scholarly journals Cross Talk between Insulin and Bone Morphogenetic Protein Signaling Systems in Brown Adipogenesis

2010 ◽  
Vol 30 (17) ◽  
pp. 4224-4233 ◽  
Author(s):  
Hongbin Zhang ◽  
Tim J. Schulz ◽  
Daniel O. Espinoza ◽  
Tian Lian Huang ◽  
Brice Emanuelli ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Cross Talk ◽  
Suppressive Effect ◽  
Bmp Signaling ◽  
Protein Signaling ◽  
Signaling Systems ◽  
Morphogenetic Protein ◽  
High Level ◽  
Signaling Components ◽  
Brown Adipogenesis

ABSTRACT Both insulin and bone morphogenetic protein (BMP) signaling systems are important for adipocyte differentiation. Analysis of gene expression in BMP7-treated fibroblasts revealed a coordinated change in insulin signaling components by BMP7. To further investigate the cross talk between insulin and BMP signaling systems in brown adipogenesis, we examined the effect of BMP7 in insulin receptor substrate 1 (IRS-1)-deficient brown preadipocytes, which exhibit a severe defect in differentiation. Treatment of these cells with BMP7 for 3 days prior to adipogenic induction restored differentiation and expression of brown adipogenic markers. The high level of adipogenic inhibitor preadipocyte factor 1 (Pref-1) in IRS-1-null cells was markedly reduced by 3 days of BMP7 treatment, and analysis of the 1.3-kb pref-1 promoter revealed 9 putative Smad binding elements (SBEs), suggesting that BMP7 could directly suppress Pref-1 expression, thereby allowing the initiation of the adipogenic program. Using a series of sequential deletion mutants of the pref-1 promoter linked to the luciferase gene and chromatin immunoprecipitation, we demonstrate that the promoter-proximal SBE (−192/−184) was critical in mediating BMP7's suppressive effect on pref-1 transcription. Together, these data suggest cross talk between the insulin and BMP signaling systems by which BMP7 can rescue brown adipogenesis in cells with insulin resistance.

scholarly journals Bone Morphogenetic Protein Signaling Restricts Proximodistal Extension of the Ventral Fin Fold

2020 ◽  
Vol 8 ◽  
Author(s):  
Jun Ka ◽  
Jun-Dae Kim ◽  
Boryeong Pak ◽  
Orjin Han ◽  
Woosoung Choi ◽  
...  
Keyword(s):  
Cell Division ◽  
Bone Morphogenetic Protein ◽  
Molecular Mechanisms ◽  
Bmp Signaling ◽  
Protein Signaling ◽  
Morphogenetic Protein ◽  
Distal Migration ◽  
Cellular Behaviors ◽  
And Shifts ◽  
Migration Of Cells

Unpaired fins, which are the most ancient form of locomotory appendages in chordates, had emerged at least 500 million years ago. While it has been suggested that unpaired fins and paired fins share structural similarities, cellular and molecular mechanisms that regulate the outgrowth of the former have not been fully elucidated yet. Using the ventral fin fold in zebrafish as a model, here, we investigate how the outgrowth of the unpaired fin is modulated. We show that Bone Morphogenetic Protein (BMP) signaling restricts extension of the ventral fin fold along the proximodistal axis by modulating diverse aspects of cellular behaviors. We find that lack of BMP signaling, either caused by genetic or chemical manipulation, prolongs the proliferative capacity of epithelial cells and substantially increases the number of cells within the ventral fin fold. In addition, inhibition of BMP signaling attenuates the innate propensity of cell division along the anteroposterior axis and shifts the orientation of cell division toward the proximodistal axis. Moreover, abrogating BMP signaling appears to induce excessive distal migration of cells within the ventral fin fold, and therefore precipitates extension along the proximodistal axis. Taken together, our data suggest that BMP signaling restricts the outgrowth of the ventral fin fold during zebrafish development.

scholarly journals Bone morphogenetic protein signaling in inflammation

2019 ◽  
Vol 244 (2) ◽  
pp. 147-156 ◽  
Author(s):  
David H Wu ◽  
Antonis K Hatzopoulos
Keyword(s):  
Bone Morphogenetic Protein ◽  
Bmp Signaling ◽  
Therapeutic Interventions ◽  
Protein Signaling ◽  
Bone Morphogenetic Protein Signaling ◽  
Morphogenetic Protein ◽  
Therapeutic Value ◽  
Organ Systems ◽  
Different Tissues

Bone morphogenetic protein signaling has long been established as a crucial pathway during embryonic development. In recent years, our knowledge of the function of bone morphogenetic protein signaling has expanded dramatically beyond solely its important role in development. Today, the pathway is known to have important homeostatic functions across multiple different tissues in the adult. Even more importantly, bone morphogenetic protein signaling is now known to function as a driver of diseases in the adult spanning different organ systems. In this review, we will explore the functions of bone morphogenetic protein signaling in diseases of inflammation. Through this exploration, we will highlight the value and challenges in targeting bone morphogenetic protein signaling for therapeutic interventions. Impact statement By compiling findings from recent studies, this review will garner novel insight on the dynamic and complex role of BMP signaling in diseases of inflammation, highlighting the specific roles played by both individual ligands and endogenous antagonists. Ultimately, this summary will help inform the high therapeutic value of targeting this pathway for modulating diseases of inflammation.

