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Physiological aspects of blastema formation in mice
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
A second remarkable effect of HBO treatment on digit regeneration is an enhancement of bone degradation during the pre-blastema phase of regeneration (Sammarco et al. 2014, 2015). Bone degradation is an extreme example of tissue histolysis that remodels the amputation wound before blastema formation. It is reasonable to assume that all tissues involved in the regenerative response undergo some form of histolysis to establish a functional interface between the mature tissues of the stump and the newly developing tissues of the regenerate. Bone degradation involves the activity of highly specialized multinucleated cells called osteoclasts, which are derived from monocytes and attack mineralized bone. Osteoclasts attach to bone and create a focal resorptive compartment that establishes an acidic microenvironment that releases bone minerals and exposes the organic matrix of the bone for proteolytic digestion by cathepsin K, an acid protease secreted by osteoclasts. The activity of osteoclasts has been studied in the context of normal and abnormal bone turnovers, particularly in the context of bone diseases such as osteoporosis and osteopetrosis (Charles and Aliprantis 2014). During normal bone turnover, osteoclast degradation of bone is coupled with the formation of new bone tissue by osteoblasts; thus, these two cell types interact to coordinate the progressive resorption and laying down of new bone tissue in adults. Osteoclastogenesis is regulated in part by the activation of the RANK cell surface receptor (receptor activator of nuclear factor κβ) expressed by osteoclasts and its ligand, RANKL. RANK/RANKL signaling is negatively regulated by a secreted RANK decoy receptor called osteoprotegerin (OPG), which competitively binds RANKL (Honma et al. 2014).
Infection in the Hematopoeitic Stem Cell Transplant Recipient with Autoimmune Disease
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Valentina Stosor, Teresa R. Zembower
Etanercept and infliximab both inhibit tumor necrosis factor α (TNF-α). Etanercept is a form of soluble TNF receptor (a decoy receptor for TNF-α), and infliximab is a monoclonal antibody that binds to TNF-α. Infliximab-bound TNF-α is thus prevented from binding with the TNF receptor. The side effects of these medications include infusion reactions, headache, flushing, nausea, vomiting, diarrhea, rash, chest pain, development of antinuclear antibodies and anti-DNA antibodies, clinical symptoms of SLE, cytopenias, demyelination, tuberculosis, bacterial and fungal infections, and PCR70-73
Mechanical Control of Bone Remodeling
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
OPG is a soluble decoy receptor for RANKL and is produced by cells of the osteoblast lineage. Factors that increase OPG levels may inhibit osteoclastogenesis by disruption of RANKL signaling. Recent evidence suggests that mechanical loading regulates OPG expression. Cyclic strain increased OPG synthesis in osteoblastic cells,59,60 while oscillatory fluid flow upregulated OPG expression in osteoprogenitor cells.57 Thus, regulation of both RANKL and OPG levels in bone cells could contribute to inhibition of osteoclastogenesis by mechanical input.
Microstructured titanium functionalized by naringin inserted multilayers for promoting osteogenesis and inhibiting osteoclastogenesis
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Ke Shen, Xiaojing Zhang, Qiang Tang, Xingtang Fang, Chunlei Zhang, Zhaojing Zhu, Yanhua Hou, Min Lai
NA has been shown to promote osteogenesis of cells [28]. In order to better demonstrate the ability of LBL (NA) coated-Ti substrates to promote osteoblast differentiation, qRT-PCR was used to detect the key genes of osteoblasts at 4, 7 and 14 days. Runt-related transcription factor 2 (Runx2) is a key transcription factor which regulates downstream genes of osteoblasts differentiation [29]. Alkaline phosphatase (ALP) is a marker gene that regulates the early differentiation of osteoblasts and plays an important role in the process of osteogenic differentiation [30]. Collagen I (COL I), is a basic regulator of osteoblastic differentiation and the most abundant structural protein in the bone matrix and is crucial to the formation of osteoblasts [31]. Osteocalcin (OCN) and osteopontin (OPN) play an important role in the mineralization of osteoblasts and are important factors in the regulation of osteoblastic differentiation [32, 33]. Osteoprotegerin (OPG) is a marker of osteoblast maturation [34]. As a decoy receptor of RANKL, OPG can inhibit osteoclast differentiation and prevent bone resorption. As shown in Figure 5, the expression of Runx2, ALP, COL I, OCN, OPN and OPG significantly increased on the LBL (NA) coated-Ti substrate, indicating that LBL (NA) coated-Ti substrate have the ability to promote the differentiation of osteoblasts at different stages, especially in the early stage. This was consistent with the results of ALP activity and mineralization, which further proved that LBL (NA) coated-Ti substrate played an important role in promoting osteogenic differentiation. Previous studies have demonstrated that NA can regulate bone metabolism and promote bone formation through ERK and Akt signaling pathways [35, 36], and can prevent TNF-α osteogenic inhibition of mesenchymal stem cells by inhibiting NF-B signaling pathway [37]. In this study, NA was inserted into the CHI/GEL multilayers on microstructured titanium. As the multilayers degraded, a sustained release of NA was achieved which further promoted osteoblast differentiation.
