Fig. 3: GMRSP is required for maintaining oxidative metabolism via regulating the PKM pre-mRNA splicing in VSMCs.

A Dotplot showing metabolic characteristics of vascular smooth muscle cells from patients with/without aortic dissection using scMetabolism algorithm based on the GSE213740. The circle size and color darkness both represent the scaled metabolic score. B, C GO analysis (D) and KEGG (E) analysis between H19-positive and H19-negative vascular smooth muscle cells in GSE213740. D After transfection with the indicated constructs for 36 hours, followed by PDGF-BB (20 ng/mL) treatment for 24 h, RNA sequencing was performed in human primary VSMCs. GMRSP regulates PKM pre-mRNA splicing, promoting PKM1 isoform formation and inhibiting PKM2 isoform formation. E Representative immunofluorescent images of F-actin (red), PKM1 (yellow), and PKM2 (green) in human primary VSMCs were determined, Scale bar: 50 μm. The seahorse glycolysis stress test (n = 8 biologically independent samples) (F) and representative images of TMRE staining, Scale bar: 50 μm (G), F-actin and MitoTracker staining, Scale bar: 5 μm (H) were obtained in human primary VSMCs transfected with the indicated constructs for 36 h, followed by PDGF-BB (20 ng/mL) treatment for 24 hours. Data are presented as the mean ± SD. The p values were calculated by a two-tailed unpaired Student’s t-test in (F). The data presented in (E–G) are representative of three independent experiments. Source data are provided as a Source Data file. GO, gene ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; PDGF, platelet-derived growth factor; VSMCs, vascular smooth muscle cells; GMRSP; glucose metabolism regulatory small protein; PKM, pyruvate kinase M; TMRE, tetra-methyl-rhodamine ester.