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Regulation of Osteoblast Differentiation by Cytokine Networks

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Regulation of Osteoblast Differentiation by Cytokine Networks International Journal of Molecular Sciences Review Regulation of Osteoblast Differentiation by Cytokine Networks Dulshara Sachini Amarasekara 1, Sumi Kim 2 and Jaerang Rho 2,* 1 Department of Zoology and Environment Sciences, Faculty of Science, University of Colombo, Colombo 00300, Sri Lanka; [email protected] 2 Department of Microbiology and Molecular Biology, Chungnam National University, Daejeon 34134, Korea; [email protected] * Correspondence: [email protected]; Tel.: +82-42-821-6420; Fax: +82-42-822-7367 Abstract: Osteoblasts, which are bone-forming cells, play pivotal roles in bone modeling and remod- eling. Osteoblast differentiation, also known as osteoblastogenesis, is orchestrated by transcription factors, such as runt-related transcription factor 1/2, osterix, activating transcription factor 4, special AT-rich sequence-binding protein 2 and activator protein-1. Osteoblastogenesis is regulated by a network of cytokines under physiological and pathophysiological conditions. Osteoblastogenic cytokines, such as interleukin-10 (IL-10), IL-11, IL-18, interferon-γ (IFN-γ), cardiotrophin-1 and oncostatin M, promote osteoblastogenesis, whereas anti-osteoblastogenic cytokines, such as tumor necrosis factor-α (TNF-α), TNF-β, IL-1α, IL-4, IL-7, IL-12, IL-13, IL-23, IFN-α, IFN-β, leukemia inhibitory factor, cardiotrophin-like cytokine, and ciliary neurotrophic factor, downregulate os- teoblastogenesis. Although there are gaps in the body of knowledge regarding the interplay of cytokine networks in osteoblastogenesis, cytokines appear to be potential therapeutic targets in bone- related diseases. Thus, in this study, we review and discuss our osteoblast, osteoblast differentiation, osteoblastogenesis, cytokines, signaling pathway of cytokine networks in osteoblastogenesis. Keywords: osteoblast; osteoblast differentiation; osteoblastogenesis; cytokine; signaling pathway Citation: Amarasekara, D.S.; Kim, S.; Rho, J. Regulation of Osteoblast Differentiation by Cytokine Networks. Int. J. Mol. Sci. 2021, 22, 2851. https://doi.org/10.3390/ 1. Background ijms22062851 Bone modeling initially occurs during development, where there are two modes of bone development: intramembranous ossification and endochondral ossification [1]. Academic Editor: Antonella Forlino In intramembranous ossification, mesenchymal tissues are directly converted to bone, while in endochondral ossification, mesenchymal tissues are differentiated into cartilage Received: 23 February 2021 before being replaced by bone [1]. Bone remodeling is a life-long process in which the Accepted: 8 March 2021 volume of bone resorbed by osteoclasts (OCs) is restored by bone-forming osteoblasts Published: 11 March 2021 (OBs) [2]. A balance between OC and OB activity is crucial in maintaining physiological bone turnover rates, and a flaw in this balance can lead to debilitating bone diseases, such Publisher’s Note: MDPI stays neutral as rheumatoid arthritis (RA), periodontal diseases, and osteoporosis [3]. Thus, maintaining with regard to jurisdictional claims in the biomechanical integrity of bone by either modeling or remodeling is a complex process published maps and institutional affil- regulated by numerous cell lineages, transcription regulation, a network of cytokines, and iations. growth factors [2,4]. Adequate understanding of the regulation of OC and OB activity in bone tissue is crucial for the development of novel therapeutics to manage bone-related diseases. We have previously reviewed the role played by cytokines in regulating OC dif- ferentiation, also known as osteoclastogenesis, under physiological and pathophysiological Copyright: © 2021 by the authors. conditions [2,3]. In this article, we review the current knowledge of the impact of cytokines Licensee MDPI, Basel, Switzerland. in OB differentiation, also known as osteoblastogenesis. This article is an open access article distributed under the terms and 2. OB Differentiation and Function conditions of the Creative Commons OBs, which are bone-forming cells, are small mononucleated cells of mesenchymal Attribution (CC BY) license (https:// stem cell (MSC) origin [4]. OBs are usually cuboid in shape but can be found in morpho- creativecommons.org/licenses/by/ logically diverse round, flat and cylindrical forms [5]. The sequential action of cytokine 4.0/). Int. J. Mol. Sci. 2021, 22, 2851. https://doi.org/10.3390/ijms22062851 https://www.mdpi.com/journal/ijms Int. J. Mol. Sci. 2021, 22, x FOR PEER REVIEW 2 of 16 2. OB Differentiation and Function Int. J. Mol. Sci. 2021, 22, 2851 OBs, which are bone-forming cells, are small mononucleated cells of mesenchymal2 of 16 stem cell (MSC) origin [4]. OBs are usually cuboid in shape but can be found in morpho- logically diverse round, flat and cylindrical forms [5]. The sequential action of cytokine networksnetworks and and transcription transcription factors factors results results in in the the differentiation of of OB lineage cells from mesenchymalmesenchymal precursors precursors (Figure 11))[ [4].4]. FigureFigure 1. 