scholarly journals Essential Roles of Epithelial Bone Morphogenetic Protein Signaling During Prostatic Development

Endocrinology ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 2534-2544 ◽  
Author(s):  
Akiko Omori ◽  
Shinichi Miyagawa ◽  
Yukiko Ogino ◽  
Masayo Harada ◽  
Kenichiro Ishii ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Regulatory Gene ◽  
Epithelial Differentiation ◽  
Bmp Signaling ◽  
Urogenital Sinus ◽  
Protein Signaling ◽  
Morphogenetic Protein ◽  
Key Factor ◽  
Male Sex ◽  
Luminal Cells

Prostate is a male sex-accessory organ. The prostatic epithelia consist primarily of basal and luminal cells that differentiate from embryonic urogenital sinus epithelia. Prostate tumors are believed to originate in the basal and luminal cells. However, factors that promote normal epithelial differentiation have not been well elucidated, particularly for bone morphogenetic protein (Bmp) signaling. This study shows that Bmp signaling prominently increases during prostatic differentiation in the luminal epithelia, which is monitored by the expression of phosphorylated Smad1/5/8. To elucidate the mechanism of epithelial differentiation and the function of Bmp signaling during prostatic development, conditional male mutant mouse analysis for the epithelial-specific Bmp receptor 1a (Bmpr1a) was performed. We demonstrate that Bmp signaling is indispensable for luminal cell maturation, which regulates basal cell proliferation. Expression of the prostatic epithelial regulatory gene Nkx3.1 was significantly reduced in the Bmpr1a mutants. These results indicate that Bmp signaling is a key factor for prostatic epithelial differentiation, possibly by controlling the prostatic regulatory gene Nkx3.1.

scholarly journals Bone morphogenetic protein signaling regulates Id1 mediated neural stem cell quiescence in the adult zebrafish brain via a phylogenetically conserved enhancer module

2019 ◽  
Author(s):  
Gaoqun Zhang ◽  
Marco Ferg ◽  
Luisa Lübke ◽  
Masanari Takamiya ◽  
Tanja Beil ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Bmp Signaling ◽  
Transgenic Zebrafish ◽  
Deletion Mapping ◽  
Protein Signaling ◽  
Adult Zebrafish ◽  
Specific Expression ◽  
Radial Glial Cells ◽  
Morphogenetic Protein ◽  
Stem Cell Quiescence

AbstractIn the telencephalon of adult zebrafish, the inhibitor of DNA binding 1 (id1) gene is expressed in radial glial cells (RGCs), behaving as neural stem cells (NSCs), during constitutive and regenerative neurogenesis. Id1 controls the balance between resting and proliferating states of RGCs by promoting quiescence. Here, we identified a phylogenetically conserved cis-regulatory module (CRM) mediating the specific expression of id1 in RGCs. Systematic deletion mapping and mutation of conserved transcription factor binding sites in stable transgenic zebrafish lines reveal that this CRM operates via conserved smad1/5 and 4 binding motifs (SBMs) under both homeostatic and regenerative conditions. Transcriptome analysis of injured and uninjured telencephala as well as pharmacological inhibition experiments identify a crucial role of bone morphogenetic protein (BMP) signaling for the function of the CRM. Our data highlight that BMP signals control id1 expression and thus NSC proliferation during constitutive and induced neurogenesis.

scholarly journals Notch and bone morphogenetic protein differentially act on dermomyotome cells to generate endothelium, smooth, and striated muscle

2008 ◽  
Vol 180 (3) ◽  
pp. 607-618 ◽  
Author(s):  
Raz Ben-Yair ◽  
Chaya Kalcheim
Keyword(s):  
Smooth Muscle ◽  
Cell Differentiation ◽  
Bone Morphogenetic Protein ◽  
Striated Muscle ◽  
Muscle Differentiation ◽  
Protein Signaling ◽  
Mural Cell ◽  
Initial Development ◽  
Signaling Systems ◽  
Morphogenetic Protein

We address the mechanisms underlying generation of skeletal muscle, smooth muscle, and endothelium from epithelial progenitors in the dermomyotome. Lineage analysis shows that of all epithelial domains, the lateral region is the most prolific producer of smooth muscle and endothelium. Importantly, individual labeled lateral somitic cells give rise to only endothelial or mural cells (not both), and endothelial and mural cell differentiation is driven by distinct signaling systems. Notch activity is necessary for smooth muscle production while inhibiting striated muscle differentiation, yet it does not affect initial development of endothelial cells. On the other hand, bone morphogenetic protein signaling is required for endothelial cell differentiation and/or migration but inhibits striated muscle differentiation and fails to impact smooth muscle cell production. Hence, although different mechanisms are responsible for smooth muscle and endothelium generation, the choice to become smooth versus striated muscle depends on a single signaling system. Altogether, these findings underscore the spatial and temporal complexity of lineage diversification in an apparently homogeneous epithelium.

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