Myosin IIA Regulated Tight Junction in Oxygen Glucose-Deprived Brain Endothelial Cells Via Activation of TLR4/PI3K/Akt/JNK1/2/14-3-3ε/NF-κB/MMP9 Signal Transduction Pathway

Lv, Yanni; Li, Wen; Ruan, Zhaohui; Xu, Zixuan; Fu, Longsheng

doi:10.1007/s10571-019-00654-y

Cited by 36 publications

(26 citation statements)

References 40 publications

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“…MMP9 and MMP2, which were involved in the process of cell migration and TNF signaling pathway in our study, were observed increased in the retina and vitreous in DR and may increase the vascular permeability through disruption of tight junction complexes [35]. One report revealed that TLR4, toll-like receptor 4, also regulated tight junctions via TLR4/PI3K/Akt/JNK1/2/14-3-3ε/NF-κB/MMP9 pathway [36]. Therefore, we suspect that the MMP9-, MMP2-and TLR4-mediated signaling pathways may play an important roles in the cell tight junctions of DR. TGFB1, transforming growth factor beta 1, promotes the recruitment of endothelial cells and proliferation [37], which are elevated in DR. [6] PDGFB, platelet-derived growth factor subunit B, also regulates the proliferation and migration of pericytes via the TGFB pathway [38].…”

Section: Discussionsupporting

confidence: 61%

Comprehensive analysis of angiogenesis-related genes and pathways in early diabetic retinopathy

Lhamo

Zou

et al. 2020

BMC Med Genomics

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Background Angiogenesis is an important parameter in the development of diabetic retinopathy (DR), and it is indicative of an early stage evolving into a late phase. Therefore, examining the role of angiogenic factors in early DR is crucial to understanding the mechanism of neovascularization. Methods The present study identified hub genes and pathways associated with angiogenesis in early DR using bioinformatics analysis. Genes from published literature and Gene Expression Omnibus (GEO) were collected and analysed. Results We collected 73 genes from 70 published studies in PubMed, which were referred to as DR-related gene set 1 (DRgset1). The gene expression profile of GSE12610 was downloaded, and 578 differentially expressed genes (DEGs) between diabetic and normal samples were identified. DEGs and DRgset1 were further combined to create DR-related gene set 2 (DRgset2). After an enrichment analysis, we identified 12 GO terms and 2 pathways associated with neovascularization in DRgset1, and 8 GO terms and 2 pathways in DRgset2. We found 39 new genes associated with angiogenesis and verified 8 candidate angiogenesis-related genes in DR cells using real-time PCR: PIK3CB, ALDH3A1, ITGA7, FGF23, THBS1, COL1A1, MAPK13, and AIF1. We identified 10 hub genes associated with neovascularization by constructing a protein-protein interaction (PPI) network: TNF, VEGFA, PIK3CB, TGFB1, EDN1, MMP9, TLR4, PDGFB, MMP2, and THBS1. Conclusions The present study analysed angiogenesis-related genes and pathways in early DR in a comprehensive and systematic manner. PIK3CB, ALDH3A1, ITGA7, FGF23, THBS1, COL1A1, MAPK13, and AIF1 may be the candidate genes to further explore the mechanisms of angiogenesis in early DR. TNF, PIK3CB, TGFB1, EDN1, MMP9, TLR4, PDGFB, MMP2, and THBS1 may be new targets for early neovascularization therapy in the future.

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Section: Discussionsupporting

confidence: 61%

Comprehensive analysis of angiogenesis-related genes and pathways in early diabetic retinopathy

Lhamo

Zou

et al. 2020

BMC Med Genomics

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“…Combined with H&E liver staining, ruscogenin could obviously decrease the acreage of tumor nodule, the high dosage 20 mg/kg ruscogenin had the strongest functions on the suppression of tumor migration. Tight junctions (TJs) are important intercellular junction complexes, which are composed of transmembrane proteins, cytoplasmic attachment proteins, and cytoskeleton proteins (18). Transmembrane proteins include occludin, claudin, and jam, while there are three kinds of cytoplasmic attachment proteins, namely, ZO-1, ZO-2, and ZO-3 (8).…”

Section: Discussionmentioning

confidence: 99%

Ruscogenin attenuated tight junction injury and tumor migration in colorectal liver metastasis mice via regulating TRAP1

