased, which could promote the translocation of YB-1 to the nucleus that reduces the expression of PLA2R1 at the cellular transcriptional level, thereby inhibiting podocyte apoptosis. Our study is the first to report that APC can improve membranous nephropathy by affecting podocyte apoptosis through the ERK1/2/YB-1/PLA2R1 axis. This study will provide a new targeted therapy for IMN patients with high PLA2R1 expression.

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Section: Discussionmentioning

confidence: 99%

APC ameliorates idiopathic membranous nephropathy by affecting podocyte apoptosis through the ERK1/2/YB-1/PLA2R1 axis

Shen

Liao

et al. 2023

Mol Cell Biochem

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“…All these protein modi cations are postulated to contribute to several eye diseases (38,39). AGEs activate their receptor RAGE (40), which contributes to in ammation, a process that is also in uenced by YB-1 (41)(42)(43).…”

Section: Discussionmentioning

confidence: 99%

YB-1 expression analysis in the developing mouse eye by immunohistochemistry

Nass,

Wolf,

Sel

et al. 2024

Preprint

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Objective: Cold shock proteins such as YB-1 (ybx1) function in the regulation of transcription, mRNA stability, and translation. Consequently, YB-1 contributes to differentiation, stress responses and oncogenesis. Eye development is a complex process involving the differentiation of a signifiant number of cell-types with distinct functions. Additionally, the adult eye is exposed to UV-radiation causing significant oxidative stress. We therefore hypothesized that YB-1 plays a role in eye development as well as stress defence. As a first step to understand YB-1 function in this context, we analyzed its expression in the developing and adult mouse eye by immunohistochemistry. Results: Expression of the YB-1 protein in the developing mouse eye at stages (E12, E15 and E18) and in adult eyes (P14) was detected in all retinal cells and in cells of the cornea and the lens epithelium at all stages investigated. These findings support a significant function of YB-1 in the eye, may be related to development and differentiation.

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“…YB-1 is a member of the cold-shock protein family, which includes both transcription and translation factors that are widely involved in regulating gene expression ( 19 , 27 , 28 ). YB-1 is involved in the fibrosis of solid organs, including the kidney and liver, and acts as a crucial orchestrator of the expression of several fibrosis-related genes ( 19 , 24 , 26 , 29 , 30 ). It has been reported that YB-1 affects the activity of the TGF-β/SMAD pathway via the regulation of collagen and/or the activation of HSCs.…”

Section: Discussionmentioning

confidence: 99%

Promotion of liver fibrosis by Y-box binding protein 1 via the attenuation of transforming growth factor-beta 3 transcription

Liao¹,

Ye²,

Li³

et al. 2023

Ann Transl Med

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Background: Spurred by the seriousness of liver fibrosis, we evaluated the correlation between Y-box binding protein 1 (YB-1) and transforming growth factor-beta 3 (TGF-β3) expression levels in the signaling pathways of the disease. Methods:Based on a mouse model of carbon tetrachloride-induced liver fibrosis, YB-1 overexpression lentivirus was used to explore the effect of YB-1 on liver fibrosis in vivo. In addition, a hepatic stellate cell (HSC) activation model in the HSC line LX-2 was developed using TGF-β1. Western blot assays were used to investigate the effects of YB-1 overexpression and knockdown on liver fibrosis. Finally, chromatin immunoprecipitation and luciferase reporter assays were used to elucidate the relationship between YB-1 and its downstream signaling pathways.Results: YB-1 was overexpressed in fibrotic liver tissue, which enhanced both fibrosis and the relative protein expressions of the TGF-β pathway. Moreover, YB-1 overexpression promoted HSC activation in response to TGF-β1 stimulation, but its knockdown inhibited liver fibrosis in vitro. Both in vitro and in vivo experiments indicated the expression of TGF-β3 in the YB-1 overexpression group to be suppressed, and liver fibrosis was more obvious in the YB-1-overexpression group than in the YB-1-inhibition group. YB-1 attenuated TGF-β3 transcription by binding to its promoter, which is involved in the effect of YB-1 on liver fibrosis.Conclusions: YB-1 overexpression in HSCs promoted liver fibrosis by attenuating TGF-β3 transcription.

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Role of YB-1 Protein in Inflammation

Cited by 10 publications

References 62 publications

APC ameliorates idiopathic membranous nephropathy by affecting podocyte apoptosis through the ERK1/2/YB-1/PLA2R1 axis

APC ameliorates idiopathic membranous nephropathy by affecting podocyte apoptosis through the ERK1/2/YB-1/PLA2R1 axis

YB-1 expression analysis in the developing mouse eye by immunohistochemistry

Promotion of liver fibrosis by Y-box binding protein 1 via the attenuation of transforming growth factor-beta 3 transcription

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