1. SchematicSchematic representation representation of of osteoblast osteoblast (OB) (OB) differentiation. differentiation. MSC, MSC, mesenchymal mesenchymal stem stem cell. cell.BMP, BMP, bone bone morphogenetic morphogenetic protein. protein. FGF, FGF, fibroblast fibroblast growth growth factor. factor. RUNX2, RUNX2, runt-related runt-related transcription tran- scriptionfactor 2. PTH,factor parathyroid 2. PTH, parathyroid hormone. hormone. TGF, transforming TGF, transforming growth factor. growth Hh, factor. hedgehog. Hh, SATB2,hedgehog. special SATB2, special AT-rich sequence-binding protein 2. OSX, osterix. ATF4, activating transcription AT-rich sequence-binding protein 2. OSX, osterix. ATF4, activating transcription factor 4. CREB, factor 4. CREB, cAMP-responsive element-binding. ALP, alkaline phosphatase. OPN, osteopontin. cAMP-responsive element-binding. ALP, alkaline phosphatase. OPN, osteopontin. OCN, osteocalcin. OCN, osteocalcin. ONN, osteonectin. BSP, bone sialoprotein. COL1A1, collagen type 1 alpha 1 chain.ONN, osteonectin. BSP, bone sialoprotein. COL1A1, collagen type 1 alpha 1 chain. OB lineage progenitor cells undergo three developmental stages: (1) cell proliferation, OB lineage progenitor cells undergo three developmental stages: (1) cell prolifera- (2) extracellular matrix (ECM) secretion and matrix maturation and (3) matrix mineral- tion, (2) extracellular matrix (ECM) secretion and matrix maturation and (3) matrix min- ization [6]. Following OB lineage commitment, pre-OBs undergo active proliferation and eralization [6]. Following OB lineage commitment, pre-OBs undergo active proliferation express collagen, fibronectin, osteopontin (OPN) and transforming growth factor-β (TGF-β) and express collagen, fibronectin, osteopontin (OPN) and transforming growth factor-β receptor 1 [7–9]. In the second stage, cell proliferation is downregulated, and immature (TGF-β) receptor 1 [7–9]. In the second stage, cell proliferation is downregulated, and im- OBs differentiate into mature OBs that secrete collagen type 1 alpha 1 chain (COL1A1) mature OBs differentiate into mature OBs that secrete collagen type 1 alpha 1 chain as the major constituent of the ECM and express alkaline phosphatase (ALP) to mature (COL1A1) as the major constituent of the ECM and express alkaline phosphatase (ALP) the ECM [7–9]. Upon completion of matrix maturation, matrix mineralization occurs in to mature the ECM [7–9]. Upon completion of matrix maturation, matrix mineralization a highly ordered process via the expression of various osteoblastogenic markers, such as occursOPN, osteocalcinin a highly ordered (OCN), andprocess bone via sialoprotein the expression (BSP), of withvarious continued osteoblastogenic expression markers, of ALP suchand COL1A1as OPN, osteocalcin [4,7]. OCN (OCN), regulates and calcium bone sialoprotein metabolism (BSP), and promotes with continued the deposition expression of ofminerals ALP and in theCOL1A1 ECM, OPN[4,7]. promotesOCN regulates bone formation calcium metabolism and mineralization, and promotes and BSP the promotes deposi- tionmineralization of minerals regulatingin the ECM, hydroxyapatite OPN promotes crystal bone formation formation and [10, 11mineralization,]. Finally, mature and OBsBSP promotesundergo apoptosis,mineralization become regulati bone-liningng hydroxyapatite cells or progressively crystal formation incorporate [10,11]. into Finally, the bone ma- turematrix OBs as undergo terminally apoptosis, differentiated become osteocytes bone-lining (OSs) cells [6]. or progressively incorporate into the boneOBs matrix orchestrate as terminally the bone differentiated remodeling process osteocytes by regulating (OSs) [6]. bone-resorbing OC differ- entiationOBs andorchestrate function the through bone remodeling the production process of two by essential regulating cytokines: bone-resorbing receptor activatorOC dif- ferentiationof nuclear factor-kappa and function B through (RANK) the ligand producti (RANKL)on of andtwo macrophageessential cytokines: colony-stimulating receptor ac- tivatorfactor (M-CSF)of nuclear [2 factor-kappa]. The binding B (RANK) of RANKL ligand and (RANKL) M-CSF to and receptors macrophage RANK colony-stim- and c-fms, ulatingrespectively, factor on (M-CSF) the surface [2]. The of OC binding progenitors, of RANKL induces and a M-CSF number to of receptors downstream RANK signaling and c- fms,cascades, respectively, ultimately on activatingthe surface nuclear of OC prog factorenitors, of activated induces T cellsa
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