Skip to main content
. 2023 Feb 27;29(7):1830–1847. doi: 10.1111/cns.14142

FIGURE 6.

FIGURE 6

LncRNA INPP5F interacted with and negatively regulated miR‐335. (A) qRT‐PCR analysis of miR‐335 expression in RVLM of SIH and control rats. (B) Schematic of lncRNA INPP5F‐WT and lncRNA INPP5F‐MUT binding sites for miR‐335. (C) Biotinylated miR‐335 transfected into B104 cells with lncRNA INPP5F overexpression. LncRNA INPP5F expression was examined by qRT‐PCR after streptavidin capture. (D) Luciferase assay of B104 cells co‐transfected with lncRNA INPP5F‐WT reporter or lncRNA INPP5F‐MUT reporter and miR‐335 agomir or agomir NC. (E, F) qRT‐PCR analysis of miR‐335 expression in B104 cells with lncRNA INPP5F overexpression or silencing. (G) MiR‐335 expression was evaluated using qRT‐PCR after microinjection of pLV‐lncRNA INPP5F plasmid in RVLM of SIH rats. Data were presented as mean ± SEM. Statistical significance was determined by two‐tailed unpaired Student's t‐test (A, C–F) and one‐way ANOVA, followed by post hoc Bonferroni test (G). n = 6 rats per group (A, G). n = 6 of independent cell culture preparations (C–F). **p < 0.01, ns means non‐significant versus SIH group. ### p < 0.001, ns means non‐significant versus agomir NC group. ΔΔ p < 0.01 versus pLV‐NC group. && p < 0.01 versus ASO NC group. ASO, antisense oligonucleotide; MUT, mutant; NC, negative control; qRT‐PCR, quantitative reverse transcription polymerase chain reaction; RVLM, rostral ventrolateral medulla; SEM, standard error of the mean; SIH, stress‐induced hypertension; WT, wild type.