1. Academic Validation
  2. SCF/c-kit signaling pathway participates in ICC damage in neurogenic bladder

SCF/c-kit signaling pathway participates in ICC damage in neurogenic bladder

  • Cell Cycle. 2020 Aug;19(16):2074-2080. doi: 10.1080/15384101.2020.1793059.
Yuan Ma 1 Yan Chen 1 Yan Zheng 2 Yibo Wen 3 Yunlong Li 3 Jinjin Feng 3 Yulin He 3 Jianguo Wen 4
Affiliations

Affiliations

  • 1 Institute of Clinical Medicine, Urodynamic Center and Department of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
  • 2 Immunization Key Lab of Kidney Disease of Henan Province, People's Hospital of Henan Province, Zhengzhou University , Zhengzhou, China.
  • 3 Department of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
  • 4 Institute of Clinical Medicine, Urodynamic Center and Department of Urology, Institute of Clinical Medicine, Pediatric Urodynamic Center and Department of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Abstract

Neurogenic bladder (NB) is a type of double renal dysfunction caused by nerve lesions. The interstitial cells of Cajal (ICC) damage are involved in bladder dysfunction. The aim of this study is to investigate the effect of stem cell factor (SCF)/c-Kit signaling pathway on ICC damage in NB model rats. Maximum cystometric capacity (MCC), bladder leak point pressures (BLPP), and bladder compliance (BC) were measured in sham-operated and NB model rats. Immunofluorescent staining for c-Kit was performed to determine ICC count in rat bladder trigone. The morphology and ultrastructure changes of ICCs were observed under an electron microscope. The mRNA levels of c-Kit and SCF in bladder tissues were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The protein levels of c-Kit, SCF, p-JAK, p-STAT1, and p-STAT3 in bladder tissues were determined by western blot. ICC proliferation was detected by CCK-8 assay. NB resulted in changes in ultrastructure changes of ICCs and a decrease in the number of ICCs and in expression of c-Kit, SCF, p-JAK, p-STAT1, and p-STAT3 in NB tissues. Inhibition of SCF/c-Kit signaling pathway suppressed ICC proliferation by inhibiting JAK/STAT3 pathway. Moreover, inhibition of SCF/c-Kit signaling pathway impaired the SCF-induced attenuation of ICC damage in NB model rats. Collectively, our data indicate that SCF/c-Kit signaling pathway participates in ICC damage in NB.

Keywords

Stem cell factor/c-kit; interstitial cells of Cajal; neurogenic bladder.

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