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| Title: | The attenuation of renal fibrosis by histone deacetylase inhibitors is associated with the plasticity of FOXP3+IL-17+ T cells |
| Authors: | Wen-Pyng Wu;Yi-Giien Tsai;Tze-Yi Lin;Ming-Ju Wu;Ching-Yuang Lin |
| Contributors: | 醫學系 |
| Keywords: | Unilateral ureteric obstruction, Renal fibrosis, Tgf-β, FOXP3+ IL-17+ T cells |
| Date: | 2017-07-10 |
| Issue Date: | 2020-08-10T03:25:42Z (UTC)
|
| Publisher: | BMC Nephrology |
| Abstract: | Abstract
Background: The histone deacetylase (HDAC) inhibitor, which has potential effects on epigenetic modifications,
had been reported to attenuate renal fibrosis. CD4+ forkhead box P3 (FOXP3)+ T regulatory (Treg) cells may be
converted to inflammation-associated T helper 17 cells (Th17) with tissue fibrosis properties. The association between
FOXP3+
IL-17+ T cells and the attenuation of renal fibrosis by the HDAC inhibitor is not clear.
Methods: This study evaluated the roles of the HDAC inhibitor, Treg cells and their differentiation into Th17 cells,
which aggravate chronic inflammation and renal fibrosis in a unilateral ureteral obstruction (UUO) mouse model. The
study groups included control and UUO mice that were monitored for 7, 14 or 21 days.
Results: Juxtaglomerular (JG) hyperplasia, angiotensin II type 1 receptor (AT1R) expression and lymphocyte infiltration
were observed in renal tissues after UUO but were decreased after trichostatin A (TSA) treatment, a HDAC inhibitor. The
number of CD4+
FOXP3+ T cells increased progressively, along with the number of FOXP3+
interleukin (IL)-17+ T cells,
after 14 days, and their numbers then progressively decreased with increasing CD4+
IL-17+ T cell numbers, as
demonstrated by double immunohistochemistry. Progressive renal fibrosis was associated with the loss of CD4 +
FOXP3+
IL-17+ T cells in splenic single-cell suspensions. FOXP3+
IL-17+ T cells expressed TGF-β1 both in vitro and
in vivo, and TGF-β1 expression was significantly knockdown by IL-17 siRNA in vitro. These cells were found to
play a role in converting Tregs into IL-17- and TGF-β1-producing cells.
Conclusions: TSA treatment decreased JG hyperplasia, the percentage of FOXP3+
IL-17+ cells and the degree of
fibrosis, suggesting that therapeutic benefits may result from epigenetic modifications. |
| URI: | https://ir.csmu.edu.tw:8080/ir/handle/310902500/21030 |
| Relation: | BMC Nephrology volume 18, Article number: 225 (2017) |
| Appears in Collections: | [醫學系] 期刊論文
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