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

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 Free hemoglobin induction of pulmonary vascular disease: evidence for an inflammatory mechanism

2012 ◽  
Vol 303 (4) ◽  
pp. L312-L326 ◽  
Author(s):  
Paul W. Buehler ◽  
Jin Hyen Baek ◽  
Christina Lisk ◽  
Ian Connor ◽  
Tim Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Disease ◽  
Vascular Remodeling ◽  
Pulmonary Vascular Disease ◽  
Wall Thickening ◽  
Sprague Dawley ◽  
Free Hemoglobin ◽  
Pulmonary Vessel ◽  
Pulmonary Arterial ◽  
No Bioavailability

Cell-free hemoglobin (Hb) exposure may be a pathogenic mediator in the development of pulmonary arterial hypertension (PAH), and when combined with chronic hypoxia the potential for exacerbation of PAH and vascular remodeling is likely more pronounced. We hypothesized that Hb may contribute to hypoxia-driven PAH collectively as a prooxidant, inflammatory, and nitric oxide (NO) scavenger. Using programmable micropump technology, we exposed male Sprague-Dawley rats housed under room air or hypoxia to 12 or 30 mg per day Hb for 3, 5, and 7 wk. Blood pressure, cardiac output, right ventricular hypertrophy, and indexes of pulmonary vascular remodeling were evaluated. Additionally, markers of oxidative stress, NO bioavailability and inflammation were determined. Hb increased pulmonary arterial (PA) pressure, pulmonary vessel wall stiffening, and right heart hypertrophy with temporal and dose dependence in both room air and hypoxic cohorts. Hb induced a modest increase in plasma oxidative stress markers (malondialdehyde and 4-hydroxynonenal), no change in NO bioavailability, and increased lung ICAM protein expression. Treatment with the antioxidant Tempol attenuated Hb-induced pulmonary arterial wall thickening, but not PA pressures or ICAM expression. Chronic exposure to low plasma Hb concentrations (range = 3–10 μM) lasting up to 7 wk in rodents induces pulmonary vascular disease via inflammation and to a lesser extent by Hb-mediated oxidation. Tempol demonstrated a modest effect on the attenuation of Hb-induced pulmonary vascular disease. NO bioavailability was found to be of minimal importance in this model.

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

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.

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