Growth factors in development: the role of TGF-β related polypeptide signalling molecules in embryogenesis

Development ◽  
1994 ◽  
Vol 1994 (Supplement) ◽  
pp. 53-60 ◽  
Author(s):  
Brigid L. M. Hogan ◽  
Manfred Blessing ◽  
Glenn E. Winnier ◽  
Noboru Suzuki ◽  
C. Michael Jones
Keyword(s):  
Growth Factors ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Related Gene ◽  
Genetic Studies ◽  
Signalling Molecules ◽  
Embryonic Tissues ◽  
Morphogenetic Protein ◽  
Large Families

Embryonic induction, the process by which signals from one cell population influence the fate of another, plays an essential role in the development of all organisms so far studied. In many cases, the signalling molecules belong to large families of highly conserved proteins, originally identified as mammalian growth factors. The largest known family is related to Transforming Growth Factor-β (TGF-β) and currently consists of at least 24 different members. Genetic studies in Drosophila on the TGF-β related gene, decapentaplegic (dpp), reveal the existence of conserved mechanisms regulating both the expression of the protein during development and the way in which it interacts with other signalling molecules to generate pattern within embryonic tissues. Comparative studies on another TGF-β related gene, known as Bone Morphogenetic Protein-4 (BMP-4), in Xenopus and mouse point to a conserved role in specifying posteroventral mesoderm during gastrulation. Analysis of other polypeptide signalling molecules during gastrulation suggests that their interaction in the generation of the overall body plan has also been conserved during vertebrate evolution.

Effects of bone morphogenetic protein 15 (BMP15) knockdown on porcine testis morphology and spermatogenesis

2020 ◽  
Vol 32 (11) ◽  
pp. 999
Author(s):  
Tao Tang ◽  
Qiyuan Lin ◽  
Yufeng Qin ◽  
Xinyu Liang ◽  
Yang Guo ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Transforming Growth Factor ◽  
Biological Function ◽  
Transforming Growth Factor Β ◽  
Reproductive Capacity ◽  
Ovary Development ◽  
Sperm Viability ◽  
Morphogenetic Protein ◽  
Bone Morphogenetic Protein 15

Bone morphogenetic protein 15 (BMP15) is a member of the transforming growth factor-β (TGFB) superfamily that plays an essential role in mammalian ovary development, oocyte maturation and litter size. However, little is known regarding the expression pattern and biological function of BMP15 in male gonads. In this study we established, for the first time, a transgenic pig model with BMP15 constitutively knocked down by short hairpin (sh) RNA. The transgenic boars were fertile, but sperm viability was decreased. Further analysis of the TGFB/SMAD pathway and markers of reproductive capacity, namely androgen receptor and protamine 2, failed to identify any differentially expressed genes. These results indicate that, in the pig, the biological function of BMP15 in the development of male gonads is not as crucial as in ovary development. However, the role of BMP15 in sperm viability requires further investigation. This study provides new insights into the role of BMP15 in male pig reproduction.

scholarly journals Activation of both transforming growth factor-β and bone morphogenetic protein signalling pathways upon traumatic brain injury restrains pro-inflammatory and boosts tissue reparatory responses of reactive astrocytes and microglia

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Georgios Divolis ◽  
Athanasios Stavropoulos ◽  
Maria Manioudaki ◽  
Anastasia Apostolidou ◽  
Athanasia Doulou ◽  
...  
Keyword(s):  
Brain Injury ◽  
Growth Factor ◽  
Bone Morphogenetic Protein ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Transforming Growth Factor Β1 ◽  
Reactive Astrocytes ◽  
Glia Cells ◽  
Morphogenetic Protein

