Role of bone morphogenetic proteins in cardiac differentiation

Wijk, Bram van; Moorman, Antoon F.M.; Hoff, Maurice J.B. van den

doi:10.1016/j.cardiores.2006.11.022

Cited by 181 publications

(175 citation statements)

References 134 publications

(167 reference statements)

Supporting

Mentioning

166

Contrasting

Unclassified

Order By: Relevance

“…Next, the signal is carried to the cell nucleus using the SMAD protein [27]. Expression is located mainly in the neuroectodermis and the forming s periosteum, which suggests that BMP-3 may be engaged in www.journals.viamedica.pl [25], own modified. In canonical pathway of BMP signal is transduced through the heteromeric complex with BMP ligand and type I and type II BMP receptors.…”

Section: The Bmp Protein and Bmpr Receptor: Expression Function And mentioning

confidence: 99%

Selected Bone Morphogenetic Proteins—The Possibility of Their Use in the Diagnostics and Therapy of Severe Asthma

Koćwin

Jonakowski

Przemęcka

et al. 2017

Advances in Respiratory Medicine

View full text Add to dashboard Cite

Asthma is a chronic heterogeneous illness of the lower airway with an inflammatory basis, developing from hyperresponsiveness and bronchial obstruction. One of the more unfavourable processes occurring in the airway are the long-term changes of the respiratory tract known as remodelling, resulting in complete irreversible obstruction. Bone morphogenetic protein (BMP) is a member of the Transforming Growth Factor beta (TGF-b) superfamily, which regulates processes in embryonic and post-embryonic development. The role played by BMP is regulation of degradation and remodelling of the extracellular matrix, which is one of the elements involved in the reconstruction of the structure of the bronchi in severe asthma. This paper presents the antagonistic properties of BMP against TGF-b, anti-inflammatory and counteracting fibrosis in the respiratory tract. The current state of knowledge indicates that this group of cytokines are potential new markers of remodelling in severe asthma, and further studies on their therapeutic value are necessary.

show abstract

Section: The Bmp Protein and Bmpr Receptor: Expression Function And mentioning

confidence: 99%

Selected Bone Morphogenetic Proteins—The Possibility of Their Use in the Diagnostics and Therapy of Severe Asthma

Koćwin

Jonakowski

Przemęcka

et al. 2017

Advances in Respiratory Medicine

View full text Add to dashboard Cite

show abstract

“…BMP signaling is required for cardiac progenitor specification, proliferation and differentiation (Brand, 2003;Klaus et al, 2012;Mercola et al, 2011;Olson and Schneider, 2003;van Wijk et al, 2007). To understand how enhanced Akt activity gives rise to SHF expansion, we studied BMP signaling in the SHF of Pten deletion mice.…”

Section: Pten-akt Signaling Suppresses Bmp-smad Signaling Through Foxomentioning

confidence: 99%

Akt1 signaling coordinates BMP signaling and β-catenin activity to regulate second heart field progenitor development

et al. 2015

View full text Add to dashboard Cite

Second heart field (SHF) progenitors exhibit continued proliferation and delayed differentiation, which are modulated by FGF4/8/10, BMP and canonical Wnt/β-catenin signaling. PTEN-Akt signaling regulates the stem cell/progenitor cell homeostasis in several systems, such as hematopoietic stem cells, intestinal stem cells and neural progenitor cells. To address whether PTEN-Akt signaling is involved in regulating cardiac progenitors, we deleted Pten in SHF progenitors. Deletion of Pten caused SHF expansion and increased the size of the SHF derivatives, the right ventricle and the outflow tract. Cell proliferation of cardiac progenitors was enhanced, whereas cardiac differentiation was unaffected by Pten deletion. Removal of Akt1 rescued the phenotype and early lethality of Pten deletion mice, suggesting that Akt1 was the key downstream target that was negatively regulated by PTEN in cardiac progenitors. Furthermore, we found that inhibition of FOXO by Akt1 suppressed the expression of the gene encoding the BMP ligand (BMP7), leading to dampened BMP signaling in the hearts of Pten deletion mice. Cardiac activation of Akt also increased the Ser552 phosphorylation of β-catenin, thus enhancing its activity. Reducing β-catenin levels could partially rescue heart defects of Pten deletion mice. We conclude that Akt signaling regulates the cell proliferation of SHF progenitors through coordination of BMP signaling and β-catenin activity.

