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Nanopharmaceuticals in Alveolar Bone and Periodontal Regeneration
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
Mark A. Reynolds, Zeqing Zhao, Michael D. Weir, Tao Ma, Jin Liu, Hockin H. K. Xu, Abraham Schneider
These results were likely due to the following mechanisms. First, HPL contains a wide spectrum of growth factors that can promote the MSC proliferating rate (Altaie et al. 2016). These include VEGF, TGF, PDGF, FGF, and IGF (Altaie et al. 2016). However, high concentrations of HPL (21.25% HPL) appeared to inhibit cell proliferation. The latter suggests a differential dose response to one or more proteins in HPL (Chen et al. 2012, Lee et al. 2011). Negative feedback is a mechanism that can block activation of the incoming signalling pathway to prevent inappropriate cellular response to excessive extracellular signals (such as growth factors) (Perrimon and McMahon 1999). Second, regarding the factors in HPL, TGF, IGF, FGF, and PDGF have been shown to enhance the osteogenesis of MSCs (Xia et al. 2011). TGF induces osteogenesis by activating receptor-regulated Smads and initiating mitogen-activated protein kinase signalling cascade (Iwasaki et al. 2018). TGF can also increase the Runx2 expression (Iwasaki et al. 2018). Moreover, IGF can upregulate type I collagen transcription and stabilise β-catenin, which is essential for osteoblastogenesis (Giustina et al. 2008). FGF can activate Runx2 and upregulate the anabolic function of osteoblasts (Majidinia et al. 2018). Furthermore, PDGF can promote the osteogenic differentiation by activating the BMP-Smad1/5/8- Runx2/Osterix pathway (Majidinia et al. 2018).
Bone Regeneration Effect of Cassia occidentalis Linn. Extract and Its Isolated Compounds
Published in Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay, Phytochemistry of Plants of Genus Cassia, 2021
Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay
In human fetal bone marrow-derived MSCs, apigenin stimulated osteogenic differentiation and upregulated osteogenic genes (Runx2, osterix and osteopontin) through JNK and p38 MAPK pathways (Zhang et al., 2015). In osteoblasts, apigenin blocks the action of tumour necrosis factor α (TNFα) and interferon γ (IFNγ) by inhibiting the production of osteoclastogenic cytokines including interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), MCP-3, and regulated upon activation, normal T cell expressed (RANTES). In preadipocytes, apigenin inhibits adipocyte differentiation, production of osteoclastogenic cytokines MCP-1, MCP-3, enhanced the production of the osteogenic cytokine BMP-6. Apigenin inhibited the differentiation of preosteoclasts to mature osteoclasts and attenuated pit resorption by mature osteoclasts (Bandyopadhyay et al., 2006). These reports suggested that apigenin has multiple effects on bone cells that could result in osteoanabolic as well as osteoprotective outcomes in diseases of bone loss.
Definition, risk factors, and epidemiology of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
The Wnt pathways enhance the osteoblast differentiation of bone marrow mesenchymal stem cells (MSCs) and the proliferation and differentiation of osteoblast progenitors by binding the Wnt ligand to its membrane receptor complex. The receptor is a complex of specific Frizzled (FZD) proteins and the low-density lipoprotein receptor-related protein 5/6 (LRP-5/6). Activated membrane ligand-receptor complexes release and stabilize β-catenin (OPG inhibitor) as intracellular signaling to regulate the Runx2 and Osterix gene coding proteins at the nuclei level, together with transcription factor 4 (TCF-4) or lymphoid enhancer binding factor 1 (LEF-1). Wnt signaling also reduces bone resorption by the competitive binding of secreted Frizzled-related protein 1 (Sfrp1) to RANKL expressed in osteoclast activity. Other regulators of this pathway include insulin-like growth factor 1 (IGF-1), Notch, and Sclerostin. BMPs are cytokines belonging to the transforming growth factor-beta (TGF-β) superfamily, which stimulates the phosphorylation of R-Smads (Samd1, Smad5, and Smad8), which, in turn, form complexes with Co-Smad (Smad4) modulating gene expression at the nuclei level, and thus increase osteogenesis. In this pathway, Runx2 regulates the gene expression of osteopontin (OPN), bone sialoprotein (BSP), osteocalcin (OCN), and PI3K/Akt and the activation of Smads.
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
Runt-related transcription factor 2 (Runx2) is a transcription factor that is essential for osteoblast differentiation and chondrocyte maturation [11]. Runx2 regulates the expression of Ihh, Col10α1, Spp1, Ibsp, MMP13 and VEGF-A in growth plate [12]. Studies have found that Runx2 plays an important role in bone metastasis of breast and prostate cancer [13]. In addition, Runx2 is one of the genes leading to osteoarthritis (OA) [14]. Studies have found that inhibition of the PI3K/AKT and ERK signalling pathway can significantly inhibit the apoptosis of chondrocytes and inhibit the progress of osteoarthritis [15]. In addition, Runx2 can play a carcinogenic role in oesophageal cancer by activating the PI3K/AKT and ERK pathways, indicating that Runx2 has a regulatory role in PI3K/AKT and ERK pathways [16].
The Genes Involved in Dentinogenesis
Published in Organogenesis, 2022
Shuang Chen, Han Xie, Shouliang Zhao, Shuai Wang, Xiaoling Wei, Shangfeng Liu
Runt-related transcription factor 2 (Runx2) participates in dentin formation, mineralization, and the development of odontoblasts.32 Runx2 is also essential for the differentiation of osteoblasts and odontoblasts, and it regulates the expression of numerous bone- and tooth-related genes. Runx2 determines the lineage of osteoblasts and odontoblasts in the mesenchymal cells. Osterix (OSX), a downstream gene of Runx2 in the osteoblast differentiation signaling pathway, is involved in the differentiation, maturation, and intercellular signal transduction of odontoblasts.41 Osteoprotegerin (OPG) is expressed in both the thickened and bud epithelium, as well as in combination with receptor activator of nuclear factor-κΒ (RANK) in both the enamel and papillary stroma. Although RANK ligand (RANKL) was not detected in the tooth epithelium or mesenchyme, it was expressed in pre-osteogenic mesenchymal cells near the developing tooth germ.46
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.