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1.

001-es BibID:BIBFORM013571
Első szerző:Felszeghy Szabolcs Béla (fogorvos, anatómus, kötőszövetbiológus)
Cím:Notch signalling is required for the survival of epithelial sterm cells in the continuously growing mouse incisor / Szabolcs Felszeghy, Marika Suomalainen, Irma Thesleff
Dátum:2010
ISSN:0301-4681
Megjegyzések:The Notch pathway regulates the renewal and fate decisions of stem cells in multiple tissues. Notch1, -2, as well as the Notch target gene Hes1 are expressed in the putative stem cells in the continuously growing mouse incisors, but so far there has not been any evidence for a function of the Notch pathway in the regulation of the incisor stem cells. We have analysed the effects of the Notch pathway inhibitor DAPT on the maintenance, proliferation, and differentiation of the epithelial stem cells in explant cultures of the mouse incisor. The proximal part of the incisor containing the cervical loop stem cell niche was dissected from newborn mice and cultured for 2-6 days in vitro. DAPT inhibited the expression of Notch target gene Hes1 in the cervical loop indicating that Notch signalling was inhibited in the putative stem cells. The most striking effect of DAPT was a significant reduction in the size of the cervical loop. DAPT caused a marked but partially reversible decrease in cell proliferation, as well as massive apoptosis in the epithelial stem cell niche. Interestingly, restricted apoptosis was detected within the Notch expressing putative stem cells also in the control cultures as well as in incisors in vivo, suggesting that apoptosis may be a mechanism regulating the size of the epithelial stem cell pool in the incisor. The differentiation of the epithelial cells into enamel-forming ameloblasts was not affected by DAPT but the number of preameloblasts was progressively decreased during culture period reflecting the depletion of stem and progenitor cells. Our results indicate that Notch signalling is required for epithelial stem cell survival and enamel formation in the continuously growing mouse incisor.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Differentiation. - 80 : (4-5) (2010), p. 241-248. -
További szerzők:Suomalainen, Marika Thesleff, Irma
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

001-es BibID:BIBFORM014423
Első szerző:Munne, Pauliina M.
Cím:Splitting placodes : effects of bone morphogenetic protein and Activin on the patterning and identity of mouse incisors / Munne, Pauliina M., Felszeghy Szabolcs, Jussila, Maria, Suomalainen, Marika, Thesleff, Irma, Jernvall, Jukka
Dátum:2010
ISSN:1520-541X
Megjegyzések:The single large rodent incisor in each jaw quadrant is evolutionarily derivedfrom a mammalian ancestor with many small incisors. The embryonic placode givingrise to the mouse incisor is considerably larger than the molar placode, and thequestion remains whether this large incisor placode is a developmental requisiteto make a thick incisor. Here we used in vitro culture system to experiment withthe molecular mechanism regulating tooth placode development and how mice havethick incisors. We found that large placodes are prone to disintegration andformation of two to three small incisor placodes. The balance between one largeor multiple small placodes was altered through the regulation of bonemorphogenetic protein (BMP) and Activin signaling. Exogenous Noggin, whichinhibits BMP signaling, or exogenous Activin cause the development of two tothree incisors. These incisors were more slender than normal incisors.Additionally, two inhibitor molecules, Sostdc1 and Follistatin, which regulatethe effects of BMPs and Activin and have opposite expression patterns, are likelyto be involved in the incisor placode regulation in vivo. Furthermore, inhibitionof BMPs by recombinant Noggin has been previously suggested to cause a change inthe tooth identity from the incisor to the molar. This evidence has been used tosupport a homeobox code in determining tooth identity. Our work provides analternative interpretation, where the inhibition of BMP signaling can lead tosplitting of the large incisor placode and the formation of partly separateincisors, thereby acquiring molar-like morphology without a change in toothidentity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
0 (Bone Morphogenetic Proteins)
0 (Carrier Proteins)
0 (Follistatin)
0 (Sostdc1 protein, mouse)
104625-48-1 (Activins)
148294-77-3 (noggin protein)
Activins/genetics/metabolism/*physiology
Animals
Body Patterning
Bone Morphogenetic
Proteins/genetics/metabolism/*physiology
Carrier Proteins/metabolism
Embryo, Mammalian/metabolism
Embryonic Development
Follistatin/metabolism/physiology
Incisor/anatomy & histology/*embryology
külföldön készült közlemény
Mice
Signal Transduction
Megjelenés:Evolution & Development. - 12 (2010), p. 383-392. -
További szerzők:Felszeghy Szabolcs Béla (1972-) (fogorvos, anatómus, kötőszövetbiológus) Jussila, Maria Suomalainen, Marika Thesleff, Irma Jernvall, Jukka
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

3.

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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