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Dhh signaling pathway regulates reconstruction of seminiferous tubule-like structure
Affiliation:1. Department of Immunology, Zunyi Medical University, Zunyi, China;2. Special Key Laboratory of Gene Detection & Therapy of Guizhou Province, Zunyi Medical University, Zunyi, China;3. Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine, Zunyi Medical University, Zunyi, China;4. People’s Hospital of Qingbaijiang District, Qingbaijiang, 61300 Chengdu, China;5. Department of Histology and Embryology, Zunyi Medical University, Zunyi 563000, China;1. Department of Gynecology, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang, China;2. Department of Orthopedics, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang, China;1. Health Management Center, Huizhou Central People''s Hospital, Huizhou, Guangdong, China;2. Department of Stomatology, Huizhou Central People''s Hospital, Huizhou, Guangdong, China;3. Department of Breast Surgery, Huizhou Central People''s Hospital, Huizhou, Guangdong, China;1. Pelvic Floor and Postpartum Rehabilitation Center, Changsha Maternal and Child Health Care Hospital, Changsha, Hunan 410007, PR China;2. Department of Gynaecology, Changsha Maternal and Child Health Care Hospital, Changsha, Hunan 410007, PR China;1. Werlhof-Institute Hannover, Schillerstr. 23, 30159 Hannover, Germany;2. Institute for Anatomy, University of Veterinary Medicine Hannover Foundation, Bischofsholer Damm 15, 30173 Hannover, Germany;3. Friedrich-Loeffler-Institute (FLI), Institute of Farm Animal Genetics (ING), Höltystrasse 10, 31535 Neustadt, Germany;1. Department of Obstetrics and Gynecology, Clinical Medical College, Yangzhou University, Yangzhou 225001, China;2. State Key Laboratory of Reproductive Medicine, Clinical Center of Reproductive Medicine, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China
Abstract:The reconstruction of a tubule-like structure in vitro has provided a promising system to analyze factors that drive morphogenesis and the underlying mechanisms. In this study, we took advantage of the inhibitor cyclopamine and a smoothened agonist to detect the role of the Dhh signaling pathway in the reconstructed tubule-like structure. Sertoli cells did not show polarity, rounded peritubular myoid cells and scattered Leydig cells were observed, combined with less laminin and lower proliferation of Leydig, peritubular myoid, germ, and Sertoli cells. However, in the presence of SAG, elongated peritubular myoid cells gathered at the bottom of polarized Sertoli cells, and most of the Leydig cells gathered at the outer part of the elongated peritubular myoid cells. Moreover, SAG promoted the secretion of laminin, assisting in the formation of the basal membrane and promoting the proliferation of Leydig, peritubular myoid, and germ cells. The level of Gli1 was significantly downregulated when treated with cyclopamine, whereas it was significantly upregulated when treated with SAG. These results indicate that the Dhh signaling pathway regulates the reconstruction of tubule-like structures by regulating the expression of Gli1.
Keywords:Dhh signaling pathway  Cyclopamine  Smoothened agonist  Seminiferous tubule  Reconstruction  Dhh"  },{"  #name"  :"  keyword"  ,"  $"  :{"  id"  :"  key0035"  },"  $$"  :[{"  #name"  :"  text"  ,"  _"  :"  Desert Hedgehog  SCB"  },{"  #name"  :"  keyword"  ,"  $"  :{"  id"  :"  key0045"  },"  $$"  :[{"  #name"  :"  text"  ,"  _"  :"  Sertoli cell barrier  SAG"  },{"  #name"  :"  keyword"  ,"  $"  :{"  id"  :"  key0055"  },"  $$"  :[{"  #name"  :"  text"  ,"  _"  :"  Smoothened agonist  DMSO"  },{"  #name"  :"  keyword"  ,"  $"  :{"  id"  :"  key0065"  },"  $$"  :[{"  #name"  :"  text"  ,"  _"  :"  Dimethyl sulfoxide  DDX4"  },{"  #name"  :"  keyword"  ,"  $"  :{"  id"  :"  key0075"  },"  $$"  :[{"  #name"  :"  text"  ,"  _"  :"  Dead box polypeptide 4  Gli1"  },{"  #name"  :"  keyword"  ,"  $"  :{"  id"  :"  key0085"  },"  $$"  :[{"  #name"  :"  text"  ,"  _"  :"  Glioma-associated oncogene homolod-1
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