Linked Life Data

9698454

Source:http://linkedlifedata.com/resource/pubmed/id/9698454

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-8-31
pubmed:abstractText
In the final stages of limb morphogenesis, autopodial cells leaving the progress zone differentiate into cartilage or undergo apoptotic cell death, depending on whether they are incorporated into the digital rays or interdigital spaces. Most evidence indicates that these two opposite fates of the autopodial mesoderm are controlled by BMP signaling. However, the molecular basis for these two distinct actions of BMPs, including the receptors involved in the process, is controversial. In this study we have addressed this question by exploring the presence in the developing autopod of diffusible signals able to modulate BMP function and by analyzing the effects of their exogenous administration on the pattern of expression of BMP receptor genes. Our findings show that tgfbeta2 and noggin genes are expressed in the condensing region of the developing digital rays in addition to the well-known distribution in the autopodial tissues of FGFs (apical ectodermal ridge, AER) and BMPs (AER, progress zone mesoderm, and interdigital regions). Exogenous administration of all the factors causes changes in the expression of the bmpR-1b gene which are followed by parallel alterations of the skeletal phenotype: FGFs inhibit the expression of bmpR-1b compatible with their function in the maintenance of the progress zone mesoderm in an undifferentiated state; and TGFbetas induce the expression of bmpR-1b and promote ectopic chondrogenesis, compatible with a function in the establishment of the position of the digital rays. In addition we provide evidence for the occurrence of an interactive loop between BMPs and noggin accounting for the spatial distribution of bmpR-1b which may control the size and shape of the skeletal pieces. In contrast to the bmpR-1b gene, the bmpR-1a gene is expressed at low levels in the autopodial mesoderm and its expression is not modified by any of the tested factors regardless of their effects on chondrogenesis or cell death. Finally, the role of BMPs in programmed cell death is confirmed here by the intense inhibitory effect of noggin on apoptosis, but the lack of correlation between changes in the pattern of cell death induced by treatment with the studied factors and the expression of either bmpR-1a or bmpR-1b genes suggest that a still-unidentified BMP receptor may account for this BMP function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0012-1606
pubmed:author
pubmed:copyrightInfo
Copyright 1998 Academic Press.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
200
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
35-45
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9698454-Animals, pubmed-meshheading:9698454-Apoptosis, pubmed-meshheading:9698454-Bone Morphogenetic Protein Receptors, pubmed-meshheading:9698454-Bone Morphogenetic Proteins, pubmed-meshheading:9698454-Carrier Proteins, pubmed-meshheading:9698454-Cartilage, pubmed-meshheading:9698454-Chick Embryo, pubmed-meshheading:9698454-Extremities, pubmed-meshheading:9698454-Fibroblast Growth Factors, pubmed-meshheading:9698454-Gene Expression Regulation, Developmental, pubmed-meshheading:9698454-Models, Biological, pubmed-meshheading:9698454-Morphogenesis, pubmed-meshheading:9698454-Protein Biosynthesis, pubmed-meshheading:9698454-Proteins, pubmed-meshheading:9698454-Receptors, Cell Surface, pubmed-meshheading:9698454-Receptors, Growth Factor, pubmed-meshheading:9698454-Signal Transduction, pubmed-meshheading:9698454-Toes, pubmed-meshheading:9698454-Transforming Growth Factor beta
pubmed:year
1998
pubmed:articleTitle
Morphogenesis of digits in the avian limb is controlled by FGFs, TGFbetas, and noggin through BMP signaling.
pubmed:affiliation
Facultad de Medicina, Universidad de Cantabria, C/Cardenal Herrera Oria s/n, Santander, 39011, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't