show abstract

“…Bone morphogenesis proteins (BMP), a large subgroup in the TGF-b superfamily, have been shown to mediate a variety of biologic functions, which regulate cell proliferation, differentiation, and the determination of cell fate (10,11). In particular, BMP signaling has been implicated in the regulation of early liver development and has been shown to play a vital role in the determination of liver bud morphogenesis and to promote hepatoblast migration, proliferation, and survival (12,13).…”

Section: Introductionmentioning

confidence: 99%

The Activation of MEK/ERK Signaling Pathway by Bone Morphogenetic Protein 4 to Increase Hepatocellular Carcinoma Cell Proliferation and Migration

Chiu

Kuo

et al. 2012

Molecular Cancer Research

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is one of the most common visceral malignancies worldwide, with a very high incidence and poor prognosis. Bone morphogenesis protein 4 (BMP4), which belongs to the TGF-b superfamily of proteins, is a multifunctional cytokine, which exerts its biologic effects through SMAD-and non-SMADdependent pathways, and is also known to be involved in human carcinogenesis. However, the effects of the BMP4 signaling in liver carcinogenesis are not yet clearly defined. Here, we first show that BMP4 and its receptor, BMPR1A, are overexpressed in a majority of primary HCCs and that it promotes the growth and migration of HCC cell lines in vitro. We also establish that BMP4 can induce HCC cyclin-dependent kinase (CDK)1 and cyclin B1 upregulation to accelerate cell-cycle progression. Our study indicates that the induction of HCC cell proliferation is independent of the SMAD signaling pathway, as Smad4 knockdown of HCC cell lines still leads to the upregulation of CDK1 and cyclin B1 expression after BMP4 treatment. Using mitogen-activated protein/extracellular signalregulated kinase (MEK) selective inhibitors, the induction of CDK1, cyclin B1 mRNA and protein were shown to be dependent on the activation of MEK/extracellular signal-regulated kinase (ERK) signaling. In vivo xenograft studies confirmed that the BMPR1A-knockdown cells were significantly less tumorigenic than the control groups. Our findings show that the upregulation of BMP4 and BMPR1A in HCC promotes the proliferation and metastasis of HCC cells and that CDK1 and cyclin B1 are important SMAD-independent molecular targets in BMP4 signaling pathways, during the HCC tumorigenesis. It is proposed that BMP4 signaling pathways may have potential as new therapeutic targets in HCC treatment. Mol Cancer Res; 10(3); 415-27. Ó2012 AACR. IntroductionHepatic cancer, particularly hepatocellular carcinoma (HCC), is one of the most common tumors worldwide and the third most common cause of cancer-related deaths. Diagnosis of advanced stage of HCC is a devastating experience for both patients and family. More than 80% of HCC cases originate in developing countries (1, 2). Chronic infections with hepatitis B virus or hepatitis C virus are responsible for the majority of HCC cases in those countries, especially in Asia (3, 4). Other risk factors include prolonged

show abstract

Role of bone morphogenetic proteins in cardiac differentiation

Cited by 181 publications

References 134 publications

Selected Bone Morphogenetic Proteins—The Possibility of Their Use in the Diagnostics and Therapy of Severe Asthma

Selected Bone Morphogenetic Proteins—The Possibility of Their Use in the Diagnostics and Therapy of Severe Asthma

Akt1 signaling coordinates BMP signaling and β-catenin activity to regulate second heart field progenitor development

The Activation of MEK/ERK Signaling Pathway by Bone Morphogenetic Protein 4 to Increase Hepatocellular Carcinoma Cell Proliferation and Migration

Contact Info

Product

Resources

About