Modulation of cartilage differentiation by melanoma inhibiting activity/cartilage-derived retinoic acid-sensitive protein (MIA/CD-RAP)

Schubert, Thomas; Schlegel, Jacqueline; Schmid, Rainer; Opolka, Alfred; Grässel, Susanne; Humphries, Martin J.; Bosserhoff, Anja‐Katrin

doi:10.3858/emm.2010.42.3.017

Cited by 26 publications

(30 citation statements)

References 31 publications

(44 reference statements)

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“…Mia1 stabilizes cartilage differentiation and inhibits cartilage differentiation into bone (Schubert et al, 2010). Sox9 regulates Mia1 expression through binding to a SOX consensus sequence in the Mia1 promoter (Xie et al, 1999).…”

Section: Sox9 Regulates the Expression Of Cartilage-associated Factormentioning

confidence: 99%

FGF signaling activates a Sox9-Sox10 pathway for the formation and branching morphogenesis of mouse ocular glands

et al. 2014

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Murine lacrimal, harderian and meibomian glands develop from the prospective conjunctival and eyelid epithelia and produce secretions that lubricate and protect the ocular surface. Sox9 expression localizes to the presumptive conjunctival epithelium as early as E11.5 and is detected in the lacrimal and harderian glands as they form. Conditional deletion showed that Sox9 is required for the development of the lacrimal and harderian glands and contributes to the formation of the meibomian glands. Sox9 regulates the expression of Sox10 to promote the formation of secretory acinar lobes in the lacrimal gland. Sox9 and FGF signaling were required for the expression of cartilageassociated extracellular matrix components during early stage lacrimal gland development. Fgfr2 deletion in the ocular surface epithelium reduced Sox9 and eliminated Sox10 expression. Sox9 deletion from the ectoderm did not affect Fgf10 expression in the adjacent mesenchyme or Fgfr2 expression in the epithelium, but appeared to reduce FGF signaling. Sox9 heterozygotes showed a haploinsufficient phenotype, in which the exorbital branch of the lacrimal gland was absent in most cases. However, enhancement of epithelial FGF signaling by expression of a constitutively active FGF receptor only partially rescued the lacrimal gland defects in Sox9 heterozygotes, suggesting a crucial role of Sox9, downstream of FGF signaling, in regulating lacrimal gland branching and differentiation.

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Section: Sox9 Regulates the Expression Of Cartilage-associated Factormentioning

confidence: 99%

FGF signaling activates a Sox9-Sox10 pathway for the formation and branching morphogenesis of mouse ocular glands

et al. 2014

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“…Itga2b and Itgb3 are known to be down-regulated by RA in a leukemia cell line (Liu et al, 2000; Csomos et al, 2010), though expression during inner ear development has not been characterized. However, integrins are known to play important roles in mesenchymal condensation and chondrogenesis, suggesting possible expression of both Itga2b and Itgb3 in the POM (Schubert et al, 2010). In summary, all gene expression changes detected by microarray analysis were in the direction predicted downstream of increased RA levels, some of which may be effectors of cochlear or vestibular morphogenesis based on tissue expression patterns.…”

Section: Resultsmentioning

confidence: 99%

Identification of putative retinoic acid target genes downstream of mesenchymal Tbx1 during inner ear development

Monks

Morrow

2012

Developmental Dynamics

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The T-box transcription factor Tbx1 is expressed in the otic vesicle and surrounding mesoderm of the periotic mesenchyme (POM) during inner ear development. Mesenchymal Tbx1 is essential for inner ear development, with conditional mutants displaying defects in both the auditory and vestibular systems. We have previously reported that mesodermal Tbx1 loss of function mutants (Mest-KO) have reduced expression of retinoic acid (RA) metabolic genes, Cyp26a1 and Cyp26c1, in the POM, consistent with other studies showing an increase in mesodermal RA reporter expression in Tbx1-/- embryos. However, putative RA effector genes whose expression is altered downstream of increased otic mesenchymal-epithelial RA signaling have remained elusive. Here we report the identification of eighteen retinoic acid responsive genes altered in Mest-KO conditional mutants by microarray gene profiling. Nine were chosen for biological validation including quantitative RT-PCR and in situ hybridization (Otor, Mia, Col2a1, Clu, Adm, Myt1, Dlx3, Itgb3 and Itga2b). This study provides a series of newly identified RA effector genes for inner ear development downstream of mesenchymal Tbx1 that may contribute to the inner ear phenotype observed in Tbx1 loss of function mouse models.

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“…They observed an increase of Agg and a decrease of osteocalcin compared to untreated dedifferentiated HACs [18]. …”

Section: Discussionmentioning

confidence: 99%

Redifferentiation of aged human articular chondrocytes by combining bone morphogenetic protein-2 and melanoma inhibitory activity protein in 3D-culture

et al. 2017

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Melanoma inhibitory activity (MIA) affects the differentiation to hyaline cartilage and can inhibit the osteogenic potential of bone morphogenetic protein (BMP)-2 in mesenchymal stem cells (MSC). The aim of this study was to investigate if MIA also inhibits the osteogenic potential of BMP-2 in human articular chondrocytes during redifferentiation, which may lead to a higher grade of differentiation without calcification. HAC of four female patients (mean age: 73.75 ±6.98) were seeded into 3D culture for 28 days; after adding the recombinant proteins, four groups were formed (Control, BMP-2, MIA, BMP-2+MIA). Samples were analysed for gene expression, glycosaminoglycan (GAG) content and histology on day 0, 14 and 28. Collagen type 2 (COL2A1) was significantly increased in the BMP-2 containing groups on day 28; BMP-2 (100-fold, p = 0.001), BMP-2+MIA (65-fold, p = 0.009) and similar to the level of native cartilage. Higher aggrecan (Agg) levels were present in the BMP-2 (3-fold, p = 0.007) and BMP-2+MIA (4-fold, p = 0.002) group after 14 days and in the BMP-2 (9-fold, p = 0.001) group after 28 days. Collagen type 10 (COL10A1) was increased in the BMP-2 containing groups (6-fold, p = 0.006) but these levels were significantly below native cartilage. Alkaline phosphatase (ALP), collagen type 1 (COL1A1) and the glycosaminoglycan (GAG) content did not reveal any relevant differences between groups. BMP-2 is a potent inducer for differentiation of HAC. A significant enhancement of this effect in combination with MIA could not be observed. Furthermore no significant reduction of osteogenic markers during re-differentiation of chondrocytes was present combining BMP-2 and MIA.

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Modulation of cartilage differentiation by melanoma inhibiting activity/cartilage-derived retinoic acid-sensitive protein (MIA/CD-RAP)

Cited by 26 publications

References 31 publications

FGF signaling activates a Sox9-Sox10 pathway for the formation and branching morphogenesis of mouse ocular glands

FGF signaling activates a Sox9-Sox10 pathway for the formation and branching morphogenesis of mouse ocular glands

Identification of putative retinoic acid target genes downstream of mesenchymal Tbx1 during inner ear development

Redifferentiation of aged human articular chondrocytes by combining bone morphogenetic protein-2 and melanoma inhibitory activity protein in 3D-culture

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