Figure 6.

Prenatal e-cigarette exposure induced microglial cell death and elevated susceptibility to cerebral ischemic injury

(A) Manhattan plot showing the top Gene Ontology (GO) terms (MF, molecular function; CC, cellular component; BP, biological process), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Reactome, enriched from the genes within DARs in microglia between control and e-cigarette exposed P7 rat brains.

(B) IPA using DE-Gs determined in microglia (snRNA-seq dataset) between control and e-cigarette exposed P7 rat brains.

(C) Enrichment of the transcription factor binding motifs from microglia differential peaks. The height of the letters was scaled to the frequency of each base at a given position.

(D) Prenatal e-cigarette exposure aggravated neonatal cerebral ischemic injury. Transient Middle Cerebral Artery Occlusion (tMCAO) was conducted on the postnatal day 9 rat pups of both genders with or without prenatal e-cigarette exposure. The brain infarct size was determined by TTC staining 48 h after tMCAO. The Relative infarct areas (calculated as the ratio of infarct area to the total brain area studied) were shown as Means ± SD in the barplot. ∗∗∗p < 0.001, e-cigarette exposure versus control. Control group: n = 5 male and 5 female pups. E-cigarette group: n = 4 male and 5 female pups. P values were calculated using two-tailed Student's t-test.