title: Blocking P2X receptors can inhibit the injury-induced proliferation of olfactory epithelium progenitor cells in adult mouse.
abstract: OBJECTIVE
  The olfactory epithelium (OE) is unusual for its remarkable regenerative capacity and sustained neurogenesis of olfactory receptor neurons (ORNs) throughout adult life. Regeneration of ORNs is accomplished by basal cells in the OE, including stem cells and progenitor cells. Although there is considerable knowledge about the roles of OE basal cells in ORN turnover, the molecular mechanism that regulates the proliferation and differentiation of adult OE basal cells is not fully understood. As intercellular signaling molecules, purines have been reported to meditate proliferation, differentiation and migration of many kinds of neural stem cells. However, it is still unclear whether ATP, which could be released by injured ORNs, plays a role in regulating neurogenesis in ORN turnover.
  
  
  METHODS
  RT-PCR and immunohistochemistry were used to detect the expression of ionotropic purinergic receptors-P2X receptors in adult mouse OE. By using the olfactory bulbectomy model and in vivo administration of P2X receptors antagonists, the function of P2X receptors in regulating the proliferation of OE progenitor cell was evaluated.
  
  
  RESULTS
  We found that basal cells in the adult mouse OE express functional P2X receptors, and blocking the activities of P2X receptors can significantly inhibit the injury-induced proliferation of OE basal cells.
  
  
  CONCLUSIONS
  Our research provides evidence in support of the hypothesis that purinergic signaling can serve as a paracrine signal in regulating the neurogenesis of OE in adult mouse.
authors.affiliation: Institute of Neuroscience, Neuroscience Research Center of Changzheng Hospital, Second Military Medical University, Shanghai, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Gao
authors.forename: Li
authors.initials: L
authors.lastname: Cao
authors.forename: Yang
authors.initials: Y
authors.lastname: Qiu
authors.forename: Zhida
authors.initials: Z
authors.lastname: Su
authors.forename: Geoffrey
authors.initials: G
authors.lastname: Burnstock
authors.forename: Zhenghua
authors.initials: Z
authors.lastname: Xiang
authors.forename: Cheng
authors.initials: C
authors.lastname: He
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009830:Olfactory Bulb / Q000601:surgery; D009831:Olfactory Mucosa / Q000166:cytology* / Q000378:metabolism; D018034:Olfactory Receptor Neurons / Q000166:cytology / Q000473:pathology; D016133:Polymerase Chain Reaction; D058920:Purinergic P2X Receptor Antagonists / Q000494:pharmacology*; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D058469:Receptors, Purinergic P2X / Q000378:metabolism; D013234:Stem Cells / Q000187:drug effects* / Q000378:metabolism; D013498:Suramin / Q000494:pharmacology
chemical_list: D058920:Purinergic P2X Receptor Antagonists; D012333:RNA, Messenger; D058469:Receptors, Purinergic P2X; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; D011732:Pyridoxal Phosphate; D013498:Suramin; C505409:Casp3 protein, mouse; D053148:Caspase 3