To investigate the potential role and mechanism of C1q/tumor necrosis factor‑related protein‑9 (CTRP9) in diabetes‑induced endothelial‑mesenchymal transition (EndMT).
Methods
2
The experimental mice were randomly divided into four groups (Control
DM
Ad‑GFP+DM
and Ad‑CTRP9+DM). At 16 weeks of age
the mice were injected with Ad‑CTRP9 (1×10
9
pfu) or Ad‑GFP (1×10
9
pfu) via the tail vein. Four weeks after the first adenovirus injection
a cardiac ultrasound was performed. Then
the mice were anesthetized and sacrificed at the age of 20 weeks. The heart tissues were obtained for Masson staining and immunohistochemical staining. The EndMT‑related markers (CD31
α‑SMA
FSP1
Collagen Ⅰ
Collagen Ⅲ
TGF‑β1
and CTGF) were detected by Western Blot and quantitative real‑time PCR (RT‑PCR).
Results
2
The plasma level of CTRP9 was decreased in diabetic mice. Hyperglycemia prom
oted endothelial⁃to⁃mesenchymal transition (EndMT) and exacerbated collagen deposition
in vivo
whereas CTRP9 overexpression attenuated these effects without influencing cardiac function in diabetic mice.
Conclusion
2
The CTRP9 can alleviate diabetes‑induced EndMT.
关键词
Keywords
references
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