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001-es BibID:BIBFORM015600
035-os BibID:17564495
Első szerző:Wang, Xiu-Ping
Cím:An integrated gene regulatory network controls stem cell proliferation in teeth / Wang X. P., Suomalainen M., Felszeghy Sz., Zelarayan L. C., Alonso M. T., Plikus M. V., Maas R. L., Chuong C. M., Schimmang T., Thesleff I.
Dátum:2007
ISSN:1544-9173 (Linking)
Megjegyzések:Epithelial stem cells reside in specific niches that regulate their self-renewal and differentiation, and are responsible for the continuous regeneration oftissues such as hair, skin, and gut. Although the regenerative potential ofmammalian teeth is limited, mouse incisors grow continuously throughout life andcontain stem cells at their proximal ends in the cervical loops. In the labialcervical loop, the epithelial stem cells proliferate and migrate along the labialsurface, differentiating into enamel-forming ameloblasts. In contrast, thelingual cervical loop contains fewer proliferating stem cells, and the lingualincisor surface lacks ameloblasts and enamel. Here we have used a combination ofmouse mutant analyses, organ culture experiments, and expression studies toidentify the key signaling molecules that regulate stem cell proliferation in therodent incisor stem cell niche, and to elucidate their role in the generation ofthe intrinsic asymmetry of the incisors. We show that epithelial stem cellproliferation in the cervical loops is controlled by an integrated generegulatory network consisting of Activin, bone morphogenetic protein (BMP),fibroblast growth factor (FGF), and Follistatin within the incisor stem cellniche. Mesenchymal FGF3 stimulates epithelial stem cell proliferation, and BMP4represses Fgf3 expression. In turn, Activin, which is strongly expressed inlabial mesenchyme, inhibits the repressive effect of BMP4 and restricts Fgf3expression to labial dental mesenchyme, resulting in increased stem cellproliferation and a large, labial stem cell niche. Follistatin limits the numberof lingual stem cells, further contributing to the characteristic asymmetry ofmouse incisors, and on the basis of our findings, we suggest a model in whichFollistatin antagonizes the activity of Activin. These results show how thespatially restricted and balanced effects of specific components of a signalingnetwork can regulate stem cell proliferation in the niche and account forasymmetric organogenesis. Subtle variations in this or related regulatorynetworks may explain the different regenerative capacities of various organs andanimal species.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
0 (Bone Morphogenetic Proteins)
0 (Follistatin)
104625-48-1 (Activins)
62031-54-3 (Fibroblast Growth Factors)
Activins/metabolism
Animals
Bone Morphogenetic Proteins/metabolism
Cell Proliferation
Fibroblast Growth Factors/metabolism
Follistatin/metabolism
Gene Expression Regulation, Developmental
Gene Regulatory Networks/*genetics
In Situ Hybridization
Incisor/cytology/*growth & development
Mice
Mice, Transgenic
Models, Biological
Signal Transduction/genetics/*physiology
Stem Cells/*physiology
Tissue Culture Techniques
külföldön készült közlemény
Megjelenés:PLOS Biology. - 5 : 6 (2007), p. 1324-1333. -
További szerzők:Suomalainen, Marika Felszeghy Szabolcs Béla (1972-) (fogorvos, anatómus, kötőszövetbiológus) Zelarayan, Laura C. Alonso, Maria T. Plikus, Maxim V. Maas, Richard L. Chuong, Cheng-Ming Schimmang, Thomas Thesleff, Irma
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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