scholarly journals HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Yi Liu ◽  
Guo-Bin Zhuang ◽  
Xue-Zhi Zhou
Keyword(s):  
Current Knowledge ◽  
High Mobility ◽  
Retinal Cell ◽  
Ocular Diseases ◽  
Wide Range ◽  
Glycation End Products ◽  
Cell Layers ◽  
Proinflammatory Activity ◽  
And Migration ◽  
Proliferation And Migration

High-mobility group box 1 (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation, and migration in eye diseases. It induces signaling pathways by binding to the receptor for advanced glycation end products (RAGE) and Toll-like receptors (TLRs) 2, 4, and 9. This proinflammatory activity is considered to be important in the pathogenesis of a wide range of ocular diseases resulting from hemodynamic changes, presence of neovascular endothelial cells, secretion of intraocular immune factors or inflammation, and apoptosis of retinal cell layers. Further work is needed to elucidate in detail how HMGB1 contributes to ocular disease and how its damaging activity can be modulated. In this review, we summarize current knowledge on HMGB1 as a ligand that can evoke inflammation and immune responses in ocular diseases.

scholarly journals Paradoxical role of high mobility group box 1 in glioma: a suppressor or a promoter?

2017 ◽  
Author(s):  
Richard A. Seidu ◽  
Min Wu ◽  
Zhaoliang Su ◽  
Huaxi Xu
Keyword(s):  
Molecular Mechanisms ◽  
High Mobility ◽  
Treatment Resistance ◽  
High Mobility Group ◽  
Tissue Invasion ◽  
Self Sufficiency ◽  
Glycation End Products ◽  
And Migration ◽  
Proliferation And Migration

Gliomas represent 60% of primary intracranial brain tumors and 80% of all malignant types, with highest morbidity and mortality worldwide. Although glioma has been extensively studied, the molecular mechanisms underlying its pathology remain poorly understood. Clarification of the molecular mechanisms involved in their development and/or treatment resistance is highly required. High mobility group box 1 protein (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation and migration, through receptor for advanced glycation end products and toll like receptors in a number of cancers including gliomas. It is known that excessive release of HMGB1 in cancer leads to unlimited replicative potential, ability to develop blood vessels (angiogenesis), evasion of programmed cell death (apoptosis), self-sufficiency in growth signals, insensitivity to inhibitors of growth, inflammation, tissue invasion and metastasis. In this review we explore the mechanisms by which HMGB1 regulates apoptosis and autophagy in glioma. We also looked at how HMGB1 mediates glioma regression and promotes angiogenesis as well as possible signaling pathways with an attempt to provide potential therapeutic targets for the treatment of glioma.

scholarly journals Perivascular adipose tissue: more than just structural support

2011 ◽  
Vol 122 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Theodora Szasz ◽  
R. Clinton Webb
Keyword(s):  
Adipose Tissue ◽  
Current Knowledge ◽  
Vascular Biology ◽  
Biologically Active ◽  
Perivascular Adipose Tissue ◽  
Structural Support ◽  
Wide Range ◽  
And Migration ◽  
Obesity Hypertension ◽  
And Function

PVAT (perivascular adipose tissue) has recently been recognized as a novel factor in vascular biology, with implications in the pathophysiology of cardiovascular disease. Composed mainly of adipocytes, PVAT releases a wide range of biologically active molecules that modulate vascular smooth muscle cell contraction, proliferation and migration. PVAT exerts an anti-contractile effect in various vascular beds which seems to be mediated by an as yet elusive PVRF [PVAT-derived relaxing factor(s)]. Considerable progress has been made on deciphering the nature and mechanisms of action of PVRF, and the PVRFs proposed until now are reviewed here. However, complex pathways seem to regulate PVAT function and more than one mechanism is probably responsible for PVAT actions in vascular biology. The present review describes our current knowledge on the structure and function of PVAT, with a focus on its role in modulating vascular tone. Potential involvements of PVAT dysfunction in obesity, hypertension and atherosclerosis will be highlighted.