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
OCs, which are derived from hematopoietic stem cells (HSCs), are responsible for bone resorption. Stimulated by the macrophage colony-stimulating factor (M-CSF), HSCs first differentiate into mononuclear precursor cells (MPCs) (Boyle et al., 2003). Thereafter, M-CSF and RANKL induce MPCs to further differentiate into osteoclast progenitors (OCPs) which ultimately become functional multinuclear osteoclasts (MOCs) following fusion and polarization (Figure 6) (Crockett et al., 2011; Tang et al., 2014). OC differentiation initially depends on signaling via colony-stimulating factor 1 receptor (CSF1R) − the receptor for M-CSF − in MPCs to upregulate the expression of RANK. Its ligand, RANKL (RANK competes with a decoy receptor, OPG, for RANKL), is expressed in OBs and stromal cells in response to PTH and stimulation by the active dihydroxy form of vitamin D3 (1,25 Vit D3) (Crockett et al., 2011; Hrdlicka et al., 2019). Upon binding of RANK to RANKL, tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) forms a complex with transforming growth factor-β-activated kinase 1 (TAK1) and TGF-β activated kinase 1 binding protein 1 (TAB1). They subsequently recruit SMAD3 and facilitate the downstream ubiquitination and degradation of IκBα, the inhibitor of transcription factors nuclear factor κB (NF-κB). The free NF-κB then translocates from the cytosol to the nucleus and promotes the transcription of the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) (Hrdlicka et al., 2019; Lozano et al., 2019). Alternatively, together with the immunoreceptor tyrosine-based activation motif (ITAM)-containing adaptors, DNAX-activating protein of 12 kDa (DAP12) and Fc receptor γ chain (FcRγ), binding of RANKL to RANK activates NF-κB, activator protein 1 (AP-1, composed of C-FOS and C-JUN) and NFATc1 (Lozano et al., 2019). All of these transcription factors induce the expression of key OC genes, which include dendritic cell-specific transmembrane protein (DC-STAMP), tartrate-resistant acid phosphatase (TRAcP), cathepsin K (CTSK), matrix metalloproteinases (MMPs), and β3 integrin in MOCs (Crockett et al., 2011; Hrdlicka et al., 2019).
Effects of running a marathon on sclerostin and parathyroid hormone concentration in males aged over 50
Published in Journal of Sports Sciences, 2023
Aleksandra Zagrodna, Anna Książek, Małgorzata Słowińska-Lisowska, Jan Chmura, Piotr Ponikowski, Giovanni Lombardi
Expression of sclerostin is also subjected to a strict endocrine regulation and, among the hormones parathyroid hormone (PTH) is of particular relevance since it is a master regulator of calcium metabolism (Sims & Chia, 2012). Parathyroid hormone is an 84-amino acid peptide hormone synthesized in the chief cells of the parathyroid glands. It is essential for the maintenance of serum calcium concentration within a narrow range through direct actions on bone, kidney, and, indirectly, on small intestine (Anastasilakis et al., 2014). Parathyroid hormone acts via the parathyroid hormone 1 receptor (PTH1R) expressed by mesenchymal stem cells and cells of the osteoblastic lineage (eg osteoprogenitors, lining cells, immature and mature osteoblasts, and osteocytes). Parathyroid hormone stimulates proliferation, osteoblast differentiation, osteoblast activity, ECM deposition, and mineralisation. However, PTH can also induce the expression of the tumour-necrosis factor (TNF)-related ligand of the receptor activator of nuclear factor κB (RANκL) that stimulates osteoclast differentiation and activity via RANκ, and inhibits osteoprotegerin, a decoy receptor for RANκL. Osteoclast activity causes the release of calcium (Ca2+) from the resorbing bone, which, in turn, inhibits the expression of PTH in the parathyroid glands (Lombardi et al., 2020). While PTH stimulates both bone resorption and bone formation, the final outcome on bone mass, catabolic or anabolic, depends on the dose and periodicity of the PTH signal. Continuous exposure to PTH results in catabolic effects on the skeleton, while intermittent, low doses of PTH result in osteoanabolic effects (Miyamoto-Mikami et al., 2015). Parathyroid hormone negatively regulates sclerostin expression in rodent bone tissue (Gardinier et al., 2015), and serum sclerostin concentrations in humans (Yu et al., 2011). Parathyroid hormone responses to acute exercise stimuli in humans show variable patterns depending on the type of exercise (Lombardi et al., 2020). The available literature contains little available data on changes in PTH concentration during the postexercise period caused by long-term stimulus, and such studies on the middle-aged population have not yet been published.