Store-Operated Calcium Channel Inhibition Attenuates Neutrophil Function and Postshock Acute Lung Injury

Lee, Cindy; Xu, Dazhong; Feketeova, Eleonora; Kannan, Kolenkode B.; Fekete, Zoltán; Deitch, Edwin A.; Livingston, David H.; Hauser, Carl J.

doi:10.1097/01.ta.0000171456.54921.fe

Cited by 31 publications

(13 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, HG activates PKC, PKC-␣ activation also enhances Ca i 2ϩ via the activation of TRPC1 in human endothelial cells, and elevated PKC activity has been linked to the development of diabetes-related vascular disease (2,12,27). A potential link between an enhanced SOCE in endothelial cells and endothelial dysfunction is that, at least in neutrophils, SOCE is involved in the activation of NADPH oxidase; an increase in NADPH oxidase has been associated with endothelial dysfunction in streptozotocin-induced diabetic rats, and HG increased the expression of NADPH oxidase in an endothelial cell culture protocol (24,29).…”

Section: Discussionmentioning

confidence: 99%

Glucose enhances expression of TRPC1 and calcium entry in endothelial cells

Bishara

Ding

2010

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Hyperglycemia is a major risk factor for endothelial dysfunction and vascular disease, and in the current study, the link to glucose-induced abnormal intracellular Ca2+ (Cai2+) homeostasis was explored in bovine aortic endothelial cells in high glucose (HG; 25 mmol/l) versus low glucose (LG; 5.5 mmol/l; control). Transient receptor potential 1 (TRPC1) ion channel protein, but not TRPC3, TRPC4, or TRPC6 expression, was significantly increased in HG versus LG at 72 h. HG for 4, 24, and 72 h did not change basal Cai2+ or ATP-induced Cai2+ release; however, the amplitude of sustained Cai2+ was significantly increased at 24 and 72 h and reduced by low concentration of the putative, but nonspecific, TRPC blockers, gadolinium, SKF-96365, and 2-aminoethoxydiphenyl borate. Treatment with TRPC1 antisense significantly reduced TRPC1 protein expression and ATP-induced Ca2+ entry in bovine aortic endothelial cells. Although the link between HG-induced changes in TRPC1 expression, enhanced Ca2+ entry, and endothelial dysfunction require further study, the current data are suggestive that targeting these pathways may reduce the impact of HG on endothelial function.

show abstract

Section: Discussionmentioning

confidence: 99%

Glucose enhances expression of TRPC1 and calcium entry in endothelial cells

Bishara

Ding

2010

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…However, Ca 2ϩ imbalance is thought to be related to the pathogenesis of several types of viral infection (3,7,25) and various pathophysiologies (35,52,63), including acute lung injury (41,42 ] i is maintained when Ca 2ϩ is actively pumped out of the cell and into the ER. During H5N1-AIV infection (lower panel), an undetermined factor(s) may interfere with the Ca 2ϩ transport mechanisms on the plasma membrane, which in turn induces the influx of extracellular Ca 2ϩ followed by an elevation in [Ca 2ϩ ] i .…”

Section: Discussionmentioning

confidence: 99%

Highly Pathogenic H5N1 Avian Influenza Virus Induces Extracellular Ca ²⁺ Influx, Leading to Apoptosis in Avian Cells

Ueda

Daidoji²,

et al. 2010

J Virol

View full text Add to dashboard Cite

In this study, we show that the highly pathogenic H5N1 avian influenza virus (AIV) . Thus, we investigated the molecular mechanisms of apoptosis induced by H5N1-AIV infection. Caspase-dependent and -independent pathways contributed to the cytopathic effects. We further showed that, in the induction of apoptosis, the hemagglutinin of H5N1-AIV played a major role and its cleavage sequence was not critical. We also observed outer membrane permeabilization and loss of the transmembrane potential of the mitochondria of infected DEF, indicating that mitochondrial dysfunction was caused by the H5N1-AIV infection. (

show abstract

“…The SKI, 2-(p-hydroxyanilino)-4-(p-chlorophenyl) thiazole, which was formally named SKI-II, was developed and synthesized by our group as described previously (French et al, 2003) and was used as a specific sphingosine kinase inhibitor previously (Lee et al, 2004(Lee et al, , 2005Francy et al, 2007;Jung et al, 2007). In this article, we described SKI-II as SKI for simplicity.…”

