TGF-β-induced interleukin-6 participates in transdifferentiation of human tenon’s fibroblasts to myofibroblasts

Molecular vision

Kim, Sung-Joo¹  Hong, Samin¹  Jung, Sun-Ah¹  Lim, Eunhae¹  Lee, Jung-Jin¹  Seong, Gong Je¹  Lee, Joon H.¹ 

DOI  :  

学科分类：生物化学/生物物理

来源: Molecular Vision

【 摘 要 】

Purpose: To gain a better understandingof the roles of interleukins (ILs) in subconjunctival fibrosis, weinvestigated their expression in transforming growth factor-β1(TGF-β1)-stimulated Tenon’s fibroblasts and examined their associationwith the transdifferentiation of fibroblasts to myofibroblasts. Methods: After primary culture,fibroblasts derived from human Tenon’s capsule were exposed to TGF-β1.The expression of α-smooth muscle actin (α-SMA) protein was assessed bywestern immunoblots and immunofluorescence. The mRNA levels of variousILs were also evaluated by multiplex reverse transcription (RT)-PCR.Using the small interfering RNAs (siRNAs) specific for IL-6 andIL-11 and the promoter deletion assay, the contributions of IL-6and IL-11 to TGF-β1-induced induction of α-SMA were determined.Results: In human Tenon’s fibroblasts,TGF-β1 stimulated the expression of α-SMA protein determined by westernblot analysis and also increased the mRNA levels of IL-6 and IL-11determined by multiplex RT-PCR. On the western immunoblots andimmunofluorescence, the increased expression of α-SMA was attenuatedonly by the siRNAs specific for IL-6 but not by the siRNAsspecific for IL-11. When the activator protein-1 binding sitesof the IL-6 promoter region were deleted, the stimulationeffects of TGF-β1 decreased. Conclusions: Our data show thatautocrine IL-6 may participate in the TGF-β1-inducedtransdifferentiation of human Tenon’s fibroblasts to myofibroblasts,which is known to be an essential step for subconjunctival fibrosis.

【 授权许可】

Unknown