Fig. 3: tsRNA-0032 inhibits pathological lymphangiogenesis in vivo.
From: Targeting glycolytic reprogramming by tsRNA-0032 for treating pathological lymphangiogenesis
A C57BL/6 mice were transfected with negative control (NC) agomir, tsRNA-0032 agomir, NC antagomir, or tsRNA-0032 antagomir using subconjunctival injection, or left untreated (Ctrl). qRT-PCRs were conducted to detect tsRNA-0032 expression levels (n = 5, *P < 0.05, one-way ANOVA followed by post hoc Bonferroni test). B–D C57BL/6 mice underwent corneal suture placement, which remained in place for 7 days. Neolymphatic vessels in the flat-mounted cornea were visualized using the fluorescence signal of LYVE-1 (n = 5). Scale bar: 200 μm. Quantification of neolymphatic vessel coverage area (C) and total length (D) was conducted (n = 5). E, F C57BL/6 mice received subcutaneous injections with Matrigel, mixed with NC agomir, tsRNA-0032 agomir, NC antagomir, tsRNA-0032 antagomir, or left untreated (Ctrl). The matrigel plugs were harvested at day 14 after injection. The frozen sections were stained with DAPI (blue) and LYVE-1 antibody (red) (n = 5). Quantification of neolymphatic vessel coverage area was conducted (n = 5, *P < 0.05, one-way ANOVA followed by post hoc Bonferroni test, *P < 0.05 versus Ctrl group).
