Fig 1: Interferon-beta (IFN-ß) plus nicotinamide riboside (NR) restores cecal ligation puncture-(CLP)-induced endothelial glycocalyx damage by modulating the sirtuin 1 (SIRT1)/heparinase 1 pathway. (A) The expression of heparan sulfate proteoglycan (HSPG) in the lungs of wild-type (WT) and endothelial cell-specific Sirt1 conditional knockout (EC-Sirt1 cKO) mice. The HSPG expression was assessed by immunostaining (upper panel). The HSPG expression was quantified as the fluorescent intensity (lower panel). Mean values ± standard error of the mean are shown. n = 3. Cell nuclei were identified using 4’,6-diamidino-2-phenylindole (DAPI) (blue). Scale bar = 10 µm. (B) The effect of IFN-ß and/or NR on the expression of HSPG in the lungs of mice subject to CLP-induced sepsis. IFN-ß (2 µg/kg) plus NR (40 µmole/kg) were intravenously administered at 6 h and 16 h after CLP. At 18 h after CLP, HSPG was immunostained. (C) The Sirt1 knockdown abolished lipopolysaccharide-(LPS)-induced increase of Heparinase 1 (HPA1) in murine yolk sac endothelial cells (MYSECs). The MYSECs were transfected with control or Sirt1 SiRNA for 48 h and treated with 300 ng/ml of LPS in the presence or absence of 40 ng/ml of IFN-ß plus 800 µM NR for 24 h. The levels of SIRT1, HPA1, and ß-actin were measured by Western blot. A typical example of a Western blot analysis (upper panel) and the summarized data (lower panel) are shown. n = 3. **P < 0.01.
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