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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).
The therapeutic role of the components of Aloe vera in activating the factors that induce osteoarthritic joint remodeling
Published in Badal Jageshwar Prasad Dewangan, Maheshkumar Narsingrao Yenkie, Novel Applications in Polymers and Waste Management, 2018
Abhipriya Chatterjee, Patit Paban Kundu
TGF-βΙ and 3 has a role in maintaining the balance of anabolism in cartilage and synthesis of extracellular matrix. In vitro studies suggested that in normal cartilage, the level of TGFβ was high, which was drasti cally decreased in osteoarthritic cartilage. Even if TGFβ pathway was blocked in normal cartilage, it became more prone to damage and suscep tible to osteoarthritis.64 This indicates that TGFβ is a major factor in maintaining cartilage homeostasis. TGFβ can suppress the expression of cytokines like IL1 and 6 and induce extracellular matrix synthesis and chondrogenesis. TGFβ signaling is mediated by Smad (mothers against decapentaplegic homolog) via activinlike kinase 1 and 5 receptors.65-67 In spite of all these beneficial activities of TGFβ, it can also be harmful as it highly increases chondrocyte proliferation which can result in formation of osteophyte.62
Reduction and Fixation of Sacroiliac joint Dislocation by the Combined Use of S1 Pedicle Screws and an Iliac Rod
Published in Kai-Uwe Lewandrowski, Donald L. Wise, Debra J. Trantolo, Michael J. Yaszemski, Augustus A. White, Advances in Spinal Fusion, 2003
Kai-Uwe Lewandrowski, Donald L. Wise, Debra J. Trantolo, Michael J. Yaszemski, Augustus A. White
The most commonly described intracellular targets for the TβRI kinase are the receptor-associated Smad proteins (rSmad). Studies first done in Drosophila led to the discovery of a group of related proteins called mothers against decapentaplegic (dpp), or Mad proteins, that were targets of receptor serine/threonine kinases (RSK) [16]. Subsequent identification of specific Mad-binding DNA domains demonstrated their direct regulation of gene transcription [16]. Smad proteins are the vertebrate homologs of Mad. Several Smad proteins have been discovered, and some of the receptor associated Smads, rSmads, are unique for specific TGFβ superfamily members. The rSmads specific for TGF-pl are Smad 2 and Smad 3. Activated TβRI phosphoryl
Benzo[a]pyrene osteotoxicity and the regulatory roles of genetic and epigenetic factors: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Jiezhang Mo, Doris Wai-Ting Au, Jiahua Guo, Christoph Winkler, Richard Yuen-Chong Kong, Frauke Seemann
OBs that originate from multipotent MSCs are responsible for the production of bone matrix constituents (Figure 5). The commitment of MSCs into osteochondral progenitor cells (OPCs) is mainly controlled by the TGF-β superfamily and bone morphogenetic proteins (BMPs) (Baek & Kim, 2011). BMPs function by recruiting and activating the heterodimeric mothers against decapentaplegic homolog (SMAD) proteins that control the expression of a key transcription factor, RUNX2/CBFA-1, so that OPCs can differentiate into premature osteoblasts (POBs) (Crockett et al., 2011; Gámez et al., 2014). The canonical Wnt/β-catenin signaling pathway is also indispensable for OB differentiation during osteogenesis and continues to serve important roles in mature OBs. The downstream transcription factors, OSX, and ATF4, control the further differentiation and maturation of OBs (Baek & Kim, 2011; Gámez et al., 2014). POBs and mature osteoblasts (MOBs) first produce and maturate the osteoid matrix, which is followed by mineralizing the matrix (composed of phosphate, released by alkaline phosphatases which combine with calcium to form hydroxyapatite) (Teti, 2011). At the end of the bone-forming phase, MOBs differentiate into osteocytes, which are either entrapped in the new bone matrix and become bone lining cells on the bone surface or undergo apoptosis (Baek & Kim, 2011; Crockett et al., 2011). It is noteworthy that some teleost such as medaka do not have osteocytes in their bone tissues during entire life cycle (Witten & Huysseune, 2009). OBs produce a variety of growth factors under different stimuli such as the IGF, platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), TGF-β, and BMPs. OB function is regulated by these growth factors since these receptors were experimentally proven to be expressed in OBs (Crockett et al., 2011). Receptors of canonical hormones including parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), thyroid hormone (TH), growth hormone (GH), insulin, progesterone (P4), and prolactin have also been identified on OBs. Additionally, OBs have nuclear steroid hormone receptors, such as receptors for estrogens (ER), androgens (AR), vitamin D3 (VDR), and retinoids (RARs) (Hadjidakis & Androulakis, 2006).