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Definition, risk factors, and epidemiology of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
New candidates associated with BMD have also been suggested, including wntless Wnt ligand secretion mediator (GPR177) genes, and SRY-box 6 (SOX6), a transcriptional activator that is required for normal development of chondrogenesis and maintenance of skeletal muscle cells (73). A panel of more than 25 genes has been associated with BMD by GWAS analysis in postmenopausal women, including ARHGAP1, CLCN7, CTNNB1, ESR1, FAM3C, FLJ42280, FOXL1, GALNT3, GPR177, HDAC5, IBSP, JAG1, LRP5, LTBP3, MARK3, MEF2C, MEPE, OPG, RANK, RANKL, RSPO3, SOST, SOX4, SOX6, SP7 (Osterix), TARD3NL, and ZBTB40 (74).
Tumors with adipocyte, myxoid, muscular, osseous, and cartilaginous features
Published in Eckart Haneke, Histopathology of the NailOnychopathology, 2017
Histologic sections show a sharply delimited central growth area, the nidus, consisting of a meshwork of trabeculae of osteoid with a variable degree of calcification. They are surrounded by plump osteoblasts and dispersed in a very vascular connective tissue usually without any sign of inflammation.112 Most of the osteoid osteomas are positive for CD138 (syndecan-1), which is a surface proteoglycan and specific for plasmocytic differentiation in hematologic disorders, but also in the majority of epithelial tumors.113 Most osteoid osteomas express nuclear Runx2 (runt-related transcription factor 2) and Osterix (Sp7 transcription factor), two master transcription factors for bone formation, whereas they are negative for Sox9, which is positive in chondromyxoid fibromas and chondroblastoma.114
KLF2 reduces dexamethasone-induced injury to growth plate chondrocytes by inhibiting the Runx2-mediated PI3K/AKT and ERK signalling pathways
Published in Autoimmunity, 2023
Yulong Ma, Tao Peng, Xudong Yao, Chaonan Sun, Xiaowei Wang
To explore the underlying molecular mechanisms of KLF2 in Dex-induced chondrocytes, we studied the regulator that bind to KLF2. Consistent with previous data [10], our results also show that KLF2 significantly promoted the expression of Runx2 in GPCs. Runx2 is the key to osteoblast differentiation and chondrocyte maturation [25]. During the differentiation of osteoblasts, Runx2 was weakly expressed in undifferentiated mesenchymal cells, up-regulated in pre-osteoblasts, highly expresses in immature osteoblasts, and down-regulated in mature osteoblasts [26]. Runx2 enhances the proliferation of osteoblast progenitor cells by directly regulating FGFR2 and FGFR3 [12]. Furthermore, it has been reported that Runx2 induces Sp7 and activates canonical Wnt signal to guide cells to differentiate into osteoblasts, thereby inhibiting chondrocyte differentiation [11]. In the present study, our findings indicated that KLF2 affected Dex-treated rat GPCs functions through targeting Runx2.
Molecular Genetics of Cleidocranial Dysplasia
Published in Fetal and Pediatric Pathology, 2021
Jamshid Motaei, Arash Salmaninejad, Ebrahim Jamali, Imaneh Khorsand, Mohammad Ahmadvand, Sasan Shabani, Farshid Karimi, Mohammad Sadegh Nazari, Golsa Ketabchi, Fatemeh Naqipour
RUNX2 gene plays an important role in osteoblast differentiation. The expression of Indian hedgehog (Ihh) in chondrocytes induces expression of RUNX2 in mesenchymal stem cells during the development of the endochondral bone. Then, Runx2, by inhibiting the differentiation of the mesenchymal stem cells into chondrocytes and adipocytes, induces them to osteoblast progenitors. In knockout mice for Ihh-/-, osteoblasts and expression of Runx2 in perichondrium are completely absent [30]. Sp7, Runx2 and canonical Wnt signaling cause osteoblast progenitors differentiation into immature osteoblasts. Expression of Sp7 is regulated by Runx2. Osteoblast progenitors have the ability to differentiate into chondrocytes that are inhibited by canonical Wnt signaling and Sp7 (27). Notch signaling inhibits Runx2 through the Hes and Hey transcriptional inhibitors, as a result, with the proliferation of mesenchymal cells, their differentiation into osteoblasts are inhibited [31]. Runx2 expression decreases during osteoblasts maturation [32]. In the process of endochondral ossification, Runx2 plays an important role in the chondrocytes maturation. Sox5, Sox6 and Sox9 control the differentiation of mesenchymal cells into immature chondrocytes [27]. Overexpression of RUNX2 in transgenic mice increased the chondrocyte maturation and endochondral bone formation. While the expression of dominant-negative Runx2 in mice inhibited chondrocyte maturation and delayed endochondral ossification [33]. Therefore, Runx2 plays an important role in the development of chondrocytes from immature chondrocytes.
The role of imaging in early diagnosis and prevention of joint damage in inflammatory arthritis
Published in Expert Review of Clinical Immunology, 2018
Jiang Yue, Dongze Wu, Lai-Shan Tam
Osteoblasts are cells of mesenchymal origin responsible for bone formation by secreting bone matrix proteins and promoting mineralization. Several factors, such as Osterix (also known as SP7), control the differentiation and proliferation of osteoblasts. Differentiated osteoblasts embedded in the bone matrix are called osteocytes, and they play an important function within bone as mechanosensors initiating bone remodeling [10].