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The Induction of Bone Formation
Published in Ugo Ripamonti, The Geometric Induction of Bone Formation, 2020
Are bone morphogenetic proteins, either naturally derived from mammalian bone matrices or recombinantly produced by DNA technology, the only proteins endowed with the striking prerogative of inducing bone formation when implanted heterotopically in animal models to set into motion the induction of bone formation where there is no bone? That is, in intramuscular or subcutaneous sites?
Introduction to Oral and Craniofacial Tissue Engineering
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
María Verónica Cuevas González, Eduardo Villarreal-Ramírez, Adriana Pérez-Soria, Pedro Alberto López Reynoso, Vincenzo Guarino, Marco Antonio Alvarez-Pérez
Bone Morphogenetic Proteins (BMP) are a group of proteins involved in multiple development processes which include skeletal formation, embryogenesis, hematopoiesis and neurogenesis. These proteins belong to the Transforming Growth Factor Beta superfamily, and over 20 members have been characterized. Four groups are formed to classify these proteins based on its amino acid sequence similarity: BMP2/4, BMP5/6/7/8a/8b, BMP9/10, and BMP12/13/14. These proteins are synthetized as a large precursor from 400–500 aa, which has three main domains, N-terminal secretion signal, a prodomain and a C-terminal region that constitutes the mature protein. Most of BMPs have seven cysteine residues in the C-terminal region, which are involved in its self-assembly and is known as a cysteine knot. BMPs functioning depends on the structural arrangement as homo- or heterodimers, which in turn are associated with specific membrane serine/threonine receptors denoted as type I and type II to trigger two main signal pathways: Smad (mothers against decapentaplegic) dependent pathway and Mitogen-Activated Protein Kinase (MAPK) pathway. This BMPs-MAPK signal pathway has shown its potential as an inductor of mesenchymal stem cells differentiation into osteoblasts, this extracellular signal is transduced inside the nucleus via the activation of ERK1/2, p38, INK 1/2/3 cascades which activate specific transcriptional factors (RUNX2, DLX5, and Osterix) related with the osteoblastic commitment and initiate the production of bone matrix proteins, leading to bone morphogenesis (Ripamonti 2019; Anusuya et al. 2016).
Mouse Knockout Models of Biliary Epithelial Cell Formation and Disease
Published in Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso, The Pathophysiology of Biliary Epithelia, 2020
Bone morphogenetic proteins (Bmps) are members of the TGF-beta superfamily of secreted signaling molecules and, together with FGFs, have many morphogenetic roles in the developing embryo. Bmp2 and Bmp4 are strongly expressed in the cardiac mesoderm. FGFs are also expressed before and during hepatic induction, and while liver gene induction occurs normally in the ventral foregut endoderm of Bmp4-homozygous mutant embryos, the initial induction of hepatic genes is inhibited in ventral foregut expiants that are treated with a Bmp inhibitor, noggin. Adding Bmp2 or Bmp4 back to the noggin-inhibited expiants restores hepatic gene induction. These data suggest Bmp signaling is both redundant as well as important for liver induction, possibly through enhancing the hepatic competence of the endoderm.23–25
Impregnation of polyethylene terephthalate (PET) grafts with BMP-2 loaded functional nanoparticles for reconstruction of anterior cruciate ligament
Published in Journal of Microencapsulation, 2023
Zeynep Karahaliloglu, Batur Ercan, Baki Hazer
In addition to ARS staining, osteogenic differentiation was also confirmed by calcium kit for up to 21 days. As shown in Figure 10(C), the calcium content for all groups at 21 days was significantly increased higher compared to 7 and 14 days (**p < 0.005). The mineralized calcium deposition on the 0.1BMP2-PLinaS-g-PEG-NPs modified PET sheets was found to be better from 14 to 21 days (*p < 0.05). Meanwhile, especially BMP-2 loaded groups had more mineralization compared all other groups at 7, 14, and 21 days, and promote cell mineralization. In this line, Huh et al. used recombinant human-bone morphogenic protein-2 immobilized heparin-grafted bone substrate (Bio-Oss®, Geistlich, Wolhusen, Switzerland) to enhance the osteoblastic functions in their study. The calcium accumulation of osteoblast-like cells exposed to Bio-Oss® were examined by ARS staining, and it observed that the calcium deposits increased in the MG63 osteoblast-like cells cultured in the Bio-Oss® groups with rhBMP-2 on day 31 after culture (Huh et al. 2011).
