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<p>Neurogenic bladder (NB) is a lower urinary tract dysfunction caused by lesions in the nervous system that regulate urine storage and micturition. Fibrosis is considered the basic pathological alteration of NB, whereas the underlying mechanism remains unclear. Here, we find that Wnt11 is significantly up-regulated in the rat fibrotic bladders induced by bilateral pelvic nerve injury (BPNI) and spinal cord injury (SCI) and promotes bladder fibroblasts (BFs)-to-myofibroblasts transition and smooth muscle cells (SMCs) phenotypic transformation. Selective inhibition or gene silencing of Wnt11 in vivo and in vitro attenuates BFs and SMCs activation, and mitigates the development of NB fibrosis. Mechanistically, Wnt11 specifically binds to Vangl2 receptor to activate downstream JNK/c-JUN signaling via the membrane recruitment of DVL2. Further research shows that Wnt11 signaling interacts with transforming growth factor beta 1 (TGF-β1)/Smad-dependent pathway through the binding of membrane receptors (Vangl2 and TβR1) and the crosstalk of nuclear transcription factors. These findings uncover the regulatory mechanism and may provide a new therapeutic strategy for NB fibrosis.</p>

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Wnt11 mediates fibroblast–smooth muscle cell interaction to promote neurogenic bladder fibrosis in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月9日

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  • Qingyu Ge,
  • Junjie Zhang,
  • Zongyao Fan,
  • Yan Wang,
  • Xinglin Chen,
  • Dongdong Guo,
  • Tao Wang,
  • Cheng Ma,
  • Xinyu Zhai,
  • Guanqun Ju,
  • Baixin Shen,
  • Mingyue Tan,
  • Zhongqing Wei,
  • Dongliang Xu

摘要

Neurogenic bladder (NB) is a lower urinary tract dysfunction caused by lesions in the nervous system that regulate urine storage and micturition. Fibrosis is considered the basic pathological alteration of NB, whereas the underlying mechanism remains unclear. Here, we find that Wnt11 is significantly up-regulated in the rat fibrotic bladders induced by bilateral pelvic nerve injury (BPNI) and spinal cord injury (SCI) and promotes bladder fibroblasts (BFs)-to-myofibroblasts transition and smooth muscle cells (SMCs) phenotypic transformation. Selective inhibition or gene silencing of Wnt11 in vivo and in vitro attenuates BFs and SMCs activation, and mitigates the development of NB fibrosis. Mechanistically, Wnt11 specifically binds to Vangl2 receptor to activate downstream JNK/c-JUN signaling via the membrane recruitment of DVL2. Further research shows that Wnt11 signaling interacts with transforming growth factor beta 1 (TGF-β1)/Smad-dependent pathway through the binding of membrane receptors (Vangl2 and TβR1) and the crosstalk of nuclear transcription factors. These findings uncover the regulatory mechanism and may provide a new therapeutic strategy for NB fibrosis.