POLYAMINE REGULATORY PROCESSES AND OXIDATIVE STRESS IN MONOCROTALINE-TREATED PULMONARY ARTERY ENDOTHELIAL CELLS

[Ca2+]i (cytosolic [Ca2+]) and OS (oxidative stress) were measured simultaneously in calf pulmonary artery endothelial cells using fura-2 and carboxy-2´,7´-dichlorodihydrofluorescein. ATP stimulated a [Ca2+]i increase that was followed a few seconds later by an increase in OS. Pre-exposure to 5 μM H2O2 potentiated these responses to ATP. Elevating or removing extracellular Ca2+ increased or reduced the [Ca2+]i response to ATP and caused parallel changes in the OS response, suggesting that this response was a consequence of the [Ca2+]i response. Inhibition of mitochondria with rotenone or antimycin A affected the responses but not in a manner that allowed a simple interpretation of the role of mitochondria. These data show an initimate connection between [Ca2+]i and OS that can be modulated by low levels of exogenously applied OS, allowing the possibility of positive feedback.

Download Full-text

Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

Journal of Immunology Research ◽

10.1155/2021/2389029 ◽

2021 ◽

Vol 2021 ◽

pp. 1-10

Author(s):

Haijun Zhao ◽

Yanhui He

Keyword(s):

Oxidative Stress ◽

Stem Cells ◽

Bone Marrow ◽

Endothelial Cells ◽

Inflammatory Response ◽

Protective Effects ◽

Stress Injury ◽

Oxidative Stress Injury ◽

Marrow Mesenchymal Stem Cells ◽

And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

Download Full-text

New Perspectives of S-Adenosylmethionine (SAMe) Applications to Attenuate Fatty Acid-Induced Steatosis and Oxidative Stress in Hepatic and Endothelial Cells

Molecules ◽

10.3390/molecules25184237 ◽

2020 ◽

Vol 25 (18) ◽

pp. 4237 ◽

Cited By ~ 1

Author(s):

Laura Vergani ◽

Francesca Baldini ◽

Mohamad Khalil ◽

Adriana Voci ◽

Pietro Putignano ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Fatty Acid ◽

Lipid Accumulation ◽

Endothelium Dysfunction ◽

Beneficial Effects ◽

Mitochondrial Fatty Acid ◽

Oxidant Production ◽

Pleiotropic Functions ◽

And Oxidative Stress

S-adenosylmethionine (SAMe) is an endogenous methyl donor derived from ATP and methionine that has pleiotropic functions. Most SAMe is synthetized and consumed in the liver, where it acts as the main methylating agent and in protection against the free radical toxicity. Previous studies have shown that the administration of SAMe as a supernutrient exerted many beneficial effects in various tissues, mainly in the liver. In the present study, we aimed to clarify the direct effects of SAMe on fatty acid-induced steatosis and oxidative stress in hepatic and endothelial cells. Hepatoma FaO cells and endothelial HECV cells exposed to a mixture of oleate/palmitate are reliable models for hepatic steatosis and endothelium dysfunction, respectively. Our findings indicate that SAMe was able to significantly ameliorate lipid accumulation and oxidative stress in hepatic cells, mainly through promoting mitochondrial fatty acid entry for β-oxidation and external triglyceride release. SAMe also reverted both lipid accumulation and oxidant production (i.e., ROS and NO) in endothelial cells. In conclusion, these outcomes suggest promising beneficial applications of SAMe as a nutraceutical for metabolic disorders occurring in fatty liver and endothelium dysfunction.

Download Full-text

Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/2304018 ◽

2019 ◽

Vol 2019 ◽

pp. 1-14 ◽

Cited By ~ 8

Author(s):

Dehai Xian ◽

Jing Song ◽

Lingyu Yang ◽

Xia Xiong ◽

Rui Lai ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Growth Factors ◽

Molecular Mechanisms ◽

Capillary Tube ◽

Proteolytic Enzymes ◽

Skin Tumor ◽

Antioxidant Systems ◽

Antiangiogenic Factors ◽

And Oxidative Stress

Angiogenesis is the process of new vessel formation, which sprouts from preexisting vessels. This process is highly complex and primarily involves several key steps, including stimulation of endothelial cells by growth factors, degradation of the extracellular matrix by proteolytic enzymes, migration and proliferation of endothelial cells, and capillary tube formation. Currently, it is considered that multiple cytokines play a vital role in this process, which consist of proangiogenic factors (e.g., vascular endothelial growth factor, fibroblast growth factors, and angiopoietins) and antiangiogenic factors (e.g., endostatin, thrombospondin, and angiostatin). Angiogenesis is essential for most physiological events, such as body growth and development, tissue repair, and wound healing. However, uncontrolled neovascularization may contribute to angiogenic disorders. In physiological conditions, the above promoters and inhibitors function in a coordinated way to induce and sustain angiogenesis within a limited period of time. Conversely, the imbalance between proangiogenic and antiangiogenic factors could cause pathological angiogenesis and trigger several diseases. With insights into the molecular mechanisms of angiogenesis, increasing reports have shown that a close relationship exists between angiogenesis and oxidative stress (OS) in both physiological and pathological conditions. OS, an imbalance between prooxidant and antioxidant systems, is a cause and consequence of many vascular complains and serves as one of the biomarkers for these diseases. Furthermore, emerging evidence supports that OS and angiogenesis play vital roles in many dermatoses, such as psoriasis, atopic dermatitis, and skin tumor. This review summarizes recent findings on the role of OS as a trigger of angiogenesis in skin disorders, highlights newly identified mechanisms, and introduces the antiangiogenic and antioxidant therapeutic strategies.

Download Full-text