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  • Open Access

    COMMENTARY

    Retinal Focus on Relationships between Diet-Induced, Advanced Glycation End Products and Supplemental Estradiol

    Nicholas T. Bello1, Bonnie L. Firestein2, Maribel Vazquez3,*

    BIOCELL, Vol.49, No.3, pp. 349-354, 2025, DOI:10.32604/biocell.2025.061810 - 31 March 2025

    Abstract Neurodegeneration of retinal tissue leads to progressive vision loss in millions of working-age adults each year. Metabolic alterations caused by modern diets that are high in fats and sugars contribute to the development of diabetic retinopathy. Chronic, diet-induced metabolic changes are linked to high glucose and harmful, pro-inflammatory compounds in the blood, called advanced glycation end products (AGEs), that can alter the integrity of neurovascular barriers. AGEs-induced changes to the permeability of the inner blood-retinal barrier can lead to progressive vision loss with disparate impacts in patients with low estrogen, such as via natural aging More >

  • Open Access

    REVIEW

    Effect of proinflammatory cytokines on blood-brain barrier integrity

    Małgorzata Gryka-Marton, Anna Grabowska, Dariusz Szukiewicz

    European Cytokine Network, Vol.35, No.3, pp. 38-47, 2024, DOI:10.1684/ecn.2024.0498

    Abstract The blood-brain barrier (BBB) consists of a unique system of brain microvascular endothelial cells, capillary basement membranes, and terminal branches (“end-feet”) of astrocytes. The BBB’s primary function is to protect the central nervous system from potentially harmful or toxic substances in the bloodstream by selectively controlling the entry of cells and molecules, including nutrients and immune system components. During neuroinflammation, the BBB loses its integrity, resulting in increased permeability, mostly due to the activity of inflammatory cytokines. However, the pathomechanism of structural and functional changes in the BBB caused by individual cytokines is poorly understood.… More >

  • Open Access

    ARTICLE

    Integrated Bioinformatics Analysis Identifies Vascular Endothelial Cell-Related Biomarkers for Hypertrophic Cardiomyopathy

    Ying Wang1, Weijun Zhang1, Fei Cai1, Yong Tao2,*

    Congenital Heart Disease, Vol.19, No.6, pp. 653-669, 2024, DOI:10.32604/chd.2025.060406 - 27 January 2025

    Abstract Background: Previous studies combined integrated scRNA-seq with bulk RNA data to screen biomarkers for cardiomyopathy. This study extended this approach to identify biomarkers specific for hypertrophic cardiomyopathy (HCM). Methods: Datasets GSE36961, GSE130036, GSE249925 and GSE203274 were analyzed in this study. ScRNA-seq analysis was employed to identify distinct cell populations. Differentially expression analysis was conducted to screen vascular endothelial cells (VECs)-related feature genes. After calculating VECs score, WGCNA was used to correlate gene modules with the VECs score. Key HCM biomarkers were determined using random forest analysis, and LASSO regression analyses to construct a diagnostic model… More >

  • Open Access

    ARTICLE

    MiR-30a-5p alleviates LPS-induced HPMEC injury through regulation of autophagy via Beclin-1

    RAN PAN1,#, JIAYAN MAO2,#, YUELIANG ZHENG3, WEI CHEN2, JUNPING GUO1,*, LIJUN WANG3,*

    BIOCELL, Vol.48, No.3, pp. 431-441, 2024, DOI:10.32604/biocell.2023.046484 - 15 March 2024

    Abstract Background: Sepsis, a type of systemic disease, can impact nearly all organs, tissues and cells. Among them, endothelial cells are amongst the first to be affected and respond to the insult. In this study, we investigated the protective effects of microRNA-30a-5p (miR-30a-5p) on human pulmonary microvascular endothelial cells (HPMECs) treated with lipolysaccharide (LPS). Methods: An in vitro model of sepsis was established in HPMECs with the use of LPS. Transfecting with different tools (mimetic and inhibitor) to modify miR-30a-5p expression. Cell viability, proliferation and apoptosis were detected by the CCK-8 assay, the EdU kit and fluorescence… More >

  • Open Access

    ARTICLE

    Gastric cancer secreted miR-214-3p inhibits the anti-angiogenesis effect of apatinib by suppressing ferroptosis in vascular endothelial cells

    WEIXUE WANG#, TONGTONG WANG#, YAN ZHANG, TING DENG, HAIYANG ZHANG*, YI BA*

    Oncology Research, Vol.32, No.3, pp. 489-502, 2024, DOI:10.32604/or.2023.046676 - 06 February 2024

    Abstract Different from necrosis, apoptosis, autophagy and other forms of cell death, ferroptosis is a mechanism that catalyzes lipid peroxidation of polyunsaturated fatty acids under the action of iron divalent or lipoxygenase, leading to cell death. Apatinib is currently used in the third-line standard treatment of advanced gastric cancer, targeting the anti-angiogenesis pathway. However, Apatinib-mediated ferroptosis in vascular endothelial cells has not been reported yet. Tumor-secreted exosomes can be taken up into target cells to regulate tumor development, but the mechanism related to vascular endothelial cell ferroptosis has not yet been discovered. Here, we show that More >

  • Open Access

    ARTICLE

    Single-Cell RNA Sequencing Reveals Potential for Endothelial-to-Mesenchymal Transition in Tetralogy of Fallot

    Aisa Zulibiya1,2,#, Jing Wen3,#, Huiqing Yu3,#, Xiaoming Chen3, Lei Xu3, Xiao Ma1,2, Baojian Zhang1,2,*

    Congenital Heart Disease, Vol.18, No.6, pp. 611-625, 2023, DOI:10.32604/chd.2023.047689 - 19 January 2024

