Association of C-reactive protein and complement factor H gene polymorphisms with risk of lupus nephritis in Chinese population
Complement overactivation is a major driver of lupus nephritis (LN). Impaired interactions of C-reactive protein (CRP) with complement factor H (CFH) have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN. However, genetic variations of neither CRP nor C...
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Published in | World journal of clinical cases Vol. 11; no. 13; pp. 2934 - 2944 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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United States
Baishideng Publishing Group Inc
06.05.2023
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Online Access | Get full text |
ISSN | 2307-8960 2307-8960 |
DOI | 10.12998/wjcc.v11.i13.2934 |
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Abstract | Complement overactivation is a major driver of lupus nephritis (LN). Impaired interactions of C-reactive protein (CRP) with complement factor H (CFH) have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN. However, genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.
To examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.
We genotyped six CRP single nucleotide polymorphisms (SNPs) (rs1205, rs3093062, rs2794521, rs1800947, rs3093077, and rs1130864) and three CFH SNPs (rs482934, rs1061170, and rs1061147) in 270 LN patients and 303 healthy subjects.
No linkage was found among CRP and CFH SNPs, indicating lack of genetic interactions between the two genes. Moreover, CRP and CFH SNPs, neither individually nor in combination, are associated with the risk or clinical manifestations of LN. Given the unambiguous pathogenic roles of the two genes.
These findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN. |
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AbstractList | Complement overactivation is a major driver of lupus nephritis (LN). Impaired interactions of C-reactive protein (CRP) with complement factor H (CFH) have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN. However, genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.
To examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.
We genotyped six CRP single nucleotide polymorphisms (SNPs) (rs1205, rs3093062, rs2794521, rs1800947, rs3093077, and rs1130864) and three CFH SNPs (rs482934, rs1061170, and rs1061147) in 270 LN patients and 303 healthy subjects.
No linkage was found among CRP and CFH SNPs, indicating lack of genetic interactions between the two genes. Moreover, CRP and CFH SNPs, neither individually nor in combination, are associated with the risk or clinical manifestations of LN. Given the unambiguous pathogenic roles of the two genes.
These findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN. Complement overactivation is a major driver of lupus nephritis (LN). Impaired interactions of C-reactive protein (CRP) with complement factor H (CFH) have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN. However, genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.BACKGROUNDComplement overactivation is a major driver of lupus nephritis (LN). Impaired interactions of C-reactive protein (CRP) with complement factor H (CFH) have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN. However, genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.To examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.AIMTo examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.We genotyped six CRP single nucleotide polymorphisms (SNPs) (rs1205, rs3093062, rs2794521, rs1800947, rs3093077, and rs1130864) and three CFH SNPs (rs482934, rs1061170, and rs1061147) in 270 LN patients and 303 healthy subjects.METHODSWe genotyped six CRP single nucleotide polymorphisms (SNPs) (rs1205, rs3093062, rs2794521, rs1800947, rs3093077, and rs1130864) and three CFH SNPs (rs482934, rs1061170, and rs1061147) in 270 LN patients and 303 healthy subjects.No linkage was found among CRP and CFH SNPs, indicating lack of genetic interactions between the two genes. Moreover, CRP and CFH SNPs, neither individually nor in combination, are associated with the risk or clinical manifestations of LN. Given the unambiguous pathogenic roles of the two genes.RESULTSNo linkage was found among CRP and CFH SNPs, indicating lack of genetic interactions between the two genes. Moreover, CRP and CFH SNPs, neither individually nor in combination, are associated with the risk or clinical manifestations of LN. Given the unambiguous pathogenic roles of the two genes.These findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN.CONCLUSIONThese findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN. |
Author | Liu, Xiao-Ling Yu, Feng Lv, Jian-Min Li, Hai-Yun Li, Qiu-Yu |
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Cites_doi | 10.1371/journal.pone.0141547 10.1167/iovs.05-1456 10.2215/CJN.05780616 10.1086/344289 10.1177/0961203317702254 10.1016/j.molimm.2004.02.005 10.3389/fimmu.2018.00808 10.1038/sj.cr.7290272 10.1038/srep22889 10.18632/aging.103655 10.1073/pnas.95.25.14869 10.1007/s10067-017-3695-5 10.1111/j.1523-1755.2004.00443.x 10.1007/s10067-018-4059-5 10.1002/art.20511 10.1046/j.1365-2249.1998.00655.x 10.1006/jaut.2002.0608 10.1097/01.bor.0000132648.62680.81 10.1155/2014/212597 10.1371/journal.pgen.1002079 10.1002/art.1780350606 10.1186/ar4142 10.21873/invivo.12309 10.1002/art.20846 10.3899/jrheum.080262 10.1007/s002510050631 10.1002/anr.1780320909 10.1002/art.10590 10.3899/jrheum.090243 10.1002/art.1780230609 10.1007/s00109-005-0658-0 10.1056/NEJMra071297 10.1046/j.1365-2249.1996.d01-777.x 10.1002/art.11026 10.3389/fimmu.2018.00372 10.1038/sj.gene.6364459 10.1093/hmg/ddh021 10.1093/rheumatology/kes218 10.1038/nrrheum.2011.37 10.3389/fimmu.2018.01089 10.1681/ASN.2016070735 |
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Keywords | Complement factor H C-reactive protein Systemic lupus erythematosus Lupus nephritis Single nucleotide polymorphism |
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License | The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved. This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Corresponding author: Hai-Yun Li, PhD, Assistant Professor, School of Basic Medical Sciences, Xi’an Jiaotong University, No. 76 Yanta West Road, Xi'an 710061, Shaanxi Province, China. lihaiy@xjtu.edu.cn Author contributions: Yu F and Li HY designed the research. Li QY, Lv JM, and Liu XL performed the experiments. Lv JM and Li HY analyzed the data and wrote the paper. All authors reviewed and approved the final version of the manuscript. |
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Title | Association of C-reactive protein and complement factor H gene polymorphisms with risk of lupus nephritis in Chinese population |
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