scholarly journals Inflammation and oxidative stress in angiogenesis and vascular disease

2013 ◽  
Vol 91 (3) ◽  
pp. 323-328 ◽  
Author(s):  
Young-Woong Kim ◽  
Xiaoxia Z. West ◽  
Tatiana V. Byzova
Keyword(s):  
Oxidative Stress ◽  
Vascular Disease ◽  
And Oxidative Stress

Testosterone induces leucocyte migration by NADPH oxidase-driven ROS- and COX2-dependent mechanisms

2015 ◽  
Vol 129 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Andreia Z. Chignalia ◽  
Maria Aparecida Oliveira ◽  
Victor Debbas ◽  
Randal O. Dull ◽  
Francisco R.M. Laurindo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Risk ◽  
Cardiovascular Diseases ◽  
Nadph Oxidase ◽  
Vascular Disease ◽  
Leucocyte Migration ◽  
And Oxidative Stress

Testosterone triggers leucocyte migration and oxidative stress, important features in inflammation and in the development of cardiovascular diseases. The mechanisms by which testosterone increase cardiovascular risk are unknown. We describe one pathway whereby testosterone can potentially contribute to vascular disease.

scholarly journals Biomechanical Forces and Oxidative Stress: Implications for Pulmonary Vascular Disease

2019 ◽  
Vol 31 (12) ◽  
pp. 819-842 ◽  
Author(s):  
Evgeny A. Zemskov ◽  
Qing Lu ◽  
Wojciech Ornatowski ◽  
Christina N. Klinger ◽  
Ankit A. Desai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Disease ◽  
Pulmonary Vascular Disease ◽  
Biomechanical Forces ◽  
And Oxidative Stress

scholarly journals HIF-1α/JMJD1A signaling regulates inflammation and oxidative stress following hyperglycemia and hypoxia-induced vascular cell injury

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Min Zhao ◽  
Shaoting Wang ◽  
Anna Zuo ◽  
Jiaxing Zhang ◽  
Weiheng Wen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Vascular Disease ◽  
Expression Analysis ◽  
High Glucose ◽  
Gene Expression Analysis ◽  
Cell Counting ◽  
Histone Demethylases ◽  
Rna Seq ◽  
And Oxidative Stress

Abstract Background Endothelial cell (EC) injury accelerates the progression of diabetic macrovascular complications. Hypoxia is an important cause of EC injury. Hypoxia-inducible factor-1 alpha (HIF-1α) is an important hypoxia regulatory protein. Our previous studies showed that high-glucose and hypoxic conditions could upregulate HIF-1α expression and enhance EC inflammatory injury, independently of the nuclear factor kappa-B (NF-κB) pathway. However, it is not clear whether HIF-1α plays a role in vascular disease through epigenetic-related mechanisms. Methods We conducted gene expression analysis and molecular mechanistic studies in human umbilical vein endothelial cells (HUVECs) induced by hyperglycemia and hypoxia using RNA sequencing (RNA-seq) and small interfering HIF-1α (si-HIF-1α). We determined HIF-1α and Jumonji domain-containing protein 1 A (JMJD1A) expression by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot, analyzed inflammatory protein secretion in the cell supernatant by enzymelinked immunosorbent assay (ELISA), and assessed protein interaction between HIF-1α and JMJD1A by chromatin immunoprecipitation (Ch-IP). We used the Cell Counting Kit8 (CCK-8) assay to analyze cell viability, and assessed oxidative stress indicators by using a detection kit and flow cytometry. Results High glucose and hypoxia up-regulated HIF-1α expression, and down-regulated HIF-1α decreased the level of inflammation and oxidative stress in HUVECs. To determine the downstream pathways, we observed histone demethylases genes and related pathway by RNA-sEq. Among these, JMJD1A was the most upregulated gene in histone demethylases. Moreover, we observed that HIF-1α bound to the promoter of JMJD1A, and the ameliorative effects of si-HIF-1α on oxidative stress and inflammatory cytokines in high-glucose and hypoxia-induced HUVECs were reversed by JMJD1A overexpression. Furthermore, knockdown of JMJD1A decreased inflammatory and oxidative stress injury. To determine the JMJD1A-related factors, we conducted gene expression analysis on JMJD1A-knockdown HUVECs. We observed that downregulation of inflammation and the oxidative stress pathway were enriched and FOS and FOSB might be important protective transcription factors. Conclusions These findings provide novel evidence that the HIF-1α/JMJD1A signaling pathway is involved in inflammation and oxidative stress in HUVECs induced by high glucose and hypoxia. Also, this pathway might act as a novel regulator of oxidative stress and inflammatory-related events in response to diabetic vascular injury and thus contribute to the pathological progression of diabetes and vascular disease.

Association between calcitriol and paricalcitol with oxidative stress in patients with hemodialysis

2020 ◽  
pp. 1-8
Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Antioxidant Status ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Total Oxidant Status ◽  
Vitamin D Analog ◽  
Total Antioxidant ◽  
Oxidant Status ◽  
And Oxidative Stress

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.

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