The process of calcification during development of the rat tracheal cartilage characterized by distribution of alkaline phosphatase activity and immunolocalization of types I and II collagens and glycosaminoglycans of proteoglycans

Sasano, Yasuyuki; Mizoguchi, Itaru; Furusawa, Mitsuru; Aiba, Nobuhiko; Ohtani, Eriko; Iwamatsu, Yoko; Kagayama, Manabu

doi:10.1007/bf00191449

Cited by 24 publications

(20 citation statements)

References 38 publications

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“…In the rat, hypertrophic chondrocytes were reported in trachea from 2‐month‐old animals. They were associated with cartilage calcification, not with ossification (Sasano et al, ; Sasano et al, ). In contrast, no mineralization of the tracheal cartilage was observed in mice from the same age, indicating differences between species.…”

Section: Discussionmentioning

confidence: 99%

Lung development requires an active ERK/MAPK pathway in the lung mesenchyme

Boucherat

Landry-Truchon

Aoidi

et al. 2016

Developmental Dynamics

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Background: Reciprocal epithelial-mesenchymal communications are critical throughout lung development, dictating branching morphogenesis and cell specification. Numerous signaling molecules are involved in these interactions, but the way epithelialmesenchymal crosstalk is coordinated remains unclear. The ERK/MAPK pathway transduces several important signals in lung formation. Epithelial inactivation of both Mek genes, encoding ERK/MAPK kinases, causes lung agenesis and death. Conversely, Mek mutation in mesenchyme results in lung hypoplasia, trachea cartilage malformations, kyphosis, omphalocele, and death. Considering the negative impact of kyphosis and omphalocele on intrathoracic space and, consequently, on lung growth, the exact role of ERK/MAPK pathway in lung mesenchyme remains unresolved. Results: To address the role of the ERK/MAPK pathway in lung mesenchyme in absence of kyphosis and omphalocele, we used the Tbx4Cre deleter mouse line, which acts specifically in lung mesenchyme. These Mek mutants did not develop kyphosis and omphalocele but they presented lung hypoplasia, tracheal defects, and neonatal death. Tracheal cartilage anomalies suggested a role for the ERK/MAPK pathway in the control of chondrocyte hypertrophy. Moreover, expression data indicated potential interactions between the ERK/MAPK and canonical Wnt pathways during lung formation. Conclusions: Lung development necessitates a functional ERK/MAPK pathway in the lung mesenchymal layer in order to coordinate efficient epithelial-mesenchymal interactions. Developmental Dynamics 246:72-82, 2017. V C 2016 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Lung development requires an active ERK/MAPK pathway in the lung mesenchyme

Boucherat

Landry-Truchon

Aoidi

et al. 2016

Developmental Dynamics

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“…Decalcification had no effect on immunoreactivity of type I collagen. The enzymatic pretreatments using hyaluronidase and protease were well established for immunohistochemistry of extracellular matrix proteins in our previous studies (Sasano et al 1993(Sasano et al , 1997(Sasano et al , 1998. The hyaluronidase treatment was better to reveal the immunoreactivity for type I collagen, osteonectin and osteopontin whereas the protease was better for BSP and osteocalcin.…”

Section: Discussionmentioning

confidence: 99%

Expression of major bone extracellular matrix proteins during embryonic osteogenesis in rat mandibles

et al. 2000

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It is not known how bone proteins appear in the matrix before and after calcification during embryonic osteogenesis. The present study was designed to investigate expressions of the five major bone extracellular matrix proteins--i.e. type I collagen, osteonectin, osteopontin, bone sialoprotein and osteocalcin--during osteogenesis in rat embryonic mandibles immunohistochemically, and their involvement in calcification demonstrated by von Kossa staining. Wistar rat embryos 14 to 18 days post coitum were used. Osteogenesis was not seen in 14-day rat embryonic mandibles. Type I collagen was localized in the uncalcifed bone matrix in 15-day mandibles, where no other bone proteins showed immunoreactivity. Osteonectin, osteopontin, bone sialoprotein and osteocalcin appeared almost simultaneously in the calcified bone matrix of 16-day mandibles and accumulated continuously in 18-day mandibles. The present study suggested that type I collagen constitutes the basic framework of the bone matrix upon which the noncollagenous proteins are oriented to lead to calcification, whereas the noncollagenous proteins are deposited simultaneously by osteoblasts and are involved in calcification cooperatively.

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“…By combining immunofluorescence images and the corresponding images obtained by confocal laser‐scanning microscopy in transmission mode, we were able to define the histological localization of type II collagen more definitively than when we combined immunofluorescence images and the corresponding DIC images. Type II collagen is the major and unique collagenous component of cartilage and, with type I collagen, it plays an important role in chondrogenesis during embryonic development (Sasano et al. 1992, 1993; Ishizeki et al.…”

Section: Discussionmentioning

confidence: 99%

“…2007). By contrast, type II collagen is the major and unique collagenous component of cartilage and plays an important role in chondrogenesis during embryonic development (Sasano et al. 1992, 1993; Ishizeki et al.…”

Section: Introductionmentioning

confidence: 99%

Localization of type II collagen in the lingual mucosa of rats during the morphogenesis of circumvallate papillae

2010

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Iwasaki, S., Aoyagi, H. and Yoshizawa, H. 2011. Localization of type II collagen in the lingual mucosa of rats during the morphogenesis of circumvallate papillae.-Acta Zoologica (Stockholm) 92: 67-74.Immunoreactivity specific for type II collagen was recognized first in the mesenchymal connective tissue just beneath the circumvallate papilla placode in fetuses on E13. At this stage, most of the lingual epithelium was pseudostratified epithelium composed of one or two layers of cuboidal cells. However, the epithelium of the circumvallate papilla placode was composed of several layers of cuboidal cells. Immunoreactivity specific for type II collagen was detected mainly on the lamina propria just beneath the lingual epithelium of the rudiment of the circumvallate papilla in fetuses on E15 and on E17, and slight immunostaining was detected on the lamina propria around the rudiment. In fetuses on E19, immunoreactivity specific for type II collagen was widely and densely distributed on the connective tissue around the developing circumvallate papillae and on the connective tissue that surrounded the lingual muscle. Immunoreactivity specific for type II collagen was sparsely distributed on the lamina propria of central bulge. After birth, morphogenesis of the circumvallate papillae advanced gradually with the increase in size of the tongue. Immunoreactivity specific for type II collagen was distinctively distributed in the lamina propria around circumvallate papilla, in the central bulge, and in the connective tissue that surrounded the lingual muscle.Shin-ichi Iwasaki,

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The process of calcification during development of the rat tracheal cartilage characterized by distribution of alkaline phosphatase activity and immunolocalization of types I and II collagens and glycosaminoglycans of proteoglycans

Cited by 24 publications

References 38 publications

Lung development requires an active ERK/MAPK pathway in the lung mesenchyme

Lung development requires an active ERK/MAPK pathway in the lung mesenchyme

Expression of major bone extracellular matrix proteins during embryonic osteogenesis in rat mandibles

Localization of type II collagen in the lingual mucosa of rats during the morphogenesis of circumvallate papillae

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