Katariina Öörni (Finland)

Wihuri Research Institute Atherosclerosis Research Laboratory
Katariina Öörni leads the Atherosclerosis Research Laboratory of Wihuri Research Institute, Helsinki, Finland, and she is Adjunct Professor of Biochemistry at the University of Helsinki. Katariina Öörni’s research interests are centered on the development of atherosclerotic lesions, particularly in examining the retention and accumulation of apolipoprotein (apo) B-containing particles, such as low-density lipoprotein (LDL) in the arterial intima. The group has determined mechanisms of LDL aggregation, reported how modification of lipoprotein particles influences their binding to the components of the arterial wall, and analyzed the effect of extracellular conditions on modification and retention of LDL. Most recently the group has shown that the aggregation susceptibility of LDL shows wide person-to-person variation and the presence of aggregation-prone LDL predicts future cardiovascular events independent of conventional risk factors, including LDL cholesterol levels. The overall goal of Katariina Öörni’s research program is to understand how lipoproteins accumulating in the arterial wall trigger inflammatory responses during atherogenesis. Katariina Öörni is a council member of the Finnish Atherosclerosis Society and has represented Finland in the Organizing Committee of the European Lipoprotein Club in 2016-2020 and been the secretary and treasurer of the Scandinavian Society for Atherosclerosis Research in 1998-2006. She is a Co-Editor of Atherosclerosis, the official journal of EAS. She received the Esko Nikkilä Memorial Lecture Award from the Scandinavian Society for Atherosclerosis Research in 2019.

Author Of 5 Presentations

Introduction (ID 1523)

Session Type
CME Session
Session Time
12:45 - 14:00
Date
Sun, 30.05.2021
Room
Hall A (Live Q&A)
Lecture Time
12:45 - 12:48

Introduction (ID 1584)

Session Type
Vascular Biology
Session Time
10:30 - 12:00
Date
Wed, 02.06.2021
Room
Live Streamed
Lecture Time
10:30 - 10:33

Live Q&A (ID 1386)

Session Type
CME Session
Session Time
12:45 - 14:00
Date
Sun, 30.05.2021
Room
Hall A (Live Q&A)
Lecture Time
13:33 - 14:00

O053 - Lp(a) induces inflammasome activation in human macrophages (ID 474)

Session Type
Genetics
Session Time
16:00 - 17:30
Date
Tue, 01.06.2021
Room
Live Streamed
Lecture Time
16:33 - 16:41

Abstract

Background and Aims

Elevated Lp(a) serum levels are associated with increased risk for atherosclerotic coronary artery disease and stroke. Here, we analyzed the effect of plasma Lp(a) levels on caspase-1 and the pro-inflammatory cytokines it processes. We further directly compare the molecular composition of Lp(a) and LDL isolated from the same donors as well as their pro-atherogenic and pro-inflammatory potential.

Methods

Human plasmas with varying Lp(a) levels and isolated Lp(a) and LDL were incubated with THP-1 macrophages for three hours and caspase-1 activation and the release of pro-inflammatory cytokines IL-1β, IL-1α, and IL-18 was measured. Molecular composition of Lp(a) and LDL isolated from the same donors was determined by lipidomics and proteomics approaches.

Results

Plasma Lp(a) levels ranging from 1.7 to 165.3 mg/dL correlated significantly with caspase-1 activity (r = 0.496), IL-18 (r = 0.496), and IL-1α (r = 0.447) in macrophages. IL-1β secretion correlated significantly with plasma triglycerides, and not with Lp(a) levels.

Lipidomics comparison of LDL and Lp(a) indicated that Lp(a) was significantly depleted of poly-unsaturated fatty acids in all lipid classes. Proteomics analyses revealed that Lp(a) is enriched in inflammation-associated proteins. Lp(a) from induced robust and dose-dependent caspase-1 activation and release of IL-1β and IL-18 compared to a mild induction upon incubation with LDL from the same donors.

Conclusions

Our data show that plasma Lp(a) levels directly correlate with inflammasome activation in macrophages, isolated Lp(a) induces stronger dose-dependent caspase-1 activation than LDL, and LDL and Lp(a) have clear structural differences additionally to apo(a).

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O062 - Children with familial hypercholesterolemia display changes in LDL and HDL function: a cross-sectional study (ID 1406)

Session Type
Late Breaking Sessions
Session Time
10:00 - 11:15
Date
Wed, 02.06.2021
Room
Hall A (Live Q&A)
Lecture Time
10:28 - 10:35

Abstract

Background and Aims

The functional status of lipoprotein particles contributes to atherogenesis. The tendency of plasma LDL particles to aggregate and the ability of HDL particles to induce and mediate reverse cholesterol transport associate with high and low risk for cardiovascular disease in adult patients, respectively. However, it is unknown whether children with familial hypercholesterolemia (FH) display lipoprotein function alterations.

We hypothesized that FH children had disrupted lipoprotein function.

Methods

We analyzed LDL aggregation susceptibility and HDL-apoA-I exchange to apoA-I ratio (HAE/apoA-I ratio), and activity of four proteins that regulate lipoprotein metabolism (CETP, LCAT, PLTP and PON1) in plasma samples derived from children with FH (n = 47) and from healthy children (n = 56). Potential biological mechanisms behind any variation in lipoprotein functionalities were explored using an NMR-based metabolomics profiling approach.

Results

LDL aggregation was higher and HAE/apoA-I ratio was lower in FH children than in healthy children. LDL aggregation associated positively with LDL-C and negatively with triglycerides, and HAE/apoA-I ratio associated negatively with LDL-C. Generally, the metabolomic profile for LDL aggregation was a mirror image of that for HAE/apoA-I ratio.

Conclusions

FH children displayed increased atherogenicity of LDL and disrupted HDL function. These newly observed functional alterations in LDL and HDL may help explain the risk for atherosclerotic cardiovascular disease in FH children.

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Presenter Of 3 Presentations

Introduction (ID 1523)

Session Type
CME Session
Session Time
12:45 - 14:00
Date
Sun, 30.05.2021
Room
Hall A (Live Q&A)
Lecture Time
12:45 - 12:48

Introduction (ID 1584)

Session Type
Vascular Biology
Session Time
10:30 - 12:00
Date
Wed, 02.06.2021
Room
Live Streamed
Lecture Time
10:30 - 10:33

Live Q&A (ID 1386)

Session Type
CME Session
Session Time
12:45 - 14:00
Date
Sun, 30.05.2021
Room
Hall A (Live Q&A)
Lecture Time
13:33 - 14:00