Embryonic Limb Mesenchyme Micromass Culture as an In Vitro Model for Chondrogenesis and Cartilage Maturation

DeLise, Anthony M.; Stringa, E.; Woodward, Wendy A.; Mello, María Alice Rostom de; Tuan, Rocky S.

doi:10.1385/1-59259-066-7:359

Cited by 61 publications

(74 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous reports have shown micromass culture forwards to chondrocyte maturation and matrix calcification similar to in vivo development (Zhang et al, 2004, DeLise et al, 2000. These studies indicate that matrices of cartilage nodules formed in micromass culture could be similar to matrices of cartilage produced by mesenchymal cell in early chondrogenesis.…”

Section: Discussionsupporting

confidence: 53%

Immunohistochemical Study of Amelogenin and Lysosome-Associate Membrane Proteins (LAMPs) in Cartilage

Hatakeyama

Oka

et al. 2014

Int. J. Morphol.

View full text Add to dashboard Cite

SUMMARY:Amelogenin is one of the enamel matrix proteins secreted by ameloblasts during enamel formation in tooth development. Recent studies showed that the amelogenin is expressed in chondrocyte. Lysosome-associated membrane proteins (LAMPs) have been identified as binding partner proteins to amelogenin and it has been suggested they act as signaling receptors of amelogenin. The purpose of this study is to clarify the localization of amelogenin and LAMPs in growth plate cartilage and cartilaginous nodules in micromass culture. Mouse knee joints including tibia growth plate at 4 weeks old and micromass cultures of limb bud mesenchymal cells after 2 weeks were fixed in paraformaldehyde, routinely processed, sections were cut and immunostained with amelogenin, collagen type II and type X, LAMP-1 and -3. The positive immunoreaction of amelogenin was observed both in proliferation and hypertrophic zone cartilage of growth plate after enzymatic pretreatment in immunostaining. Furthermore, cartilaginous nodules in micromass culture were immunopositive to amelogenin. The chondrocytes in the proliferation zone of the growth plate were immunopositive to LAMP-1 but weakly stained in the chondrocytes of hypertrophic zone. These observations indicate that amelogenin may be present in cartilage matrix produced in vivo and in vitro and amelogenin may involve cartilage formation through the LAMP-1 signaling pathway.

show abstract

Section: Discussionsupporting

confidence: 53%

Immunohistochemical Study of Amelogenin and Lysosome-Associate Membrane Proteins (LAMPs) in Cartilage

Hatakeyama

Oka

et al. 2014

Int. J. Morphol.

View full text Add to dashboard Cite

show abstract

“…35 Previously reported point mutations in BMPR1B associated with BDA2 showed a dominantnegative effect on chondrogenesis, when overexpressed in this system. 15,21 RCASBP(A) virus expressing the chicken orthologs of BMPR1B wt , BMPR1B C53R , BMPR1B dLBD , and the BDA2-associated dominant-negative mutant BMPR1B I200K .…”

Section: Gdf5-dependent Receptor Activation Is Lost In Bmpr1b C53rmentioning

confidence: 79%

Homozygous missense and nonsense mutations in BMPR1B cause acromesomelic chondrodysplasia-type Grebe

et al. 2013

View full text Add to dashboard Cite

Acromesomelic chondrodysplasias (ACDs) are characterized by disproportionate shortening of the appendicular skeleton, predominantly affecting the middle (forearms and forelegs) and distal segments (hands and feet). Here, we present two consanguineous families with missense (c.157T4C, p.(C53R)) or nonsense (c.657G4A, p.(W219*)) mutations in BMPR1B. Homozygous affected individuals show clinical and radiographic findings consistent with ACD-type Grebe. Functional analysis of the missense mutation C53R revealed that the mutated receptor was partially located at the cell membrane. In contrast to the wild-type receptor, C53R mutation hindered the activation of the receptor by its ligand GDF5, as shown by reporter gene assay. Further, overexpression of the C53R mutation in an in vitro chondrogenesis assay showed no effect on cell differentiation, indicating a loss of function. The nonsense mutation (c.657G4A, p.(W219*)) introduces a premature stop codon, which is predicted to be subject to nonsense-mediated mRNA decay, causing reduced protein translation of the mutant allele. A lossof-function effect of both mutations causing recessive ACD-type Grebe is further supported by the mild brachydactyly or even non-penetrance of these mutations observed in the heterozygous parents. In contrast, dominant-negative BMPR1B mutations described previously are associated with autosomal-dominant brachydactyly-type A2.

show abstract

“…This process requires the initial specification of precartilaginous cells (chondroprogenitors), which are not yet fully committed toward the cartilage lineage, and the following determination of a subset of these cells to form the definite cartilaginous condensation (Akiyama et al, 2005). The limb mesenchyme appears to have an intrinsic chondrogenic potential as a default fate, as can be seen in mesenchymal micromass cultures (see e.g., DeLise et al, 2000). The initial specification of mesenchymal cells to chondroprogenitors is, however, restricted to the core of the limb bud.…”

Section: Condensation Of the Digit Anlagenmentioning

confidence: 99%

Mechanisms of digit formation: Human malformation syndromes tell the story

Stricker

Mundlos

2011

Developmental Dynamics

View full text Add to dashboard Cite

Identifying the genetic basis of human limb malformation disorders has been instrumental in improving our understanding of limb development. Abnormalities of the hands and/or feet include defects affecting patterning, establishment, elongation, and segmentation of cartilaginous condensations, as well as growth of the individual skeletal elements. While the phenotype of such malformations is highly diverse, the mutations identified to date cluster in genes implicated in a limited number of molecular pathways, namely hedgehog, Wnt, and bone morphogenetic protein. The latter pathway appears to function as a key molecular network regulating different phases of digit and joint development. Studies in animal models not only extended our insight into the pathogenesis of these conditions, but have also contributed to our understanding of the in vivo functions and interactions of these key players. This review is aimed at integrating the current understanding of human digit malformations into the increasing knowledge of the molecular mechanisms of digit development. Developmental Dynamics 240:990-1004,

show abstract

Embryonic Limb Mesenchyme Micromass Culture as an In Vitro Model for Chondrogenesis and Cartilage Maturation

Cited by 61 publications

References 22 publications

Immunohistochemical Study of Amelogenin and Lysosome-Associate Membrane Proteins (LAMPs) in Cartilage

Immunohistochemical Study of Amelogenin and Lysosome-Associate Membrane Proteins (LAMPs) in Cartilage

Homozygous missense and nonsense mutations in BMPR1B cause acromesomelic chondrodysplasia-type Grebe

Mechanisms of digit formation: Human malformation syndromes tell the story

Contact Info

Product

Resources

About