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Abstract: FR-PO1058

Inhibition of HDAC11 Attenuates Renal Fibrosis Through Blocking Partial Epithelial-Mesenchymal Transition

Session Information

Category: CKD (Non-Dialysis)

  • 2303 CKD (Non-Dialysis): Mechanisms


  • Guan, Yingjie Angie, RI Hospital, Providence, Rhode Island, United States

HDAC11 is the only member of the class IV histone deacetylases (HDACs) and is highly expressed in brain, heart, kidney et al and participates in diverse pathophysiological processes, such as tumor growth, immune regulation, oxidant stress injury However, it remains unclear whether HDAC11 involves in renal fibrosis.


In this study, we assess the role of HDAC11 in the development of renal fibrosis in Unilateral Ureteral Obstruction (UUO) mouse model. To examine the efficacy of HDAC11 in renal fibrosis after UUO injury, FT895 at 5mg/kg in 50 uL DMSO was given intraperitoneally after ureteral ligation and then administered daily for 7 days. The mice were euthanized kidney was collected on day 7.


Masson trichrome staining results showed collagen fibrils were extensively deposited within the interstitial space in the kidney after UUO injury. Immunoblot analysis of kidney tissue lysate demonstrated increased expression of αSMA, collagen I, and fibronectin in the kidney after UUO injury. However, administration of FT895 significantly reduced ECM deposition and significantly decreased the expression levels of αSMA, collagen I, and fibronectin. To determine the effect of HDAC11 inhibition on the arrest of epithelial cells at G2/M and partial epithelial-mesenchymal transition (EMT), we examined the expression of pH3Ser10, a hallmark of cells arrested at G2/M and Snail and Twist, key transcription factors that drive EMT development in the obstructed kidney. Immunoblot analysis results showed that administration of FT895 significantly reduced the expression of pH3Ser10, Snail and Twist. In addition, we further visualize the immune cell infiltration by immunohistochemistry analysis of F4/80, a macrophage marker. FT895 treatment decreased infiltration of F4/80 macrophages in the interstitial areas of the obstructed kidneys.


These data provide strong evidence that inhibition of HDAC11 attenuates development of renal fibrosis in vivo through suppression of several events associated with partial EMT development. Therefore, inhibition of HDAC11 would be a promising therapeutic strategy for the treatment of renal fibrosis.