ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2019 and some content may be unavailable. To unlock all content for 2019, please visit the archives.

Abstract: SA-PO753

Improvement of the Effect of HIF-1α Stabilizer on the Destruction of Tight Junctions in Intestinal Epithelial Cells Induced by Homocysteine

Session Information

  • CKD: Mechanisms - III
    November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2103 CKD (Non-Dialysis): Mechanisms

Authors

  • Liu, Hua, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
  • Chen, Lei, Xi'an Jiaotong University, Xi'an, China
  • Liang, Shanshan, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
  • Xue, Jinhong, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
  • Jiang, Hongli, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
Background

Based on previous findings that homocysteine (Hcy) can increase the permeability of intestinal epithelial Caco2 cell and lead to decreased expression of tight junction molecules, the role of HIF-1α in intestinal barrier dysfunction caused by homocysteine and the mechanism of intervention of HIF-1α stabilizer (FG-4592) on these effects were explored.

Methods

Caco2 cells was cultured and divided into four groups: normal control group, FG4592 group, homocysteine group (Hcy group), Hcy+FG4592 group. mRNA and protein expression levels of HIF-1α, ZO-1, claudin-1, occludin were detected by RT-qPCR and Western blotting. The expression level of miR-223 was detected by RT-qPCR.

Results

Hcy (0.5 mM) can reduce the expression of HIF-1α, claudin-1, occludin and ZO-1mRNA and protein in Caco2 cells, and FG-4592 can improve the expression of these induced by Hcy (P<0.05) through the RT-qPCR or Western bloting method (Fig.1). Hcy can reduce the expression of miR-223 mRNA (P<0.05), while the FG-4592 can increase the expression of miR-223 mRNA (P<0.05) (Fig.2).

Conclusion

miR-223 may be involved in the maintenance of intestinal epithelial barrier function in the experiment of using uremic serum to stimulate Caco2 cells. HIF-1α stabilizer can improve the Hcy-induced reduction expression of HIF-1α, ZO-1, claudin-1, Occludin, up-regulate the expression of miR-223 and down-regulate the expression of NLRP3, the mechanism may involve the mir-223/NLRP3 pathway.