Thoracic Vertebrae 11
Ontology highlight
ABSTRACT:
SUBMITTER: 
David Nickerson
PROVIDER: a77 | Physiome Model Repository |
REPOSITORIES: PMR
Similar Datasets
Project description:The number of vertebrae is precisely defined in almost all vertebrate species, but varies considerably in pigs, making this animal an excellent model for studying the mechanisms that control vertebral number. Vertnin (VRTN) variants have been associated with thoracic vertebral number (TVN) in pigs. However, the causal relation between VRTN and TVN remains to be established, and the role of VRTN in modulating TVN is not yet known. Here, we demonstrate that VRTN is one of the genes responsible for determining TVN. We show that VRTN is a DNA-binding transcription factor, which is essential for the formation of thoracic vertebrae during early embryogenesis as VRTN-null mice showed embryonic lethality at the later thoracic somite stages and had fewer somites than their wild-type and heterozygous littermates. We also show that VRTN causative variants increase Notch signaling in pig embryos, suggesting that VRTN controls segment number by altering the pace of somatic segmentation. These findings advance our understanding of the role of VRTN in the formation of thoracic vertebrae and reveal new aspects of somite developmental biology.
2019-10-09 | GSE87775 | GEO
Project description:The number of vertebrae is precisely defined in almost all vertebrate species, but varies considerably in pigs, making this animal an excellent model for studying the mechanisms that control vertebral number. Vertnin (VRTN) variants have been associated with thoracic vertebral number (TVN) in pigs. However, the causal relation between VRTN and TVN remains to be established, and the role of VRTN in modulating TVN is not yet known. Here, we demonstrate that VRTN is one of the genes responsible for determining TVN. We show that VRTN is a DNA-binding transcription factor, which is essential for the formation of thoracic vertebrae during early embryogenesis as VRTN-null mice showed embryonic lethality at the later thoracic somite stages and had fewer somites than their wild-type and heterozygous littermates. We also show that VRTN causative variants increase Notch signaling in pig embryos, suggesting that VRTN controls segment number by altering the pace of somatic segmentation. These findings advance our understanding of the role of VRTN in the formation of thoracic vertebrae and reveal new aspects of somite developmental biology.
2019-10-09 | GSE87774 | GEO
Project description:VRTN Regulates the Number of Thoracic Vertebrae During Vertebrate Development
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Project description:To compare gene expression profiling of EMB+ cells and EMB- cells whin CD45-Ter119-CD31--Thy1-6C3-CD200+CD105- population across long bone and vertebrae, we isolated related cells form long bone or vertebrae of zic1 -cre mtmg mice by FACS.
2023-04-30 | GSE230724 | GEO
Project description:Very little is known about how intervertebral disc (IVD) is formed or maintained. Members of the TGF-ß superfamily are secreted signaling proteins that regulate many aspects of development including cellular differentiation. We recently showed that deletion of Tgfbr2 in Col2a expressing tissue results in alterations in development of IVD annulus fibrosus. The results suggested TGF-ß has an important role in regulating development of the axial skeleton, however, the mechanistic basis of TGF-ß action in these specialized joints is not known. One of the hurdles to understanding development of IVD is a lack of known markers. To identify genes that are enriched in the developing IVD and to begin to understand the mechanism of TGF-ß action in IVD development, we undertook a global analysis of gene expression comparing gene expression profiles in developing vertebrae and IVD. We also compared expression profiles in tissues from wild type and Tgfbr2 mutant mice. Lists of IVD and vertebrae enriched genes were generated. Expression patterns for several genes were verified either through in situ hybridization or literature/ database searches resulting in a list of genes that can be used as markers of IVD. Cluster analysis using genes listed under the Gene Ontology terms multicellular organism development and pattern specification indicated that mutant IVD more closely resembled vertebrae than wild type IVD. We propose TGF-ß has two functions in IVD development: 1) to prevent chondrocyte differentiation in the presumptive IVD and 2) to promote differentiation of annulus fibrosus from sclerotome. We have identified genes that are enriched in the IVD and regulated by TGF-ß that warrant further investigation as regulators of IVD development. Thirteen samples were analyzed. This includes three biological replicates of laser captured IVD from E13.5 day control mice, three biological replicates of laser captured vertebrae from the same E13.5 day control mice, three biological relicates of laser captured vertebrae from E13.5 day Col2aCre;Tgfbr2lox/lox mice, and four biological replicates of laser captured IVD from E13.5 day Col2aCre;Tgfbr2lox/lox mice.
