Relationship between calcium release and NADPH oxidase inhibition in human neutrophils

Salmon, Michael D.; Ahluwalia, Jatinder

doi:10.1016/j.bbrc.2009.04.079

Cited by 8 publications

(5 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This result is consistent with the literature showing that NOX5-␤, NOX5-␦, and NOX5-S are mainly localized at ER in human endothelial cells (5). It has been shown that potent NADPH oxidase inhibitors apocynin and diphenyleneiodonium inhibit N-formyl-L-methionyl-Lleucyl-L-phenylalanine-mediated cytosolic Ca 2ϩ release in human neutrophils (38). In human endothelial cells, NA-DPH oxidase-derived H 2 O 2 increases the sensitivity of intracellular Ca 2ϩ stores to inositol 1,4,5-trisphosphate (22).…”

Section: Discussionsupporting

confidence: 93%

Role of Rac1 in regulation of NOX5-S function in Barrett's esophageal adenocarcinoma cells

Hong

Resnick

Behar³

et al. 2011

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

We have shown that a novel NADPH oxidase isoform, NOX5-S, is the major isoform of NADPH oxidases in an esophageal adenocarcinoma (EA) cell line, FLO, and is overexpressed in Barrett's mucosa with high-grade dysplasia. NOX5-S is responsible for acid-induced reactive oxygen species production. In this study, we found that mRNA levels of NOX5-S were significantly higher in FLO EA cells than in the normal human esophageal squamous cell line HET-1A or in a Barrett cell line, BAR-T. The mRNA levels of NOX5-S were also significantly increased in EA tissues. The data suggest that NOX5-S may be important in the development of EA. Mechanisms of functional regulation of NOX5-S are not fully understood. We show that small G protein Rac1 was present in HET-1A cells, BAR-T cells, and EA cell lines FLO and OE33. Rac1 protein levels were significantly higher in FLO and OE33 cells than in HET-1A or BAR-T cells. Knockdown of Rac1 with Rac1 small interfering RNA significantly decreased acid-induced increase in H2O2 production in FLO EA cells. Overexpression of constitutively active Rac1 significantly increased H2O2 production, an increase that was blocked by knockdown of NOX5-S. By immunofluorescence staining and immunoprecipitation, we found that NOX5-S was present in the cytosol of FLO EA cells and colocalized with Rac1 and SERCA1/2 Ca 2ϩ -ATPase which is located in the endoplasmic reticulum membrane. We conclude that Rac1 may be important in activation of NOX5-S in FLO EA cells.Barrett's esophagus; SERCA1/2 Ca 2ϩ -ATPase ESOPHAGEAL ADENOCARCINOMA (EA) has increased in incidence over the past four decades (6, 39). It is characterized by a poor prognosis, with a median survival time following diagnosis of Ͻ18 mo, and a 5-yr survival rate of Ͻ20% in operable tumors (44). The major risk factor for EA is gastroesophageal reflux disease (GERD) complicated by Barrett's esophagus (BE) (26). Approximately 10% of GERD patients develop BE where esophageal squamous epithelium damaged by acid reflux is replaced by a metaplastic, intestinal type epithelium. The specialized intestinal metaplasia is associated with a 30-to 125-fold increased risk for the development of esophageal adenocarcinoma, with an estimated cancer incidence of about 0.5-1.0% per year, i.e., one cancer per 100 -200 patients for each year of observation (14,16,49). A middle-aged individual with BE for 20 yr or more has an estimated 10 -20% lifetime risk of developing esophageal adenocarcinoma, which is similar to the risk of lung cancer among heavy smokers or of liver cancer among chronic hepatitis B virus carriers (49). However, the mechanisms responsible for the progression from metaplasia to adenocarcinoma are not known. Acid reflux may play an important role in the progression from metaplasia to dysplasia and to adenocarcinoma in patients with BE because of the following: 1) cultured biopsy specimens of intestinal metaplastic cells demonstrate a significant increase in tritiated thymidine uptake when explants are briefly exposed to acid (21); 2) long-term inhibition of...

show abstract

Section: Discussionsupporting

confidence: 93%

Role of Rac1 in regulation of NOX5-S function in Barrett's esophageal adenocarcinoma cells

Hong

Resnick

Behar³

et al. 2011

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

show abstract

“…If Ca 2+ and ROS represent the two most vital second messengers used by a cell in response to both intra- and extracellular signals, their interplay forms a critical cell network involved in virtually every aspect of cellular physiology ( Yan et al, 2006 ; Hidalgo and Donoso, 2008 ; Gorlach et al, 2015 ). On the one hand, Ca 2+ signals modulate the production of ROS by stimulating the Krebs cycle and oxidative phosphorylation in mitochondria ( Brookes et al, 2004 ), and by regulating NADPH oxidases at the endoplasmic and plasma membranes ( Jiang and Zhang, 2003 ; Kobayashi et al, 2007 ; Salmon and Ahluwalia, 2009 ). On the other hand, ROS signals regulate the activity of several Ca 2+ channels and transporters ( Poteser et al, 2006 ; Takahashi and Mori, 2011 ; Bogeski et al, 2012 ; Nikolaienko et al, 2018 ; Schmidt et al, 2019 ).…”

Section: Trpm2—the Master Of Ca 2+ and Ros Signali...mentioning

confidence: 99%

TRPM2: bridging calcium and ROS signaling pathways—implications for human diseases

Maliougina

Hiani

2023

Front. Physiol.

View full text Add to dashboard Cite

TRPM2 is a versatile and essential signaling molecule that plays diverse roles in Ca2+ homeostasis and oxidative stress signaling, with implications in various diseases. Research evidence has shown that TRPM2 is a promising therapeutic target. However, the decision of whether to activate or inhibit TRPM2 function depends on the context and specific disease. A deeper understanding of the molecular mechanisms governing TRPM2 activation and regulation could pave the way for the development of innovative therapeutics targeting TRPM2 to treat a broad range of diseases. In this review, we examine the structural and biophysical details of TRPM2, its involvement in neurological and cardiovascular diseases, and its role in inflammation and immune system function. In addition, we provide a comprehensive overview of the current knowledge of TRPM2 signaling pathways in cancer, including its functions in bioenergetics, oxidant defense, autophagy, and response to anticancer drugs.

show abstract

“…In these cells, increases in intracellular calcium [Ca 2+ ] i can induce several physiological responses. It is well established that several pro-inflammatory agonists such as N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP), platelet activating factor (PAF), and leukotriene B4 (LTB 4 ) cause a transitory increase in [Ca 2+ ] i , followed by a more sustained influx of Ca 2+ in human neutrophils [1]. Despite the recognition that a rise in [Ca 2+ ] i seems to be a vital link in the activation of neutrophils in response to these agonists, the precise mechanisms that are responsible for this remain nebulous.…”

Section: Introductionmentioning

confidence: 99%

Pharmacology of receptor operated calcium entry in human neutrophils

Salmon

Ahluwalia

2011

International Immunopharmacology

Self Cite

View full text Add to dashboard Cite

Relationship between calcium release and NADPH oxidase inhibition in human neutrophils

Cited by 8 publications

References 25 publications

Role of Rac1 in regulation of NOX5-S function in Barrett's esophageal adenocarcinoma cells

Role of Rac1 in regulation of NOX5-S function in Barrett's esophageal adenocarcinoma cells

TRPM2: bridging calcium and ROS signaling pathways—implications for human diseases

Pharmacology of receptor operated calcium entry in human neutrophils

Contact Info

Product

Resources

About