    Abstract Background: Tetralogy of Fallot (TOF) is a very common cyanotic congenital heart disease. Endothelial-to-mesenchymal transition (EndoMT) is recognized as a physiological mechanism involved in embryonic heart development and endothelial formation. However, there is still a gap in the reports related to the mechanism of EndoMT development in TOF. Methods: First, transcriptomic data of single cell nuclei of TOF and Donor were obtained based on the Gene Expression Omnibus (GEO) database, and the data were normalized and clustered by dimensionality reduction using the Seurat package. Subsequently, differentially expressed genes (DEGs) between TOF and Donor were screened… More >

  • Open Access

    ARTICLE

    Inhibition of VEGF-A expression in hypoxia-exposed fetal retinal microvascular endothelial cells by exosomes derived from human umbilical cord mesenchymal stem cells

    JING LI1,2, WANWAN FAN4, LILI HAO1, YONGSHENG LI5, GUOCHENG YU1, WEI SUN6, XIANQIONG LUO2,*, JINGXIANG ZHONG1,3,*

    BIOCELL, Vol.47, No.11, pp. 2485-2494, 2023, DOI:10.32604/biocell.2023.044177 - 27 November 2023

    Abstract Objective: This study aimed to investigate the potential of human umbilical cord mesenchymal stem cell (hucMSC)-derived exosomes (hucMSC-Exos) in inhibiting hypoxia-induced cell hyper proliferation and overexpression of vascular endothelial growth factor A (VEGF-A) in immature human fetal retinal microvascular endothelial cells (hfRMECs). Methods: Exosomes were isolated from hucMSCs using cryogenic ultracentrifugation and characterized through various techniques, including transmission electron microscopy, nanoparticle tracking analysis, bicinchoninic acid assays, and western blotting. The hfRMECs were identified using von Willebrand factor (vWF) co-staining and divided into four groups: a control group cultured under normoxic condition, a hypoxic model group, a hypoxic… More > Graphic Abstract

    Inhibition of VEGF-A expression in hypoxia-exposed fetal retinal microvascular endothelial cells by exosomes derived from human umbilical cord mesenchymal stem cells

  • Open Access

    Anisodine hydrobromide alleviates oxidative stress caused by hypoxia/reoxygenation in human cerebral microvascular endothelial cells predominantly via inhibition of muscarinic acetylcholine receptor 4

    WENLI JIANG1,#, JUNYI SHEN1,#, XIAOQIANG DU1,#, YAN QIU1, JIAN ZHONG1, ZHI OUYANG1, BINGMEI M. FU2, YE ZENG1,*

    BIOCELL, Vol.47, No.10, pp. 2255-2263, 2023, DOI:10.32604/biocell.2023.030880 - 08 November 2023

    Abstract Background: Anisodine hydrobromide (AT3), an anti-cholinergic agent, could be delivered to the brain across the blood-brain barrier and has been used clinically for the treatment of cerebral ischemia/reperfusion injury. Endothelial dysfunction can be caused by hypoxia/reoxygenation (H/R) via oxidative stress and metabolic alterations. The present study investigated whether AT3 regulates the production of nitric oxide (NO) and reactive oxygen species (ROS), and the HIF-1α pathway via regulation of muscarinic acetylcholine receptors (mAChRs) in brain microvascular endothelial cells after H/R exposure. Methods: Under H/R conditions, hCMEC/D3 cerebral microvascular endothelial cells were treated with AT3. Specific inhibitors… More > Graphic Abstract

    Anisodine hydrobromide alleviates oxidative stress caused by hypoxia/reoxygenation in human cerebral microvascular endothelial cells predominantly via inhibition of muscarinic acetylcholine receptor 4

  • Open Access

    ARTICLE

    In vitro study of emodin-induced nephrotoxicity in human renal glomerular endothelial cells on a microfluidic chip

    ZHUO YANG#, WEN QIN#, DI CHEN, JUNSHENG HUO, JINGBO WANG, LIYUAN WANG, QIN ZHUO, JIYONG YIN*

    BIOCELL, Vol.47, No.1, pp. 125-131, 2023, DOI:10.32604/biocell.2023.022937 - 26 September 2022

    Abstract Emodin is an effective component of rhubarb with positive pharmacological effects on human health. However, it is also toxic to different cells or tissues to varying degrees. The effects of emodin on glomerular endothelial cells (GECs) remain to be tested, and the documented works were always performed in vitro and hardly reflect the real physiological situation. To study the effects of emodin on GECs in a biomimetic environment, we utilized a microfluidic chip to assess the physiological reaction of human renal glomerular endothelial cells to various concentrations of emodin in this work. The results showed that More >

  • Open Access

    ARTICLE

    Acetylcholine suppresses LPS-induced endothelial cell activation by inhibiting the MAPK and NF-κB pathways

    Ping Li1,2,*, Kewen Zhou2,*, Jiehao Li2, Xiaodan Xu2, Ling Wang2, Tinghuai Wang2

    European Cytokine Network, Vol.33, No.4, pp. 79-89, 2022, DOI:10.1684/ecn.2023.0481

    Abstract Background and Objective: Endothelial cell activation plays a critical role in leukocyte recruitment during inflammation and infection. We previously found that cholinergic stimulation (via vagus nerve stimulation) attenuates vascular endothelial impairment and reduces the inflammatory profile in ovariectomized rats. However, the specific molecular mechanism is unclear. This study was designed to explore the effects and molecular mechanisms of cholinergic agonists (acetylcholine [ACh]) on lipopolysaccharide (LPS)-induced endothelial cell activation in vitro. Methods: Human umbilical vein endothelial cells (HUVECs) were treated with different concentrations of LPS (10/100/1000 ng/mL) to activate endothelial cells. HUVECs were untreated, treated with ACh (10⁻⁵More >

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