Identification of Differential Expression Cytokines in Hemolysis, Elevated Liver Enzymes, and Low Platelet Syndrome by Proteome Microarray Analysis and Further Verification
To screen the differential expression cytokines (DECs) in hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome, establish its differential cytokines spectra, and provide the clues for its diagnosis and pathogenic mechanism researches. Sera from four HELLP syndrome patients and four h...
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Online Access: | https://doi.org/10.1177/0963689720975398 |
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doaj-5e91f23a9f994194a0e5cdab83d3db4f2021-03-24T23:04:12ZengSAGE PublishingCell Transplantation1555-38922021-03-013010.1177/0963689720975398Identification of Differential Expression Cytokines in Hemolysis, Elevated Liver Enzymes, and Low Platelet Syndrome by Proteome Microarray Analysis and Further VerificationSuya Kang0Liping Zhou1Yun Wang2Hui Li3Hong Zhang4 Department of Gynecology and Obstetrics, , Suzhou, China Department of Obstetrics, , Suzhou, China Department of Obstetrics, , Suzhou, China Central Laboratory, , Suzhou, China Department of Gynecology and Obstetrics, , Suzhou, ChinaTo screen the differential expression cytokines (DECs) in hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome, establish its differential cytokines spectra, and provide the clues for its diagnosis and pathogenic mechanism researches. Sera from four HELLP syndrome patients and four healthy controls were detected by proteome microarray. Then the analysis of Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein–protein interaction (PPI) network were performed and possible hub proteins were selected out, further verified by Enzyme Linked Immunosorbent Assay (ELISA) in sera from 21 HELLP syndrome patients and 21 healthy controls. Thirty DECs were defined according to P -value and fold change between HELLP group and control group. GO enrichment analysis showed that DECs were mainly involved in the regulation of inflammatory response and have relationship to growth factor binding, transmembrane receptor protein kinase, and cytokine receptor activity. Seven possible hub proteins were defined by PPI analysis, including IGFBP-3/Follistatin-like 1/FLRG/Fetuin A and MMP-13/Thrombospondin-5/Aggrecan. ELISA showed higher serum levels of Fetuin A/IGFBP-3/FLGR/MMP-13/Thrombospondin-5 in HELLP group than those in controls, while the levels of Follistatin-like 1 and Aggrecan were lower in HELLP patients (all P < 0.05 or <0.01).The serological DECs spectra of HELLP syndrome was established and seven possible hub proteins that may be more closely related to the disease have been verified, providing new clues for its pathogenesis, diagnosis, and clinical treatment.https://doi.org/10.1177/0963689720975398 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Suya Kang Liping Zhou Yun Wang Hui Li Hong Zhang |
spellingShingle |
Suya Kang Liping Zhou Yun Wang Hui Li Hong Zhang Identification of Differential Expression Cytokines in Hemolysis, Elevated Liver Enzymes, and Low Platelet Syndrome by Proteome Microarray Analysis and Further Verification Cell Transplantation |
author_facet |
Suya Kang Liping Zhou Yun Wang Hui Li Hong Zhang |
author_sort |
Suya Kang |
title |
Identification of Differential Expression Cytokines in Hemolysis, Elevated Liver Enzymes, and Low Platelet Syndrome by Proteome Microarray Analysis and Further Verification |
title_short |
Identification of Differential Expression Cytokines in Hemolysis, Elevated Liver Enzymes, and Low Platelet Syndrome by Proteome Microarray Analysis and Further Verification |
title_full |
Identification of Differential Expression Cytokines in Hemolysis, Elevated Liver Enzymes, and Low Platelet Syndrome by Proteome Microarray Analysis and Further Verification |
title_fullStr |
Identification of Differential Expression Cytokines in Hemolysis, Elevated Liver Enzymes, and Low Platelet Syndrome by Proteome Microarray Analysis and Further Verification |
title_full_unstemmed |
Identification of Differential Expression Cytokines in Hemolysis, Elevated Liver Enzymes, and Low Platelet Syndrome by Proteome Microarray Analysis and Further Verification |
title_sort |
identification of differential expression cytokines in hemolysis, elevated liver enzymes, and low platelet syndrome by proteome microarray analysis and further verification |
publisher |
SAGE Publishing |
series |
Cell Transplantation |
issn |
1555-3892 |
publishDate |
2021-03-01 |
description |
To screen the differential expression cytokines (DECs) in hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome, establish its differential cytokines spectra, and provide the clues for its diagnosis and pathogenic mechanism researches. Sera from four HELLP syndrome patients and four healthy controls were detected by proteome microarray. Then the analysis of Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein–protein interaction (PPI) network were performed and possible hub proteins were selected out, further verified by Enzyme Linked Immunosorbent Assay (ELISA) in sera from 21 HELLP syndrome patients and 21 healthy controls. Thirty DECs were defined according to P -value and fold change between HELLP group and control group. GO enrichment analysis showed that DECs were mainly involved in the regulation of inflammatory response and have relationship to growth factor binding, transmembrane receptor protein kinase, and cytokine receptor activity. Seven possible hub proteins were defined by PPI analysis, including IGFBP-3/Follistatin-like 1/FLRG/Fetuin A and MMP-13/Thrombospondin-5/Aggrecan. ELISA showed higher serum levels of Fetuin A/IGFBP-3/FLGR/MMP-13/Thrombospondin-5 in HELLP group than those in controls, while the levels of Follistatin-like 1 and Aggrecan were lower in HELLP patients (all P < 0.05 or <0.01).The serological DECs spectra of HELLP syndrome was established and seven possible hub proteins that may be more closely related to the disease have been verified, providing new clues for its pathogenesis, diagnosis, and clinical treatment. |
url |
https://doi.org/10.1177/0963689720975398 |
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