Azelnidipine, a new calcium channel blocker, inhibits endothelial inflammatory response by reducing intracellular levels of reactive oxygen species

2006 ◽  
Vol 546 (1-3) ◽  
pp. 11-18 ◽  
Author(s):  
Yuji Naito ◽  
Makoto Shimozawa ◽  
Hikori Manabe ◽  
Nami Nakabe ◽  
Kazuhiro Katada ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Inflammatory Response ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Reactive Oxygen ◽  
Oxygen Species

Co-regulation of Cxcl1 and versican in inflammatory response in UVB induced reactive oxygen species in the skin

2017 ◽  
Vol 86 (2) ◽  
pp. e80
Author(s):  
Chihiro Takemori ◽  
Makoto Kunisada ◽  
Flandiana Yogianti ◽  
Sugako Oka ◽  
Kunihiko Sakumi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Inflammatory Response ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Sergio Rius-Pérez ◽  
Isabel Torres-Cuevas ◽  
Iván Millán ◽  
Ángel L. Ortega ◽  
Salvador Pérez
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Inflammatory Response ◽  
Reactive Oxygen ◽  
High Energy ◽  
Low Grade ◽  
Oxygen Species ◽  
Antioxidant Genes ◽  
Integrative View

Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is a transcriptional coactivator described as a master regulator of mitochondrial biogenesis and function, including oxidative phosphorylation and reactive oxygen species detoxification. PGC-1α is highly expressed in tissues with high energy demands, and it is clearly associated with the pathogenesis of metabolic syndrome and its principal complications including obesity, type 2 diabetes mellitus, cardiovascular disease, and hepatic steatosis. We herein review the molecular pathways regulated by PGC-1α, which connect oxidative stress and mitochondrial metabolism with inflammatory response and metabolic syndrome. PGC-1α regulates the expression of mitochondrial antioxidant genes, including manganese superoxide dismutase, catalase, peroxiredoxin 3 and 5, uncoupling protein 2, thioredoxin 2, and thioredoxin reductase and thus prevents oxidative injury and mitochondrial dysfunction. Dysregulation of PGC-1α alters redox homeostasis in cells and exacerbates inflammatory response, which is commonly accompanied by metabolic disturbances. During inflammation, low levels of PGC-1α downregulate mitochondrial antioxidant gene expression, induce oxidative stress, and promote nuclear factor kappa B activation. In metabolic syndrome, which is characterized by a chronic low grade of inflammation, PGC-1α dysregulation modifies the metabolic properties of tissues by altering mitochondrial function and promoting reactive oxygen species accumulation. In conclusion, PGC-1α acts as an essential node connecting metabolic regulation, redox control, and inflammatory pathways, and it is an interesting therapeutic target that may have significant benefits for a number of metabolic diseases.

scholarly journals Identification of a Functional Peroxisome Proliferator-Activated Receptor Response Element in the Rat Catalase Promoter

2002 ◽  
Vol 16 (12) ◽  
pp. 2793-2801 ◽  
Author(s):  
Geoffrey D. Girnun ◽  
Frederick E. Domann ◽  
Steven A. Moore ◽  
Mike E. C. Robbins
Keyword(s):  
Reactive Oxygen Species ◽  
Transcription Factors ◽  
Inflammatory Response ◽  
Reactive Oxygen ◽  
Peroxisome Proliferator ◽  
Oxygen Species ◽  
Response Element ◽  
Peroxisome Proliferator Activated Receptor ◽  
Promoter Deletion Analysis

Abstract Peroxisomal proliferator-activated receptor (PPAR)γ has been shown to decrease the inflammatory response via transrepression of proinflammatory transcription factors. However, the identity of PPARγ responsive genes that decrease the inflammatory response has remained elusive. Because generation of the reactive oxygen species hydrogen peroxide (H2O2) plays a role in the inflammatory process and activation of proinflammatory transcription factors, we wanted to determine whether the antioxidant enzyme catalase might be a PPARγ target gene. We identified a putative PPAR response element (PPRE) containing the canonical direct repeat 1 motif, AGGTGA-A-AGTTGA, in the rat catalase promoter. In vitro translated PPARγ and retinoic X receptor-α proteins were able to bind to the catalase PPRE. Promoter deletion analysis revealed that the PPRE was functional, and a heterologous promoter construct containing a multimerized catalase PPRE demonstrated that the PPRE was necessary and sufficient for PPARγ-mediated activation. Treatment of microvascular endothelial cells with PPARγ ligands led to increases in catalase mRNA and activity. These results demonstrate that PPARγ can alter catalase expression; this occurs via a PPRE in the rat catalase promoter. Thus, in addition to transrepression of proinflammatory transcription factors, PPARγ may also be modulating catalase expression, and hence down-regulating the inflammatory response via scavenging of reactive oxygen species.

scholarly journals Association of Toll-Like Receptor Signaling and Reactive Oxygen Species: A Potential Therapeutic Target for Posttrauma Acute Lung Injury

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Meng Xiang ◽  
Janet Fan ◽  
Jie Fan
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Therapeutic Target ◽  
Major Trauma ◽  
Pulmonary Inflammation ◽  
Reactive Oxygen ◽  
Oxygen Species

Acute lung injury (ALI) frequently occurs in traumatic patients and serves as an important component of systemic inflammatory response syndrome (SIRS). Hemorrhagic shock (HS) that results from major trauma promotes the development of SIRS and ALI by priming the innate immune system for an exaggerated inflammatory response. Recent studies have reported that the mechanism underlying the priming of pulmonary inflammation involves the complicated cross-talk between Toll-like receptors (TLRs) and interactions between neutrophils (PMNs) and alveolar macrophages (AMϕ) as well as endothelial cells (ECs), in which reactive oxygen species (ROS) are the key mediator. This paper summarizes some novel mechanisms underlying HS-primed lung inflammation focusing on the role of TLRs and ROS, and therefore suggests a new therapeutic target for posttrauma ALI.

scholarly journals Calcium Ion Channels: Roles in Infection and Sepsis Mechanisms of Calcium Channel Blocker Benefits in Immunocompromised Patients at Risk for Infection

2018 ◽  
Vol 19 (9) ◽  
pp. 2465 ◽  
Author(s):  
John D’Elia ◽  
Larry Weinrauch
Keyword(s):  
Vitamin D ◽  
Ion Channels ◽  
Inflammatory Response ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Calcium Ion ◽  
Defense Mechanisms ◽  
Channel Blocker ◽  
Inadequate Response ◽  
Calcium Ion Channels

Immunosuppression may occur for a number of reasons related to an individual’s frailty, debility, disease or from therapeutic iatrogenic intervention or misadventure. A large percentage of morbidity and mortality in immunodeficient populations is related to an inadequate response to infectious agents with slow response to antibiotics, enhancements of antibiotic resistance in populations, and markedly increased prevalence of acute inflammatory response, septic and infection related death. Given known relationships between intracellular calcium ion concentrations and cytotoxicity and cellular death, we looked at currently available data linking blockade of calcium ion channels and potential decrease in expression of sepsis among immunosuppressed patients. Notable are relationships between calcium, calcium channel, vitamin D mechanisms associated with sepsis and demonstration of antibiotic-resistant pathogens that may utilize channels sensitive to calcium channel blocker. We note that sepsis shock syndrome represents loss of regulation of inflammatory response to infection and that vitamin D, parathyroid hormone, fibroblast growth factor, and klotho interact with sepsis defense mechanisms in which movement of calcium and phosphorus are part of the process. Given these observations we consider that further investigation of the effect of relatively inexpensive calcium channel blockade agents of infections in immunosuppressed populations might be worthwhile.

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