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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.
Enhanced osteogenic activity and antibacterial ability of manganese–titanium dioxide microporous coating on titanium surfaces
Published in Nanotoxicology, 2020
Quan-Ming Zhao, Yu-Yu Sun, Chun-Shuai Wu, Jian Yang, Guo-Feng Bao, Zhi-Ming Cui
ALP, BMP-2, RUNX2, OCN, and COL-I are markers of osteogenic differentiation and mineralization. An increase in ALP levels is reportedly linked to the deposition of a large amount of calcium salts. The higher the activity of ALP, the higher is the local concentration of calcium and phosphorus ions. Calcium and phosphorus deposits in collagen fibrils promote the mineralization of bone tissues. ALP activity is also an early indicator of osteogenesis and osteoblast differentiation. RUNX2 is a specific transcription factor crucial for the differentiation and maturation of osteoblasts and has an important role in bone formation and growth. COL-I has a reticular structure and plays a key role in maintaining the integrity of bone structure. ALP, RUNX2, and COL-I interact with each other, and their synergistic effect is essential for ECM formation. We found that cells on the surface of different samples expressed genes encoding ALP, BMP-2, RUNX2, OCN, and COL-I after 1d of culture. The gene expression levels gradually increased with an increase in culture duration. Compared with the PT and MT groups, the gene expression levels in the Mn–TiO2 microporous biotic coating group were significantly upregulated, indicating that the coating promoted the differentiation and mineralization of osteoblasts. It is speculated that the release of Mn ions from the coating plays an integral role.
α-Lipoic acid loaded hollow gold nanoparticles designed for osteoporosis treatment: preparation, characterization and in vitro evaluation
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Yanhai Xi, Wenming Pan, Yanyan Liu, Ji Liu, Guohua Xu, Yanguo Su, Daquan Chen, Xiaojian Ye
BMP-2, Runx-2 and OCN are important transcriptional regulators in bone development and play an important role in bone formation and remodelling. BMP-2 is one of the most effective promoters of MSC differentiation into osteoblasts in vitro and upregulates the expression of Runx-2 during osteoblast differentiation [23]. As a key regulator of bone formation, Runx2 can promote the proliferation and differentiation of early osteoblasts and affect the secretion of other bone formation related cytokines. OCN is a marker of osteoblast differentiation and maturation. As shown in Figure 4(A–C), ALA, mPEG@HGNPs-ALA and mPEG@GNPs-ALA all upregulated the expression of BMP-2, Runx2 and OCN, indicating that mPEG@HGNPs-ALA is beneficial for osteoblasts at the gene level.
Therapeutic potential of RUNX1 and RUNX2 in bone metastasis of breast cancer
Published in Expert Opinion on Therapeutic Targets, 2023
Interestingly, RUNX family member is closely associated with cancer [19,20]. RUNX1 is associated with the WNT pathway and overexpressed in invasive breast cancer. Meanwhile, mutations in RUNX1 and its binding partner CBF-β are observed in luminal breast cancer patients [21,22]. On the other hand, RUNX2 is critical for osteoblast differentiation, chondrocyte maturation, and bone formation. It is overexpressed in the breast and interacts with transforming growth factor (TGF), Wnt, and p53. Also, it promotes epithelial-mesenchymal transition (EMT), upregulates extracellular matrix degrading enzymes, subsequently boosting metastatic phenotype and cancer cell invasiveness and metastasis.