Carboxyl-Terminal Cleavage of Apolipoprotein A-I by Human Mast Cell Chymase Impairs Its Anti-Inflammatory Properties

Nguyen, Su Duy; Maaninka, Katariina; Lappalainen, Jani; Nurmi, Katariina; Metso, Jari; Öörni, Katariina; Navab, Mohamad; Fogelman, Alan M.; Jauhiainen, Matti; Lee-Rueckert, Miriam; Kovanen, Petri T.

doi:10.1161/atvbaha.115.306827

Cited by 30 publications

(19 citation statements)

References 66 publications

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“…Recently, it was established that chymase cleaves ApoA-I resulting in loss of its anti-inflammatory functions [20]. Moreover, cathepsin G, another protease released from mast cells, has been reported to degrade LDL, reducing LDL-C and ApoB levels [21].…”

Section: Discussionmentioning

confidence: 99%

Systemic mastocytosis associates with cardiovascular events despite lower plasma lipid levels

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Systemic mastocytosis associates with cardiovascular events despite lower plasma lipid levels

et al. 2018

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“…TNFα played a critical role in the promotion of atherosclerosis by decreasing cellular cholesterol efflux from foam cells [ 15 , 24 ]. Accumulated oxidative stress induced by TNFα led to the endothelial impairment and resulted in atherosclerotic lesions [ 25 – 26 ].…”

Section: Discussionmentioning

confidence: 99%

A20 functions as mediator in TNFα-induced injury of human umbilical vein endothelial cells through TAK1-dependent MAPK/eNOS pathway

Huang²,

Song

et al. 2017

Oncotarget

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A20, a negative regulator of nuclear factor κB signaling, has been shown to attenuate atherosclerotic events. Transforming growth factor beta-activated kinase 1 (TAK1) plays a critical role in TNFα-induced atherosclerosis via endothelial nitric oxide (NO) synthase (eNOS) uncoupling and NO reduction. In the study, we investigated the hypothesis that A20 protected endothelial cell injury induced by TNFα through modulating eNOS activity and TAK1 signalling. Human umbilical vein endothelial cells (HUVECs) were stimulated by TNFα. The impact of A20 on cell apoptosis, eNOS expression and NO production and related TAK1 pathway were detected. Both eNOS and NO production were remarkably reduced. TAK1, p38 MAPK phosphorylation and HUVECs apoptosis were enhanced after TNFα stimulation for 2 hrs. Inhibition of A20 significantly activated TAK1, p38 MAPK phosphorylation, and cell apoptosis, but blocked eNOS expression and NO production. Furthermore, p38 MAPK expression was suppressed by A20 over-expression, but re-enhanced by inhibiting A20 or activation of TAK1. Furtherly, TNFα-induced suppression of eNOS and NO production were largely prevented by silencing p38 MAPK. Collectively, our results suggested that A20-mediated TAK1 inactivation suppresses p38 MAPK and regulated MAPK/eNOS pathway, which contributes to endothelial cell survival and function preservation.

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“…Interestingly, smokers had not only less apoA-I, but they also had fewer macrophages in their sIAs. Although smoking did not seem to affect lipid accumulation, it may inhibit the various protective functions of apoA-I, for example via activation of mast cells and subsequent release of proteases that degrade apoA-I (44), and so block its ability to induce efflux from foam cells and to act as an anti-inflammatory component in the arterial wall (45).…”

Section: Correlation With Clinical Risk Factorsmentioning

confidence: 99%

Smooth Muscle Cell Foam Cell Formation, Apolipoproteins, and ABCA1 in Intracranial Aneurysms: Implications for Lipid Accumulation as a Promoter of Aneurysm Wall Rupture

Ollikainen

Tulamo

Lehti

et al. 2016

J Neuropathol Exp Neurol

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Saccular intracranial aneurysm (sIA) aneurysm causes intracranial hemorrhages that are associated with high mortality. Lipid accumulation and chronic inflammation occur in the sIA wall. A major mechanism for lipid clearance from arteries is adenosine triphosphate-binding cassette A1 (ABCA1)-mediated lipid efflux from foam cells to apolipoprotein A-I (apoA-I). We investigated the association of wall degeneration, inflammation, and lipid-related parameters in tissue samples of 16 unruptured and 20 ruptured sIAs using histology and immunohistochemistry. Intracellular lipid accumulation was associated with wall remodeling (p ¼ 0.005) and rupture (p ¼ 0.020).

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Carboxyl-Terminal Cleavage of Apolipoprotein A-I by Human Mast Cell Chymase Impairs Its Anti-Inflammatory Properties

Abstract: Supplemental Digital Content is available in the text.

Cited by 30 publications

References 66 publications

Systemic mastocytosis associates with cardiovascular events despite lower plasma lipid levels

Systemic mastocytosis associates with cardiovascular events despite lower plasma lipid levels

A20 functions as mediator in TNFα-induced injury of human umbilical vein endothelial cells through TAK1-dependent MAPK/eNOS pathway

Smooth Muscle Cell Foam Cell Formation, Apolipoproteins, and ABCA1 in Intracranial Aneurysms: Implications for Lipid Accumulation as a Promoter of Aneurysm Wall Rupture

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