Abstract
BackgroundPlatelets are key components in atherogenesis and determine the course of its clinical sequelae acute coronary syndrome (ACS). Components of the innate immune system—the superfamily of TLR receptors–are present in platelets and represent a link between atherothrombosis and inflammation. We hypothesize that alteration in platelet TLR mRNA expression is a result of inflammation driving coronary atherosclerosis and may represent an alternative platelet activation pathway in ACS.TLR2-, TLR4- and TLR9- mRNA-expression was determined in ACS patients and compared to patients with invasive exclusion of atherosclerotic lesions of coronary arteries.MethodsA total of fifty-four patients were enrolled in this clinical retrospective cohort single centre study. Total RNA from sepharose-filtered highly purified platelets was isolated using acid guanidinium thiocyanate-phenol-chloroform extraction and transcribed to cDNA using a first strand cDNA synthesis kit. To determine absolute copy numbers of TLR2, TLR4 and TLR9 we used plasmid based quantitative PCR with normalisation to an internal control.ResultsWe found that mRNA expression levels of TLR2 but not TLR 4 and 9 are up-regulated in platelets of patients with ACS when compared to patients without coronary atherosclerosis.ConclusionOur results suggest elevated TLR2 mRNA expression in platelets as a biomarker reflecting the underlying inflammation in ACS and possibly severity of coronary atherosclerosis. Platelet TLR2 may represent a link between inflammation and atherothrombosis in ACS.
Highlights
We found that mRNA expression levels of Toll-like receptor 2 (TLR2) but not TLR 4 and 9 are up-regulated in platelets of patients with acute coronary syndrome (ACS) when compared to patients without coronary atherosclerosis
Expression of TLR2 mRNA is increased in platelets of patients with acute coronary syndrome
Expression of TLR2 mRNA is increased in platelets of patients with acute coronary syndrome and TLR-6 [35] to assembly, through a complex cascade, a multiprotein signalosom leading to the activation of transcription factors advancing the expression of an array of inflammatory genes. [23, 36]
Summary
Subject of our mRNA analyses were expression levels of members of the superfamily of Toll-like-receptors (TLR) in platelets. These membrane-spanning proteins orchestrate platelet function upon activation, partly through increased splicing and translation to protein of platelet pre mRNA. [20,21,22,23] Due to their role as mediators of a thromboinflammatory response and in being a possible link between both platelet-function and the innate immune system, TLRs are vividly focused on by research regarding their role in ACS. Recent studies provide evidence that by presenting processed pathogens via TLR receptors to members of the adaptive immune system platelets seem to link adaptive and innate immune response [34]. Up to date TLRs are thought to form homodimers -or in case of TLR-2 heterodimers- with TLR-1
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