Abstract Various ligands and receptors of the transforming growth factor-β superfamily have been found upregulated following traumatic brain injury; however, the role of this signalling system in brain injury pathophysiology is not fully characterized. To address this, we utilized an acute stab wound brain injury model to demonstrate that hallmarks of transforming growth factor-β superfamily system activation, such as levels of phosphorylated Smads, ligands and target genes for both transforming growth factor-β and bone morphogenetic protein pathways, were upregulated within injured tissues. Using a bone morphogenetic protein-responsive reporter mouse model, we showed that activation of the bone morphogenetic protein signalling pathway involves primarily astrocytes that demarcate the wound area. Insights regarding the potential role of transforming growth factor-β superfamily activation in glia cells within the injured tissues were obtained indirectly by treating purified reactive astrocytes and microglia with bone morphogenetic protein-4 or transforming growth factor-β1 and characterizing changes in their transcriptional profiles. Astrocytes responded to both ligands with considerably overlapping profiles, whereas, microglia responded selectively to transforming growth factor-β1. Novel pathways, crucial for repair of tissue-injury and blood–brain barrier, such as activation of cholesterol biosynthesis and transport, production of axonal guidance and extracellular matrix components were upregulated by transforming growth factor-β1 and/or bone morphogenetic protein-4 in astrocytes. Moreover, both ligands in astrocytes and transforming growth factor-β1 in microglia shifted the phenotype of reactive glia cells towards the anti-inflammatory and tissue reparatory ‘A2’-like and ‘M0/M2’-like phenotypes, respectively. Increased expression of selected key components of the in vitro modulated pathways and markers of ‘A2’-like astrocytes was confirmed within the wound area, suggesting that these processes could also be modulated in situ by the integrated action of transforming growth factor-β and/or bone morphogenetic protein-mediated signalling. Collectively, our study provides a comprehensive comparative analysis of transforming growth factor-β superfamily signalling in reactive astrocytes and microglia and points towards a crucial role of both transforming growth factor-β and bone morphogenetic protein pathways in modulating the inflammatory and brain injury reparatory functions of activated glia cells.

scholarly journals The structural basis of TGF-β, bone morphogenetic protein, and activin ligand binding

Reproduction ◽  
2006 ◽  
Vol 132 (2) ◽  
pp. 179-190 ◽  
Author(s):  
S Jack Lin ◽  
Thomas F Lerch ◽  
Robert W Cook ◽  
Theodore S Jardetzky ◽  
Teresa K Woodruff
Keyword(s):  
Signal Transduction ◽  
Growth Factors ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Structural Basis ◽  
Cellular Processes ◽  
Morphogenetic Protein ◽  
Check Points ◽  
Membrane Level

The transforming growth factor-β (TGF-β) superfamily is a large group of structurally related growth factors that play prominent roles in a variety of cellular processes. The importance and prevalence of TGF-β signaling are also reflected by the complex network of check points that exist along the signaling pathway, including a number of extracellular antagonists and membrane-level signaling modulators. Recently, a number of important TGF-β crystal structures have emerged and given us an unprecedented clarity on several aspects of the signal transduction process. This review will highlight these latest advances and present our current understanding on the mechanisms of specificity and regulation on TGF-β signaling outside the cell.

scholarly journals TGF-β and BMPR2 Signaling in PAH: Two Black Sheep in One Family

2018 ◽  
Vol 19 (9) ◽  
pp. 2585 ◽  
Author(s):  
Nina Rol ◽  
Konda Kurakula ◽  
Chris Happé ◽  
Harm Bogaard ◽  
Marie-José Goumans
Keyword(s):  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Bmp Signaling ◽  
Cardiovascular Research ◽  
Black Sheep ◽  
Research Fields ◽  
Morphogenetic Protein ◽  
Pulmonary Arterial ◽  
Extended View

Knowledge pertaining to the involvement of transforming growth factor β (TGF-β) and bone morphogenetic protein (BMP) signaling in pulmonary arterial hypertension (PAH) is continuously increasing. There is a growing understanding of the function of individual components involved in the pathway, but a clear synthesis of how these interact in PAH is currently lacking. Most of the focus has been on signaling downstream of BMPR2, but it is imperative to include the role of TGF-β signaling in PAH. This review gives a state of the art overview of disturbed signaling through the receptors of the TGF-β family with respect to vascular remodeling and cardiac effects as observed in PAH. Recent (pre)-clinical studies in which these two pathways were targeted will be discussed with an extended view on cardiovascular research fields outside of PAH, indicating novel future perspectives.

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