scholarly journals Advanced Glycation End Products Induce Proliferation and Migration of Human Aortic Smooth Muscle Cells through PI3K/AKT Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Gang Yuan ◽  
Guangyan Si ◽  
Qingchun Hou ◽  
Zhaonan Li ◽  
Kaiqiang Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Akt Pathway ◽  
Advanced Glycation ◽  
Cell Proliferation And Migration ◽  
Glycation End Products ◽  
And Migration ◽  
Proliferation And Migration

Advanced glycation end products (AGEs) have been widely regarded as an important inducing factor in the pathogenesis of diabetic arteriosclerosis, and the proliferation and migration of vascular smooth muscle cells (VSMCs) are also involved in this process. However, it is not clear whether AGEs promote atherosclerosis by inducing the proliferation and migration of VSMCs. To figure out this question, this study investigated the effects of AGEs on the proliferation and migration of human aorta vascular smooth muscle cells (HASMCs) and the underlying mechanisms. This study evaluated the effects of different concentrations of AGEs on cell proliferation and migration. CCK8, transwell, and western blotting assays demonstrated that AGEs significantly increased cell proliferation and migration in a concentration-dependent manner and that the optimal proproliferative and promigratory concentrations of AGEs were 10 mg/L and 20 mg/L, respectively. AGE-induced cell proliferation, migration, and expression of filament actin (F-actin) were markedly attenuated by a PI3K inhibitor (LY2940002). Additionally, the phosphorylation of AKT was reduced when the receptor of advanced glycation end product (RAGE) gene was silenced by lentivirus transfection, which led to a concomitant reduction of the expression of proliferation and migration-related proteins. These data indicate that AGEs may activate the PI3K/AKT pathway through RAGE and thus facilitate the proliferation and migration of HASMCs.

scholarly journals SOX15 regulates proliferation and migration of endometrial cancer cells

2017 ◽  
Vol 37 (5) ◽  
Author(s):  
Xiaohui Rui ◽  
Yun Xu ◽  
Xiping Jiang ◽  
Caixia Guo ◽  
Jingting Jiang
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
High Mobility ◽  
Down Regulation ◽  
Ishikawa Cell ◽  
Migration Assay ◽  
Ec Cells ◽  
And Migration ◽  
Low Expression ◽  
Proliferation And Migration

The study aimed to investigate the effects of Sry-like high mobility group box 15 (SOX15) on proliferation and migration of endometrial cancer (EC) cells. Immunohistochemistry (IHC) was applied to determine the expression of SOX15 in EC tissues and adjacent tissues. We used cell transfection method to construct the HEC-1-A and Ishikawa cell lines with stable overexpression and low expression SOX15. Reverse-transcription quantitative real-time PCR (RT-qPCR) and Western blot were performed to examine expression of SOX15 mRNA and SOX15 protein, respectively. By conducting a series of cell proliferation assay and migration assay, we analyzed the influence of SOX15 overexpression or low expression on EC cell proliferation and migration. The expression of SOX15 mRNA and protein in EC tissues was significantly lower than that in adjacent tissues. After lentivirus-transfecting SOX15, the expression level of SOX15 mRNA and protein was significantly increased in cells of SOX15 group, and decreased in sh-SOX15 group. Overexpression of SOX15 could suppress cell proliferation, while down-regulation of SOX15 increased cell proliferation. Flow cytometry results indicated that overexpression of SOX15 induced the ratio of cell-cycle arrest in G1 stage. In addition, Transwell migration assay results showed that SOX15 overexpression significantly inhibited cell migration, and also down-regulation of SOX15 promoted the migration. As a whole, SOX15 could regulate the proliferation and migration of EC cells and up- regulation of SOX15 could be valuable for EC treatment.

Sign in / Sign up

Export Citation Format

Share Document