Genome- and transcriptome-wide association studies show that pulmonary embolism is associated with bone-forming proteins
Published in Expert Review of Hematology, 2022
Ruoyang Feng, Mengnan Lu, Yanni Yang, Pan Luo, Lin Liu, Ke Xu, Peng Xu
Bone morphogenetic proteins are at the forefront of bone regeneration research because of their potent osteoinductive effects [29]. These proteins are particularly commonly enumerated in fracture studies. The BMPs were initially discovered owing to their ability to induce bone and cartilage formation at ectopic sites [30]. It has been demonstrated that some BMPs are potent inducers of MSC osteogenesis and that osteogenic BMPs (e.g. BMP-2, BMP-6, and BMP-9) regulate a diverse set of downstream targets [30]. Therefore, we performed another LDSC analysis between PE and fracture and identified a correlation between them. It has been shown that erythropoietin (EFE) inhibits the expression of iron-regulating hormones by sequestering several BMP family members, thereby increasing iron utilization by erythrocytes [31]. Moreover, this study also showed that EFE exerts osteoprotective effects by regulating BMP signaling in osteoblasts, thereby limiting osteoclast production, reducing RANKL production along with BMP, and expanding during β-thalassemia erythropoiesis to prevent excessive bone loss [31], all of which support the conclusions obtained here. PE and right ventricular (RV) function are closely related to pulmonary arterial hypertension (PAH), which is a major determinant of survival in patients with PAH. Indeed, the literature shows that pharmacological activation of BMP signaling with FK506 (tacrolimus) can improve RV function by reducing RV afterload in preclinical models [32].
Overexpression of bone morphogenetic protein receptor type 2 suppresses transforming growth factor β-induced profibrotic responses in lung fibroblasts
Published in Experimental Lung Research, 2022
Jun Fukihara, Suzanne Maiolo, Jessica Kovac, Koji Sakamoto, Keiko Wakahara, Naozumi Hashimoto, Paul N. Reynolds
Transforming growth factor-β (TGF-β) plays a central profibrotic role in the pathogenesis of pulmonary fibrosis. It promotes migration of fibrocytes to the injured lung tissue, transdifferentiation of epithelial or endothelial cells into mesenchymal cells, proliferation of fibroblasts and their differentiation into myofibroblasts and generation and accumulation of extracellular matrix (ECM), such as fibronectin, by lung fibroblasts.5,6 These profibrotic effects are mainly mediated by activation of the Smad2/3 signaling pathway, where TGF-β binds to its membrane bound receptors to signal the upregulation of phosphorylated (p-)Smad2/3.7 Some Smad-independent (non-Smad) pathways such as the mitogen-activated protein kinase (MAPK) pathway also play important roles in regulating profibrotic changes.8–11 On the contrary, the bone morphogenetic proteins (BMPs) have been demonstrated to have antifibrotic effects. BMPs (including BMP-7 and -4) signal the phosphorylation of Smad1/5/9 by binding to a key membrane bound receptor, BMP receptor type 2 (BMPR2). P-Smad1/5/9 promotes antifibrotic effects by inhibiting fibrogenic gene expression and counterbalancing TGF-β mediated Smad2/3 phosphorylation. Imbalances in profibrotic and antifibrotic phenotypes induced by TGF-β/BMPs have been reported in some fibrotic diseases, such as pulmonary arterial hypertension,12 renal fibrosis,13,14 and liver cirrhosis.15,16