13-HODE inhibits the intracellular calcium increase of activated human polymorphonuclear cells

Velde, Marco J. van de; Engels, Ferdi; Henricks, Paul A.J.; Nijkamp, Frans P.

doi:10.1002/jlb.56.2.200

Cited by 6 publications

(5 citation statements)

References 16 publications

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“…The degranulatory response of PMNs to IMLP was additive on the 13-HODE-induced degranulation. In accordance, 13-HODE does not affect the fMLP-induced [Cae+]i-increase [24].…”

Section: Discussionsupporting

confidence: 56%

“…13-HODE attenuated the degranulatory response of PMNs to PAF. Previously, we observed a strong inhibitory effect of 13-HODE on the PAF-induced [Ca-'+]i-increase [24]. Since [Ca>]i can modulate PMN degranulation, the decrease of PAF-induced degranulation caused by 13-HODE may result from the inhibitory effect of 13-HODE on the PAFinduced [Ca2+]i.…”

Section: Discussionmentioning

confidence: 78%

“…An elevation of the intracellular calcium concentration ([Ca>]0 is generally considered to be important for degranulation [23]. However, 13-HODE induced PMN degranulation without a detectabe rise of [Ca>]~ [24]. Other investigators also observed PMN degranulation without an increase of [Ca>]i [9].…”

Section: Discussionmentioning

confidence: 99%

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The linoleic acid metabolite 13‐HODE modulates degranulation of human polymorphonuclear leukocytes

et al. 1995

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The effect of the linoleic acid metabolite 13-hydroxyoetadeeadienoie acid (13-HODE) on degranulation of human polymorphonuclear ieukocytes (PMNs) was investigated by measuring the expression of CDllb and CD67 on the plasma membrane. 13-HODE (5 pM) by itself induced degranulation of PMNs, but to a lesser extent as compared to PAF and fMLP. In addition, 13-HODE was found to inhibit the PAF-indueed degrannlation whereas an additive effect on the fMLP-induced PMNs degranulation was observed. These results indicate that 13-HODE can play a modulatory role in degranulation of PMNs.

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“…The degranulatory response of PMNs to IMLP was additive on the 13-HODE-induced degranulation. In accordance, 13-HODE does not affect the fMLP-induced [Cae+]i-increase [24].…”

Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 78%

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The linoleic acid metabolite 13‐HODE modulates degranulation of human polymorphonuclear leukocytes

et al. 1995

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“…1C ). HODEs have been shown to play an important role in inhibition of the intracellular calcium increase 28 , induction of vasodilatation 29 , suppression of proliferation and induction of apoptosis 30 . This study showed that 13-HODE induced ER stress, perturbed lipid metabolism, and enhanced protein levels of Fas, c-CAS3, and c-PARP, leading to apoptosis and suggested that 13-HODE plays an important role in the pathogenesis of ALD.…”

Section: Discussionmentioning

confidence: 99%

Hepatic overproduction of 13-HODE due to ALOX15 upregulation contributes to alcohol-induced liver injury in mice

Zhang

Zhong

Sun

et al. 2017

Sci Rep

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Chronic alcohol feeding causes lipid accumulation and apoptosis in the liver. This study investigated the role of bioactive lipid metabolites in alcohol-induced liver damage and tested the potential of targeting arachidonate 15-lipoxygenase (ALOX15) in treating alcoholic liver disease (ALD). Results showed that chronic alcohol exposure induced hepatocyte apoptosis in association with increased hepatic 13-HODE. Exposure of 13-HODE to Hepa-1c1c7 cells induced oxidative stress, ER stress and apoptosis. 13-HODE also perturbed proteins related to lipid metabolism. HODE-generating ALOX15 was up-regulated by chronic alcohol exposure. Linoleic acid, but not ethanol or acetaldehyde, induced ALOX15 expression in Hepa-1c1c7 cells. ALOX15 knockout prevented alcohol-induced liver damage via attenuation of oxidative stress, ER stress, lipid metabolic disorder, and cell death signaling. ALOX15 inhibitor (PD146176) treatment also significantly alleviated alcohol-induced oxidative stress, lipid accumulation and liver damage. These results demonstrated that activation of ALOX15/13-HODE circuit critically mediates the pathogenesis of ALD. This study suggests that ALOX15 is a potential molecular target for treatment of ALD.

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“…Their results demonstrated that the highest concentration of HODE were in ALD patients [21]. HODE play an important role in increase induction of vasodilatation [22], inhibition of the intracellular calcium [23], suppression of proliferation, and apoptosis induction. Moreover, Zhang et al revealed that 13-HODE induced ER stress, perturbed lipid metabolism, and enhanced protein levels of fatty acid synthase, which progress the inflammation in the liver [24].…”

Section: Discussionmentioning

confidence: 96%

Eicosanoids in Nonalcoholic Fatty Liver Disease (NAFLD) Progression. Do Serum Eicosanoids Profile Correspond with Liver Eicosanoids Content during NAFLD Development and Progression?

et al. 2020

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Nonalcoholic fatty liver disease (NAFLD) is becoming a major public health problem worldwide. The study aimed to evaluate the concentration of eicosanoids in serum and liver tissue during steatosis progression and to assess whether eicosanoid change scores may predict liver tissue remodeling. Thirty six eight-week-old male Sprague Dawley rats were enrolled and sacrificed at different stages of NAFLD. Eicosanoid concentrations, namely lipoxin A4, hydroxyeicosatetraenoic acids (HETE), hydroxyloctadecadienoic acids (HODE), protectin DX, Maresine1, leucotriene B4, prostaglandin E2, and resolvin D1 measurement in serum and liver tissue with Agilent Technologies 1260 liquid chromatography were evaluated. For the liver and serum concentrations of 9-HODE and 13-HODE, the correlations were found to be strong and positive (r > 0.7, p < 0.05). Along with NAFLD progression, HODE concentration significantly increased, and change scores were more abundant in the liver. The moderate positive correlation between liver and serum (r = 0.52, p < 0.05) was also observed for resolvin E1. The eicosanoid concentration decreased during NAFLD progression, but mostly in serum. There were significant correlations between HETE concentrations in liver and serum, but their associations were relatively low and changes the most in liver tissue. Eicosanoids profile, predominantly 9-HODE and 13-HODE, may serve as a potential biomarker for NAFLD development.

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13-HODE inhibits the intracellular calcium increase of activated human polymorphonuclear cells

Cited by 6 publications

References 16 publications

The linoleic acid metabolite 13‐HODE modulates degranulation of human polymorphonuclear leukocytes

The linoleic acid metabolite 13‐HODE modulates degranulation of human polymorphonuclear leukocytes

Hepatic overproduction of 13-HODE due to ALOX15 upregulation contributes to alcohol-induced liver injury in mice

Eicosanoids in Nonalcoholic Fatty Liver Disease (NAFLD) Progression. Do Serum Eicosanoids Profile Correspond with Liver Eicosanoids Content during NAFLD Development and Progression?

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