Heat shock protein 70 mitigates black carbon particles-induced cardiac damage

Abstract

Studies have demonstrated the association between black carbon (BC) particles and elevated risk of cardiovascular disease. However, the mechanisms underlying this relationship remain unclear. This study aims to investigate the effects of BC exposure on gene expressions in mice myocardium. Mice were divided into 3 groups (phosphate buffer saline (PBS) group, C50 group (50 µg BC) and C100 group (100 µg BC)). RNA sequencing was employed to conduct transcriptome analysis on myocardium samples. The expression levels of candidate genes were verified by qRT-PCR. Western Blot and Immunohistochemistry techniques were utilized to evaluate the expression of heat shock protein 70 (Hsp70). BC exposure can cause an increase in the level of cardiac I-1β and IL-6. Transcriptome analysis revealed 1027 differentially expressed genes (DEGs) in the C100 group compared with the PBS group. Gene Ontology (GO) enrichment analysis demonstrated that these DEGs were primarily enriched in misfolded protein binding, respiratory chain and ATP metabolic process. Additionally, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated significant enrichment of DEGs in pathways mainly related to prion disease, oxidative phosphorylation and reactive oxygen species. HSPA1A and HSPA1B, as Hsp70 family genes, were enriched in GO term of misfolded protein binding and prion disease pathway. Moreover, the expression of cardiac Hsp70 was significantly decreased in both BC groups and showed a negative association with pro-inflammatory factors expression. BC exposure has been shown to cause inflammatory injury and may induce protein misfolding. Notably, Hsp70 was a potential cardioprotective factor and target for BC pollution-related effects.