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Pattern Recognition Molecules of Lectin Complement Pathway in Ischemic Stroke.

Gohar Tsakanova^1,2, Ani Stepanyan¹, Rudi Steffensen³

¹Institute of Molecular Biology NAS RA, Yerevan, Armenia.

Pharmacogenomics and Personalized Medicine

|October 28, 2021

Summary

This summary is machine-generated.

Pattern recognition molecules of the lectin complement pathway are linked to ischemic stroke risk. Genetic variations in MBL2 and FCN1 genes influence stroke risk and molecule levels in an Armenian population.

Keywords:

haplotypes human ischemic stroke humoral pattern recognition molecules lectin complement pathway single nucleotide polymorphisms

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Stereological and Flow Cytometry Characterization of Leukocyte Subpopulations in Models of Transient or Permanent Cerebral Ischemia

Stereological and Flow Cytometry Characterization of Leukocyte Subpopulations in Models of Transient or Permanent Cerebral Ischemia

Published on: December 28, 2014

Area of Science:

Immunology
Genetics
Neurology

Background:

The lectin complement pathway (LCP) plays a role in innate immunity.
Pattern recognition molecules (PRMs) like mannan-binding lectin (MBL) and M-ficolin are key components of the LCP.
Alterations in LCP PRMs have been implicated in various inflammatory and vascular conditions.

Purpose of the Study:

To investigate plasma levels of MBL and M-ficolin in Armenian ischemic stroke (IS) patients.
To examine the association of single nucleotide polymorphisms (SNPs) in *MBL2*, *FCN1*, and *FCN2* genes with IS risk.
To explore the impact of these genetic variations on PRM plasma levels in IS.

Main Methods:

Study included 122 IS patients and 150 healthy controls from an Armenian population.
Plasma levels of MBL and M-ficolin were measured using immunofluorometric assays (TRIFMAs).
Real-time polymerase chain reaction with TaqMan probes was used to analyze 11 SNPs in *MBL2*, *FCN1*, and *FCN2* genes.

Main Results:

M-ficolin levels were significantly higher in IS patients compared to controls.
Specific *MBL2* (rs11003125, rs12780112) and *FCN1* (rs10120023) SNPs and their minor alleles were negatively associated with IS risk.
Certain SNPs and haplotypes (*MBL2* CGTC) were found to significantly alter plasma MBL and M-ficolin levels in IS patients.

Conclusions:

LCP PRMs are associated with the risk of developing ischemic stroke.
Genetic variations in LCP PRM genes contribute to IS pathogenesis and potentially post-ischemic brain damage.
This study highlights the role of genomic and proteomic alterations in LCP PRMs in the mechanisms of ischemic stroke within the Armenian population.