Section: Methodsmentioning

confidence: 99%

Sphingosine 1-Phosphate Has Dual Functions in the Regulation of Endothelial Cell Permeability and Ca2+ Metabolism

Itagaki

Yun

Hengst

et al. 2007

The Journal of Pharmacology and Experimental Therapeutics

Self Cite

View full text Add to dashboard Cite

Ca2ϩ signaling plays an important role in endothelial cell (EC) functions including the regulation of barrier integrity. Recently, the endogenous lipid derivative, sphingosine-1-phosphate (S1P), has emerged as an important modulator of EC barrier function. We investigated the role of endogenously generated S1P in Ca 2ϩ metabolism and barrier function in human umbilical endothelial cells (HUVECs) stimulated by thrombin, histamine, or other agonists. Barrier function was assessed by dextran diffusion through HUVEC monolayers, and Ca 2ϩ transients were measured using a fluoroprobe. Thrombin or histamine increased Ca 2ϩ release from the endoplasmic reticulum (ER) and Ca 2ϩ entry through store-operated channels (SOCs) that was accompanied by increased EC permeability. Inhibition of S1P synthesis by a specific sphingosine kinase inhibitor (SKI) decreased thrombin or histamine-induced increased permeability and decreased Ca 2ϩ entry via SOC in a concentrationdependent fashion. SKI had minuscule effects on thrombin or histamine-induced Ca 2ϩ release from ER. SKI also inhibited thapsigargin or ionomycin-induced Ca 2ϩ entry via SOC without affecting Ca 2ϩ release from the ER. In contrast to the effects of endogenously generated S1P, when S1P was administered externally, it initiated Ca 2ϩ release from ER similar to thrombin and histamine while decreasing EC permeability. These observations indicate that after agonist-induced conditions, endogenously generated S1P functions as a positive modulator of Ca 2ϩ entry via SOC and a mediator of increased cell permeability. In contrast, extracellular exposure to S1P has different signaling mechanisms and effects. Thus, the potential dual roles of endogenous and exogenous S1P on EC function need to be considered in pharmacological studies targeting sphingosine metabolism.

show abstract

Store-Operated Calcium Channel Inhibition Attenuates Neutrophil Function and Postshock Acute Lung Injury

Cited by 31 publications

References 49 publications

Glucose enhances expression of TRPC1 and calcium entry in endothelial cells

Glucose enhances expression of TRPC1 and calcium entry in endothelial cells

Highly Pathogenic H5N1 Avian Influenza Virus Induces Extracellular Ca ²⁺ Influx, Leading to Apoptosis in Avian Cells

Sphingosine 1-Phosphate Has Dual Functions in the Regulation of Endothelial Cell Permeability and Ca2+ Metabolism

Contact Info

Product

Resources

About

Store-Operated Calcium Channel Inhibition Attenuates Neutrophil Function and Postshock Acute Lung Injury

Cited by 31 publications

References 49 publications

Glucose enhances expression of TRPC1 and calcium entry in endothelial cells

Glucose enhances expression of TRPC1 and calcium entry in endothelial cells

Highly Pathogenic H5N1 Avian Influenza Virus Induces Extracellular Ca 2+ Influx, Leading to Apoptosis in Avian Cells

Sphingosine 1-Phosphate Has Dual Functions in the Regulation of Endothelial Cell Permeability and Ca2+ Metabolism

Contact Info

Product

Resources

About

Highly Pathogenic H5N1 Avian Influenza Virus Induces Extracellular Ca ²⁺ Influx, Leading to Apoptosis in Avian Cells