Changes in the distribution of type IV collagen, laminin, proteoglycan, and fibronectin during mouse tooth development

Thesleff, I; Barrach, H. J.; Foidart, Jean‐Michel; Vaheri, Antti; Pratt, Robert M.; Martin, George R.

doi:10.1016/0012-1606(81)90361-4

Cited by 224 publications

(81 citation statements)

References 12 publications

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“…Therefore, this finding may reflect changes in the extracellular matrices resulting from the formation of the basal lamina. The importance of basal lamina in the morphogenesis of teeth and other epithelial tissues has been claimed by many investigators (SLAVKIN and BRINGAS, 1976;THESLEFF et al, 1981;BERNFIELD and BANERJEE, 1982;OLIVE and RUSH, 1982), but its active role in the formation of epithelial rests remains unelucidated, although regeneration of the basal lamina which was once disrupted on disintegration of Hertwig's root sheath is crucial in the maintenance of epithelial island morphology.…”

Section: Discussionmentioning

confidence: 99%

Ultrastructural and histochemical study on the morphogenesis of epithelial rests of Malassez.

Hamamoto

Nakajima

Ozawa

1989

Archives of Histology and Cytology

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Section: Discussionmentioning

confidence: 99%

Ultrastructural and histochemical study on the morphogenesis of epithelial rests of Malassez.

Hamamoto

Nakajima

Ozawa

1989

Archives of Histology and Cytology

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“…Because the stellate reticulum becomes highly vascularized during advancing tooth development (Bonnaud, 1984) and because activin A and follistatin have been implicated in the regulation of angiogenesis (Breit et al, 2000;Larsson et al, 2001;Marchuk et al, 2003), we wondered whether a lack of angiogenesis could explain the morphology of the mutant stellate reticulum and perhaps also the reduced proliferation in the enamel epithelium. Therefore, we localized blood vessels by immunohistochemistry using an antibody against the basement membrane protein laminin, which has earlier been shown to mark blood vessels in the stellate reticulum (Thesleff et al, 1981). Both wild-type and follistatin mutant molars contained numerous blood vessels in the dental papilla and stellate reticulum regions.…”

Section: Fig 5 A-dmentioning

confidence: 99%

Modulation of activin/bone morphogenetic protein signaling by follistatin is required for the morphogenesis of mouse molar teeth

Wang

Suomalainen

Jorgez

et al. 2004

Developmental Dynamics

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Teeth form as ectodermal appendages, and their morphogenesis is regulated by conserved signaling pathways. The shape of the tooth crown results from growth and folding of inner dental epithelium, and the cusp patterning is regulated by transient signaling centers, the enamel knots. Several signal proteins in the transforming growth factor-␤ (TGF␤) superfamily are required for tooth development. Follistatin is an extracellular inhibitor of TGF␤ signaling. To investigate the roles of follistatin during tooth development, we analyzed in detail the expression patterns of follistatin, activin ␤A, as well as Bmp2, Bmp4, and Bmp7 during tooth morphogenesis. We also examined the tooth phenotypes of follistatin knockout mice and of transgenic mice overexpressing follistatin in the epithelium under the keratin 14 (K14) promoter. The folding of the dental epithelium was aberrant in the molars of follistatin knockout mice, and the cusps were shallow with reduced cell proliferation and lack of anteroposterior polarization. The functions of both primary and secondary enamel knots were apparently disturbed. In K14 -follistatin transgenic mice, the molar cusp pattern was also seriously affected (although different from the follistatin knockouts) and the occlusal surfaces of the molars were whorled. Their enamel was prematurely worn. In addition, all of the third molars were missing. Our results indicate that follistatin regulates morphogenesis and shaping of the tooth crown. We propose that finely tuned antagonistic effects between follistatin and TGF␤ superfamily signals are critical for enamel knot formation and function, as well as for patterning of tooth cusps. Developmental Dynamics 231:98 -108, 2004.

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“…Earlier studies have examined various BM constituents including collagen IV and laminin to determine their roles during tooth morphogenesis and cytodifferentiation 9,17) . .…”

Section: Introductionmentioning

confidence: 99%

“…Previously, most studies used polyclonal or monoclonal antibody to type IV collagen molecule as a whole and so no significant change in alpha chains composition could be observed among the BMs 10,11,17,33) .…”

mentioning

confidence: 99%

Differential Distribution of Type IV Collagen .ALPHA.1 to .ALPHA.6 Chains Suggests Distinct Molecular Interaction between the Epithelial and Mesenchymal Components of Benign Odontogenic Tumors

Han

Tamamura

Katase

et al. 2006

J. Hard Tissue Biology.

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Changes in the distribution of type IV collagen, laminin, proteoglycan, and fibronectin during mouse tooth development

Cited by 224 publications

References 12 publications

Ultrastructural and histochemical study on the morphogenesis of epithelial rests of Malassez.

Ultrastructural and histochemical study on the morphogenesis of epithelial rests of Malassez.

Modulation of activin/bone morphogenetic protein signaling by follistatin is required for the morphogenesis of mouse molar teeth

Differential Distribution of Type IV Collagen .ALPHA.1 to .ALPHA.6 Chains Suggests Distinct Molecular Interaction between the Epithelial and Mesenchymal Components of Benign Odontogenic Tumors

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