2010-04-09 | E-GEOD-18647 | biostudies-arrayexpress
Project description:Thoracic patient-derived xenografts
| PRJNA339191 | ENA
Project description:Very little is known about how intervertebral disc (IVD) is formed or maintained. Members of the TGF-ß superfamily are secreted signaling proteins that regulate many aspects of development including cellular differentiation. We recently showed that deletion of Tgfbr2 in Col2a expressing tissue results in alterations in development of IVD annulus fibrosus. The results suggested TGF-ß has an important role in regulating development of the axial skeleton, however, the mechanistic basis of TGF-ß action in these specialized joints is not known. One of the hurdles to understanding development of IVD is a lack of known markers. To identify genes that are enriched in the developing IVD and to begin to understand the mechanism of TGF-ß action in IVD development, we undertook a global analysis of gene expression comparing gene expression profiles in developing vertebrae and IVD. We also compared expression profiles in tissues from wild type and Tgfbr2 mutant mice. Lists of IVD and vertebrae enriched genes were generated. Expression patterns for several genes were verified either through in situ hybridization or literature/ database searches resulting in a list of genes that can be used as markers of IVD. Cluster analysis using genes listed under the Gene Ontology terms multicellular organism development and pattern specification indicated that mutant IVD more closely resembled vertebrae than wild type IVD. We propose TGF-ß has two functions in IVD development: 1) to prevent chondrocyte differentiation in the presumptive IVD and 2) to promote differentiation of annulus fibrosus from sclerotome. We have identified genes that are enriched in the IVD and regulated by TGF-ß that warrant further investigation as regulators of IVD development.
2010-04-09 | GSE18647 | GEO
Project description:Hypertension, atherosclerosis, and aneurysms alter thoracic aorta structure. Aortic lesions found in these diseases show a unique anatomical distribution. For instance, calcifications and atherosclerotic lesions tend to occur more frequently in the posterior wall of the aorta compared to other regions. The role that the outer layer of the aorta, its perivascular adipose tissue (PVAT), plays in the pathogenesis of these lesions is unknown. The descending thoracic aorta's PVAT is distributed in three strips of tissue: one strip is located anterior to the aorta (AP), while the other two are positioned laterally to the vessel and are adjacent to the thoracic vertebrae (LP). Genetic tracing indicates LP's adipocytes descend from sm22a+ and Myf5+ progenitors while the anterior are from sm22a+ only. The implications of this ontology and aortic PVAT distribution on the development of adipocytes are unknown. We hypothesize that the anatomical location of adipocyte progenitors influences their adipogenic potential. PVAT from LP and AP was collected from male SD rats at 10 wks of age (n=7) to harvest progenitors by outgrowth expansion. Progenitors were differentiated for 4 d in adipogenic media. Adipogenesis was evaluated by lipid droplet and triglyceride quantification using the IncuCyte Live-Cell® system. RNA from progenitors and adipocytes was sequenced in Illumina NextSeqData, and Differential Expressed Genes (DEG) identified. Enrichment and network analyses were performed in Ingenuity Pathways (IPA). Our findings provide evidence supporting differences in adipogenic activity and extracellular matrix secretion between the LP and AP PVAT of the aorta. These differences may explain the anatomical location of aortic lesions associated with hypertension, atherosclerosis, and aneurysms.
2023-10-11 | GSE244664 | GEO