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Listen "Myocardial infarction drives trained immunity of monocytes, accelerating atherosclerosis"
Episode Synopsis
Myocardial infarction drives trained
immunity of monocytes, accelerating atherosclerosis
Eur Heart J . 2024 Mar 1;45(9):669-684.
Abstract
Background and aims: Survivors of acute coronary
syndromes face an elevated risk of recurrent atherosclerosis-related vascular events despite advanced medical treatments. The underlying causes remain
unclear. This study aims to investigate whether myocardial infarction -induced trained immunity in monocytes could sustain proatherogenic traits and expedite atherosclerosis.
Methods: Apolipoprotein-E deficient (ApoE-/-) mice
and adoptive bone marrow transfer chimeric mice underwent MI or myocardial ischaemia-reperfusion (IR). A subsequent 12-week high-fat diet (HFD) regimen
was implemented to elucidate the mechanism behind monocyte trained immunity. In addition, classical monocytes were analysed by flow cytometry in the blood of enrolled patients.
Results: In MI and IR mice, blood monocytes and bone
marrow-derived macrophages exhibited elevated spleen tyrosine kinase (SYK), lysine methyltransferase 5A (KMT5A), and CCHC-type zinc finger nucleic
acid-binding protein (CNBP) expression upon exposure to a HFD or oxidized LDL (oxLDL) stimulation. MI induced trained immunity was transmissible by transplantation of bone marrow to accelerate
atherosclerosis in naive recipients. KMT5A specifically recruited monomethylation of Lys20 of histone H4 (H4K20me) to the gene body of SYK and synergistically transactivated SYK with CNBP. In vivo small interfering RNA (siRNA) inhibition of KMT5A or CNBP potentially slowed post-MI atherosclerosis. Sympathetic denervation with 6-hydroxydopamine reduced atherosclerosis and inflammation after MI. Classical monocytes from STEMI patients with
advanced coronary lesions expressed higher SYK and KMT5A gene levels.
Conclusions: The findings underscore the crucial role
of monocyte trained immunity in accelerated atherosclerosis after myocardial infarction, implying that spleen tyrosine kinase in blood classical monocytes
may serve as a predictive factor for the progression of atherosclerosis in STEMI patients.
Disclaimer:
Lupin makes no representation or warranty of any kind, expressed or implied, regarding the accuracy, adequacy, validity, reliability, availability, or completeness of any
scientific information shared by the HCP on the STAR UPDATE podcast. You should not allow the contents of this to substitute for your own medical judgment, which you should exercise in evaluating the information on this
website.
immunity of monocytes, accelerating atherosclerosis
Eur Heart J . 2024 Mar 1;45(9):669-684.
Abstract
Background and aims: Survivors of acute coronary
syndromes face an elevated risk of recurrent atherosclerosis-related vascular events despite advanced medical treatments. The underlying causes remain
unclear. This study aims to investigate whether myocardial infarction -induced trained immunity in monocytes could sustain proatherogenic traits and expedite atherosclerosis.
Methods: Apolipoprotein-E deficient (ApoE-/-) mice
and adoptive bone marrow transfer chimeric mice underwent MI or myocardial ischaemia-reperfusion (IR). A subsequent 12-week high-fat diet (HFD) regimen
was implemented to elucidate the mechanism behind monocyte trained immunity. In addition, classical monocytes were analysed by flow cytometry in the blood of enrolled patients.
Results: In MI and IR mice, blood monocytes and bone
marrow-derived macrophages exhibited elevated spleen tyrosine kinase (SYK), lysine methyltransferase 5A (KMT5A), and CCHC-type zinc finger nucleic
acid-binding protein (CNBP) expression upon exposure to a HFD or oxidized LDL (oxLDL) stimulation. MI induced trained immunity was transmissible by transplantation of bone marrow to accelerate
atherosclerosis in naive recipients. KMT5A specifically recruited monomethylation of Lys20 of histone H4 (H4K20me) to the gene body of SYK and synergistically transactivated SYK with CNBP. In vivo small interfering RNA (siRNA) inhibition of KMT5A or CNBP potentially slowed post-MI atherosclerosis. Sympathetic denervation with 6-hydroxydopamine reduced atherosclerosis and inflammation after MI. Classical monocytes from STEMI patients with
advanced coronary lesions expressed higher SYK and KMT5A gene levels.
Conclusions: The findings underscore the crucial role
of monocyte trained immunity in accelerated atherosclerosis after myocardial infarction, implying that spleen tyrosine kinase in blood classical monocytes
may serve as a predictive factor for the progression of atherosclerosis in STEMI patients.
Disclaimer:
Lupin makes no representation or warranty of any kind, expressed or implied, regarding the accuracy, adequacy, validity, reliability, availability, or completeness of any
scientific information shared by the HCP on the STAR UPDATE podcast. You should not allow the contents of this to substitute for your own medical judgment, which you should exercise in evaluating the information on this
website.
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