Lv¹,

Wu²,

Chen³

et al. 2021

Transl Cancer Res TCR

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Background: The effect of ruscogenin on the colorectal cancer is not clear yet. The study was applied to elucidate the mechanism of ruscogenin on colorectal cancer via regulating tumor necrosis factor receptor related protein 1 (TRAP1).Methods: HCT-116 cells were inoculated under the spleen capsule to establish the colorectal liver metastasis model. The group was divided into control, inoculation model, low dose (5 mg/kg), mediate dose (10 mg/kg), and high dose ruscogenin (20 mg/kg). The body and liver weight of the animals and tumor nodules were recorded. Western blot analysis and immunofluorescence assay were applied to indicate the alternation of tight junction, migration, and proliferation proteins.Results: Following the inoculated with tumor cells, the mice in the inoculation group suffered from liver volume and weight decrease, as well as the increase of liver tumor volume (TV) and weight (TW). The administration of ruscogenin could obviously decrease body weight and increase liver weight in a dosedependent manner. Meanwhile, 5, 10, 20 mg/kg ruscogenin could reduce the acreage of tumor nodule on liver, while the high dose 20 mg/kg ruscogenin could minimize the growth of tumor nodule. The intervention of ruscogenin could relieve the decreased expression of claudin-5, occludin, and ZO-1. The administration of ruscogenin could relieve the aggravated tight junction injury by the overexpression of TRAP1, while 20 mg/kg ruscogenin could not alleviate the tight junction injury already defused by the TRAP1 antibody in the colorectal cancer mice.Conclusions: Ruscogenin could attenuate the tight junction injury via suppressing TRAP1 in the colorectal cancer mice.

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“…The PI3K/AKT signaling pathway is a key regulator involved in the metabolism, growth, proliferation and survival of cells, which can be activated by multiple receptors or proteins, including insulin, insulin-like growth factor-1, low-density lipoprotein-related receptor 1 and toll-like receptors (37)(38)(39). After being activated by insulin, the PI3K signaling pathway is involved primarily in energy metabolism in vivo.…”

Section: Discussionmentioning

confidence: 99%

CGA ameliorates cognitive decline by regulating the PI3K/AKT signaling pathway and neurotransmitter systems in rats with multi-infarct dementia

Wei

et al. 2020

Exp Ther Med

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Multi infarct dementia (MID) is a form of dementia that is preventable and treatable. However, at present, the drugs used in MID treatment were developed for Alzheimer's disease. While only a limited range of drugs is available, the incidence of MID is increasing year on year. The present study aimed to investigate the effect and underlying mechanisms of a combination of ginsenosides and astragalosides (CGA) on cognitive decline in rats with MID. A rat model of MID was established using micro-thromboembolism, and the behavioral changes in the rats were evaluated using the Morris water maze and open field tests at 60 days post-CGA intervention. The pathological morphology of the hippocampal CA1 area was observed using hematoxylin and eosin staining. The contents of ATP, ADP and AMP were determined using high-performance liquid chromatography. Mitochondrial swelling and changes in the membrane potential in the hippocampus were detected using flow cytometry, and the changes in insulin, glutamate and γ-aminobutyric acid (GABA) content were detected using ELISA. Additionally, the expression of PI3K and AKT proteins was detected using western blot analysis. In a rat model of MID, CGA shortened the escape latency, increased the frequency of platform crossing, improved the disordered vertebral cell arrangement and reduced the cell number in the hippocampal CA1 area. CGA also reduced the degree of mitochondrial swelling, increased the mitochondrial membrane potential, and elevated the energy load and ATP content in the brain of rats with MID. Furthermore, CGA increased the insulin content and upregulated the expression of PI3K and AKT in the brain of rats with MID. In addition, in the rat model of MID, CGA also enhanced the movement time and the frequency of standing, and decreased the concentration of glutamate and GABA in the brain tissue. Amelioration of the cognitive decline in rats with MID by CGA was associated with its regulatory effect on the PI3K/AKT signaling pathway and neurotransmitter systems.

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Myosin IIA Regulated Tight Junction in Oxygen Glucose-Deprived Brain Endothelial Cells Via Activation of TLR4/PI3K/Akt/JNK1/2/14-3-3ε/NF-κB/MMP9 Signal Transduction Pathway

Cited by 36 publications

References 40 publications

Comprehensive analysis of angiogenesis-related genes and pathways in early diabetic retinopathy

Comprehensive analysis of angiogenesis-related genes and pathways in early diabetic retinopathy

Ruscogenin attenuated tight junction injury and tumor migration in colorectal liver metastasis mice via regulating TRAP1

CGA ameliorates cognitive decline by regulating the PI3K/AKT signaling pathway and neurotransmitter systems in rats with multi-infarct dementia

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