Distinct spatial and temporal distributions of aggrecan and versican in the embryonic chick heart

Zanin, Mary K.B.; Bundy, Justin; Ernst, Heidemarie; Wessels, Andy; Conway, Simon J.; Hoffman, Stanley

doi:10.1002/(sici)1097-0185(19991201)256:4<366::aid-ar4>3.0.co;2-#

Cited by 51 publications

(46 citation statements)

References 53 publications

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“…Robust HA staining persisted in the AV cushions from the early cushion-forming stage (HH stage-17) to the cushion maturation stage (HH stage-29). Consistent with a previous report indicating declining mRNA expression of aggrecan in the heart after HH stage-20 [26], we found that aggrecan protein was most intensely expressed at HH stage-24 but was less abundantly expressed at HH stage-29 in the heart. …”

Section: Resultssupporting

confidence: 92%

“…HA localization was histochemically detected with hyaluronan binding protein (HABP) following the protocol described previously [25]. Production and specificity of the anti-chick versican and anti-chick aggrecan antibodies were described previously [26]. At the early stage of cardiac cushion expansion (HH stage-17), intense immunostaining of versican was observed in the basement membrane of the endocardial side of myocardium, most prominently at the distal end of the cardiac inlet and outlet (arrows in Figure 1A).…”

Section: Resultsmentioning

confidence: 99%

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BMP-2 Induces Versican and Hyaluronan That Contribute to Post-EMT AV Cushion Cell Migration

et al. 2013

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Distal outgrowth and maturation of mesenchymalized endocardial cushions are critical morphogenetic events during post-EMT atrioventricular (AV) valvuloseptal morphogenesis. We explored the role of BMP-2 in the regulation of valvulogenic extracellular matrix (ECM) components, versican and hyaluronan (HA), and cell migration during post-EMT AV cushion distal outgrowth/expansion. We observed intense staining of versican and HA in AV cushion mesenchyme from the early cushion expansion stage, Hamburger and Hamilton (HH) stage-17 to the cushion maturation stage, HH stage-29 in the chick. Based on this expression pattern we examined the role of BMP-2 in regulating versican and HA using 3D AV cushion mesenchymal cell (CMC) aggregate cultures on hydrated collagen gels. BMP-2 induced versican expression and HA deposition as well as mRNA expression of versican and Has2 by CMCs in a dose dependent manner. Noggin, an antagonist of BMP, abolished BMP-2-induced versican and HA as well as mRNA expression of versican and Has2. We further examined whether BMP-2-promoted cell migration was associated with expression of versican and HA. BMP-2- promoted cell migration was significantly impaired by treatments with versican siRNA and HA oligomer. In conclusion, we provide evidence that BMP-2 induces expression of versican and HA by AV CMCs and that these ECM components contribute to BMP-2-induced CMC migration, indicating critical roles for BMP-2 in distal outgrowth/expansion of mesenchymalized AV cushions.

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Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 99%

BMP-2 Induces Versican and Hyaluronan That Contribute to Post-EMT AV Cushion Cell Migration

et al. 2013

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“…5M,N). Overall, this expression pattern of zebrafish versican was equivalent to that of other vertebrate versican (Mjaatvedt et al, 1998;Zanin et al, 1999;Perissinotto et al, 2000).…”

Section: Expression Of Dermacan Mrna During Embryogenesismentioning

confidence: 65%

Characterization of dermacan, a novel zebrafish lectican gene, expressed in dermal bones

Kang

Oohashi

Kawakami

et al. 2004

Mechanisms of Development

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We report here the isolation and characterization of a cDNA encoding zebrafish dermacan, a novel member of hyaluronan (HA)-binding proteoglycans, which was termed after its characteristic expression in the zebrafish dermal bones. The deduced protein sequence shares the typical modular elements of lecticans. Sequence comparison covering the C-terminal globular domain demonstrated that dermacan shows high homology with zebrafish versican but is distinct from any other identified lecticans. Genomic DNA analysis demonstrated that dermacan and versican were encoded by distinct genes in the zebrafish genome. The expression of dermacan is initiated in the sclerotome and cephalic paraxial mesoderm at 16 h postfertilization. During the pharyngular period, dermacan transcripts were detected in the sclerotome, tail fin bud, pharyngular arch primordial region, and otic vesicle. In the development of craniofacial bones, dermacan expression was detected typically in the opercle and dentary. These regions belong to the craniofacial dermal bones. aggrecan expression, in contrast, was observed in the elements of craniofacial cartilage bones. In the dermacan-morpholino-injected embryos, dermal bones, e.g. opercle, dentary, and branchiostegal rays, as well as axial skeleton in the trunk, showed decreased ossification. We conclude that dermacan is a novel lectican gene, and that zebrafish lectican genes have genetically diverged. In addition, our data suggest the involvement of dermacan in zebrafish dermal bone development.

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“…The data described here supports the hypothesis that TBX20 acts upstream of aggrecan. Aggrecan is one of the main chondroitin sulfate proteoglycan constituents of the spongiosa layer in avian valves, and is required to withstand compressive forces against blood flow [32], [43], and reportedly has a role in valve cell differentiation [44], [64].…”

Section: Discussionmentioning

confidence: 99%

Effect of altered haemodynamics on the developing mitral valve in chick embryonic heart

Pang

Parnall

Loughna

2017

Journal of Molecular and Cellular Cardiology

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Intracardiac haemodynamics is crucial for normal cardiogenesis, with recent evidence showing valvulogenesis is haemodynamically dependent and inextricably linked with shear stress. Although valve anomalies have been associated with genetic mutations, often the cause is unknown. However, altered haemodynamics have been suggested as a pathogenic contributor to bicuspid aortic valve disease. Conversely, how abnormal haemodynamics impacts mitral valve development is still poorly understood. In order to analyse altered blood flow, the outflow tract of the chick heart was constricted using a ligature to increase cardiac pressure overload. Outflow tract-banding was performed at HH21, with harvesting at crucial valve development stages (HH26, HH29 and HH35). Although normal valve morphology was found in HH26 outflow tract banded hearts, smaller and dysmorphic mitral valve primordia were seen upon altered haemodynamics in histological and stereological analysis at HH29 and HH35. A decrease in apoptosis, and aberrant expression of a shear stress responsive gene and extracellular matrix markers in the endocardial cushions were seen in the chick HH29 outflow tract banded hearts. In addition, dysregulation of extracellular matrix (ECM) proteins fibrillin-2, type III collagen and tenascin were further demonstrated in more mature primordial mitral valve leaflets at HH35, with a concomitant decrease of ECM cross-linking enzyme, transglutaminase-2. These data provide compelling evidence that normal haemodynamics are a prerequisite for normal mitral valve morphogenesis, and abnormal blood flow could be a contributing factor in mitral valve defects, with differentiation as a possible underlying mechanism.

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Distinct spatial and temporal distributions of aggrecan and versican in the embryonic chick heart

Cited by 51 publications

References 53 publications

BMP-2 Induces Versican and Hyaluronan That Contribute to Post-EMT AV Cushion Cell Migration

BMP-2 Induces Versican and Hyaluronan That Contribute to Post-EMT AV Cushion Cell Migration

Characterization of dermacan, a novel zebrafish lectican gene, expressed in dermal bones

Effect of altered haemodynamics on the developing mitral valve in chick embryonic heart

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