Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Super enhancer-driven LINC01013 mediates hypoxia-induced mitochondrial dysfunction by HSPA9 to determine pulmonary arterial smooth muscle cell fate

doi: 10.1007/s00018-025-06071-3

Figure Lengend Snippet: Human LINC01013 delivery aggravates PH progression in mice. A - B Right ventricular systolic pressure (RVSP) and RV/left ventricular (LV) + Septum weight ratio in the SuHx-induced PH mouse models ( n = 6). C Pulmonary artery velocity time integral (PAVTI), pulmonary artery acceleration time (PAAT) and left ventricular ejection fraction (LVEF) of the SuHx-induced PH mice models infected with AAV5 carrying human LINC01013 ( n = 6). D Expression of PCNA in lung tissues ( n = 5). E Pulmonary arterial morphological analysis was performed by using hematoxylin and eosin (HE) and Masson staining. Scale bar, 100 μm. F-G Immunofluorescence of TNF-α, and activities of SOD and Gpx in lung tissues ( n = 6). Scale bars, 50 μm. H RNA pull-down assays detected the interaction between LINC01013 and HSPA9 protein in mouse PASMCs. All values are presented as the mean ± SEM. Statistical analysis was performed with one-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001. Nor, normoxia; SuHx, hypoxic + Su5416; NC, negative control; ▲SMC, smooth muscle cell targeting

Article Snippet: Clonal constructs of LINC01013 targeting the smooth muscle cell-specific promoter SM22α (smooth muscle 22α) were packaged into serotype 5 adeno-associated virus (AAV5) vectors and synthesized by GeneChem (Shanghai, China) (Fig. A).

Techniques: Infection, Expressing, Staining, Immunofluorescence, Negative Control