New Insights into the Role of HMGB2 in ST-Segment Elevation Myocardial Infarction.
HMGB2
ST-segment elevation myocardial infarction
STEMI
platelet
proteomics analysis
Journal
International journal of general medicine
ISSN: 1178-7074
Titre abrégé: Int J Gen Med
Pays: New Zealand
ID NLM: 101515487
Informations de publication
Date de publication:
2023
2023
Historique:
received:
09
07
2023
accepted:
31
08
2023
medline:
20
9
2023
pubmed:
20
9
2023
entrez:
20
9
2023
Statut:
epublish
Résumé
Ischemic heart disease is one of the leading causes of death in the world, of which ST-segment elevation myocardial infarction (STEMI) is an important type. Inappropriate activation and accumulation of platelets typically induced thrombosis, which may result in acute vessel occlusion and STEMI. Multiple cytokines have been shown to regulate platelet activation, but the relationship between HMGB2 and platelet activation has not been elucidated. We collected peripheral blood of STEMI patients and healthy adults, and mass spectrometry analysis of platelet proteins was conducted. The "edgeR" package was used to identify the differentially expressed proteins (DEPs). The Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene ontology (GO) and Gene Set Enrichment Analysis (GSEA) were used to identify the significantly changed pathways. Western blot and ELISA were used to detect the expression of a high mobility group box 2 (HMGB2). Flow cytometric analysis and platelet aggregation rate were performed to evaluate the activation of platelets. We identified ALOX5, HIST1H1B, S100A11, HMGB2, and RPS15A were the top five up-regulated proteins by differential expression analysis. Western blot verified that the relative protein expression of HMGB2 in platelet was significantly higher in STEMI patients compared with control adults, and the results of ELISA indicated that the serum HMGB2 level increased and significantly correlated with neutrophil count in STEMI patients. Further investigation showed that the platelet aggregation induced by ADP, the activation of integrin αIIbβ3 and CD62P expression on platelet surface were all enhanced by the recombinant HMGB2 (rHMGB2). In conclusion, HMGB2 may be the key molecule to regulate platelet activation in patients with STEMI, which may serve as a potential therapeutic target for STEMI.
Sections du résumé
Background
UNASSIGNED
Ischemic heart disease is one of the leading causes of death in the world, of which ST-segment elevation myocardial infarction (STEMI) is an important type. Inappropriate activation and accumulation of platelets typically induced thrombosis, which may result in acute vessel occlusion and STEMI. Multiple cytokines have been shown to regulate platelet activation, but the relationship between HMGB2 and platelet activation has not been elucidated.
Methods
UNASSIGNED
We collected peripheral blood of STEMI patients and healthy adults, and mass spectrometry analysis of platelet proteins was conducted. The "edgeR" package was used to identify the differentially expressed proteins (DEPs). The Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene ontology (GO) and Gene Set Enrichment Analysis (GSEA) were used to identify the significantly changed pathways. Western blot and ELISA were used to detect the expression of a high mobility group box 2 (HMGB2). Flow cytometric analysis and platelet aggregation rate were performed to evaluate the activation of platelets.
Results
UNASSIGNED
We identified ALOX5, HIST1H1B, S100A11, HMGB2, and RPS15A were the top five up-regulated proteins by differential expression analysis. Western blot verified that the relative protein expression of HMGB2 in platelet was significantly higher in STEMI patients compared with control adults, and the results of ELISA indicated that the serum HMGB2 level increased and significantly correlated with neutrophil count in STEMI patients. Further investigation showed that the platelet aggregation induced by ADP, the activation of integrin αIIbβ3 and CD62P expression on platelet surface were all enhanced by the recombinant HMGB2 (rHMGB2).
Conclusion
UNASSIGNED
In conclusion, HMGB2 may be the key molecule to regulate platelet activation in patients with STEMI, which may serve as a potential therapeutic target for STEMI.
Identifiants
pubmed: 37727529
doi: 10.2147/IJGM.S429761
pii: 429761
pmc: PMC10506601
doi:
Types de publication
Journal Article
Langues
eng
Pagination
4181-4191Informations de copyright
© 2023 Qin et al.
Déclaration de conflit d'intérêts
The authors declare that there are no conflicts of interest in this study.
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