Inhibition of high-mobility group box 1 expression by siRNA in rat hepatic stellate cells

Ge, Wensong

doi:10.3748/wjg.v17.i36.4090

Cited by 37 publications

(27 citation statements)

References 35 publications

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“…To measure cell proliferation, the CM in each 96-well plate was changed to serum-free conditions after 24 h of seeding, and MTT (Invitrogen) assay was performed after different conditional treatments. MTT assay was performed at the end of each treatment following routine procedure (35). The experiment was repeated six times to ensure data reproducibility.…”

Section: Mtt Assay To Assess Cell Viabilitymentioning

confidence: 99%

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Jiang¹,

Cai

Zhu

et al. 2014

The Journal of Immunology

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High mobility group box 1 (HMGB1) plays an important role in the pathologic processes of endothelial permeability under oxidative stress. Trophoblast oxidative stress has been implicated in the pathophysiology of preeclampsia (PE). HMGB1 serum levels are increased in PE. However, the potential roles of HMGB1 in endothelial permeability in PE remain unclear. We assessed the effects of the hypoxic trophoblast on the permeability of the endothelial monolayer. Our results showed that the hypoxic trophoblast displayed higher HMGB1 mRNA, intracellular HMGB1 protein, and HMGB1 in conditioned medium than those of the normoxic trophoblast did. The hypoxic trophoblast conditioned medium increased the endothelial monolayer permeability and increased TLR 4 and caveolin-1 (CAV-1) protein expression in endothelial cells, which was inhibited by glycyrrhizic acid and HMGB1 small interfering RNA transfection to trophoblasts before hypoxia. The increased endothelial permeability induced by hypoxic trophoblast conditioned medium could be inhibited with TLR4 or CAV-1 gene silencing in endothelial cells. Immunoprecipitation showed that CAV-1 and TLR4 are colocalized in HUVECs and C57BL/6 mouse kidney. TLR4 small interfering RNA suppressed CAV-1 protein expression in endothelial cells upon stimulation of hypoxic trophoblast conditioned medium or HMGB1. We conclude that hypoxic trophoblasts play an important role in the mechanism of general edema (including protein urine) in PE via increasing endothelial monolayer permeability through the HMGB1/TLR4/CAV-1 pathway.

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Section: Mtt Assay To Assess Cell Viabilitymentioning

confidence: 99%

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Jiang¹,

Cai

Zhu

et al. 2014

The Journal of Immunology

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“…In a rat model of hepatic fibrosis, the level of HMGB1 is upregulated, and its expression is closely correlated with the deposition of collagen. Suppression of HMGB1 expression by small interfering RNA (siRNA) significantly inhibits synthesis of α-SMA and collagen (types I and III) in HSCs (71). In addition, HMGB1 released during the rejection phase of orthotropic liver transplantation has the ability to activate HSCs and exhibit profibrogenic effects on liver grafts (70).…”

Section: Hmgb1 and Liver Fibrosismentioning

confidence: 99%

Emerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases

Chen

Hou

Zhang

et al. 2013

Mol Med

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Damage-associated molecular pattern (DAMP) molecules are essential for the initiation of innate inflammatory responses to infection and injury. The prototypic DAMP molecule, high-mobility group box 1 (HMGB1), is an abundant architectural chromosomal protein that has location-specific biological functions: within the nucleus as a DNA chaperone, within the cytosol to sustain autophagy and outside the cell as a DAMP molecule. Recent research indicates that aberrant activation of HMGB1 signaling can promote the onset of inflammatory and autoimmune diseases, raising interest in the development of therapeutic strategies to control their function. The importance of HMGB1 activation in various forms of liver disease in relation to liver damage, steatosis, inflammation, fibrosis, tumorigenesis and regeneration is discussed in this review.

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“…Cell stress can trigger passive or active release of HMGB1 by lung immune cells, bronchial and alveolar type II epithelial cells, fibroblasts, and airway smooth muscle (ASM) cells (2,14,25). Extracellular HMGB1 induces the release of ECM proteins (17), can modulate integrin function (6), promotes airway remodeling (36), and contributes to bleomycin-induced lung fibrosis in mice (22).…”

mentioning

confidence: 99%

High-mobility group box 1 promotes extracellular matrix synthesis and wound repair in human bronchial epithelial cells

Ojo

Ryu

Jha

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Ojo OO, Ryu MH, Jha A, Unruh H, Halayko AJ. High-mobility group box 1 promotes extracellular matrix synthesis and wound repair in human bronchial epithelial cells. Am J Physiol Lung Cell Mol Physiol 309: L1354 -L1366, 2015. First published October 2, 2015; doi:10.1152/ajplung.00054.2015.-High mobility group box 1 (HMGB1) is a damage-associated molecular pattern (DAMP) protein that binds Toll-like receptors (e.g., TLR4) and the receptor for advanced glycated end products (RAGE). The direct effects of HMGB1 on airway structural cells are not fully known. As epithelial cell responses are fundamental drivers of asthma, including abnormal repair-restitution linked to changes in extracellular matrix (ECM) synthesis, we tested the hypothesis that HMGB1 promotes bronchial epithelial cell wound repair via TLR4 and/or RAGE signaling that regulates ECM (fibronectin and the ␥2-chain of laminin-5) and integrin protein abundance. To assess impact of HMGB1 we used molecular and pharmacological inhibitors of RAGE or TLR4 signaling in scratch wound, immunofluorescence, and immunoblotting assays to assess wound repair, ECM synthesis, and phosphorylation of intracellular signaling. HMGB1 increased wound closure, and this effect was attenuated by blocking RAGE and TLR4 signaling. HMGB1-induced fibronectin and laminin-5 (␥2 chain) was diminished by blocking RAGE and/or blunting TLR4 signaling. Similarly, induction of ␣3-integrin receptor for fibronectin and laminin-5 was also diminished by blocking TLR4 signaling and RAGE. Lastly, rapid and/or sustained phosphorylation of SMAD2, ERK1/2, and JNK signaling modulated HMGB1-induced wound closure. Our findings suggest a role for HMGB1 in human airway epithelial cell repair and restitution via multiple pathways mediated by TLR4 and RAGE that underpin increased ECM synthesis and modulation of cell-matrix adhesion.

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Inhibition of high-mobility group box 1 expression by siRNA in rat hepatic stellate cells

Abstract: This study suggests a significant fun-ctional role for HMGB1 in the development of liver fibrosis. It also demonstrates that downregulation of HMGB1 expression might be a potential strategy to treat liver fibrosis.

Cited by 37 publications

References 35 publications

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Emerging Role of High-Mobility Group Box 1 (HMGB1) in Liver Diseases

High-mobility group box 1 promotes extracellular matrix synthesis and wound repair in human bronchial epithelial cells

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