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Blastema formation in mammalian digit-tip regeneration
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
Blastema cells that formed after distal amputation express Msx1, Msx2, and BMP4 in fetal mice (Han et al. 2003). Postnatally, BMP4 and BMP2 are expressed in the distal and proximal regions of the blastema, whereas the expression of Msx1 and Msx2 is not detectable (Han et al. 2008, Yu et al. 2010). The majority of blastemal cells also co-express the stem cell marker Sca1 and the endothelial marker CD31 (Table 21.1) (Fernando et al. 2011). The accumulation of Sca1-positive cells is also found in the amputation site after P2 amputation in mice; however, blastema formation does not occur after this level of amputation (Table 21.1) (Agrawal et al. 2010, 2011, 2012, Mu et al. 2013). Agrawal et al. showed that Sca1+ cells that did not express epithelial or hematopoietic progenitor cell marker CD133 or c-kit but did express Sox2 and the periosteal mesenchymal stem cell marker CD90 accumulated at the amputation site after P2 amputation in adult mice (Biernaskie et al. 2009, Spangrude et al. 1988, Zhang et al. 2005, Agrawal et al. 2010, 2012). When an amputated digit was treated with a peptide that is identical to a string of amino acids from the C-terminal telopeptide of collagen III alpha, the number of Sca1+ cells increased, and these cells proliferated actively. They also showed that these cells were capable of differentiating into mesenchymal lineage cells, such as neuroectoderm, adipocyte, and osteoblast, in vitro. Moreover, Mu et al. (2013) demonstrated that treatment with matrix metalloproteinase 1 (MMP1) promoted the accumulation of Sca1+ cells at the amputation site and the formation of CD31+ capillary vessels but not bone regeneration.
Differential time responses in inflammatory and oxidative stress markers after a marathon: An observational study
Published in Journal of Sports Sciences, 2020
Emil List Larsen, Henrik Enghusen Poulsen, Cristina Michaelsen, Laura Kofoed Kjær, Mark Lyngbæk, Emilie Skytte Andersen, Christina Petersen-Bønding, Clara Lemoine, Matthew Gillum, Niklas Rye Jørgensen, Thorkil Ploug, Tina Vilsbøll, Filip Krag Knop, Kristian Karstoft
Blood samples were collected at each study visit from an antecubital vein. The blood samples were centrifuged at 2,000 g, 4°C for 15 minutes, and plasma samples were stored at -80°C until analyses. Plasma samples from the marathon visit (i.e., ‘study visit 2ʹ) were stored on dry ice before and during transportation to the laboratory following the marathon before storage at -80°C. C-terminal telopeptide of type 1 collagen (CTX), and N-terminal propeptide of type 1 procollagen (P1NP), osteocalcin, sclerostin, FGF21, high sensitivity C-reactive protein (hsCRP), tumour necrosis factor alpha (TNFα), interleukin (IL)-6, and IL-10 were determined on plasma from EDTA tubes, albumin was determined on plasma from lithium heparin tubes. TNFα, IL-6, and IL-10 were determined using a multi-spot immunoassay (V-PLEX, Meso Scale Discovery, Rockville, MD, USA) in single determinations. HsCRP was determined using solid-phase sandwich enzyme-linked immunosorbent assay (ELISA) (CRP Human ELISA Kit, Thermo Fisher Scientific, MA, USA) in duplicate determinations. FGF21 was determined as full length 1–181 FGF21 by ELISA method (Human Intact Fibroblast Growth Factor (FGF-21) ELISA, Eagle Biosciences, NH, USA) in single determinations. CTX, P1NP, and osteocalcin were determined using IDS-iSYS CTX, IDS-iSYS intact P1NP, and IDS-iSYS N-mid Osteocalcin (Immunodiagnostic Systems, plc, Tyne and Wear, UK) in single determinations. Finally, sclerostin was determined in double determinations in one batch using the TECOMedical Sclerostin HS EIA assay (Quidel Corporation, San Diego, CA, USA).
The effect of intermittent running on biomarkers of bone turnover
Published in European Journal of Sport Science, 2020
W. Evans, A. Nevill, S. J. McLaren, M. Ditroilo
The use of C-terminal telopeptide of Type I collagen (CTX-I), which represents type I collagen degradation, and procollogen type 1 amino-terminal propeptide (P1NP), which reflects changes in type I collagen synthesis, are currently recommended for markers of bone resorption and bone formation, respectively (Vasikaran et al., 2011). Venepuncture was performed and blood samples were collected 30 min prior to exercise (pre), 1, 2 and 24 h post exercise, similar to previous studies (Mezil et al., 2015; Rogers, Dawson, Wang, Thyfault, & Hinton, 2011; Scott et al., 2012). Plasma was used for the measurement of CTX-I and P1NP on the IDS-iSYS multi-discipline automated analyser. The reportable range of the IDS-iSYS CTX-I assay kit is 0.033–6.000 ng mL−1. The expected mean (95% CI) for fasted healthy males is reported as 0.294 ng mL−1 (0.115–0.748). Intra-assay precision (% coefficient of variance) for CTX-I ranged from 3.2% to 3.5%, with the inter-assay precision of the assay ranging from 4.4% to 5.3%. For P1NP the detectable reference range is 27.7–127.6 ng mL−1, the intra-assay precision 3.4–5.3% and the inter-assay precision range 3.9–5.5%.
The potential osteoporosis due to exposure to particulate matter in ambient air: Mechanisms and preventive methods
Published in Journal of the Air & Waste Management Association, 2022
Javad Torkashvand, Ahmad Jonidi Jafari, Hasan Pasalari, Abbas Shahsavani, Yasaman Oshidari, Vida Amoohadi, Majid Kermani
In the direct mechanism, PM may lead to biochemical processes in the body, which accordingly result in osteoporosis. Although, the biological mechanisms of the association of airborne particles with bone mineral metabolism are not well understood, inflammatory responses and pro-inflammatory cytokines on osteoclastogenesis are some of the cases that mentioned for this association (Qiao et al. 2020). Researchers have tried to find the true mechanism for the effect of airborne particles on osteoporosis. For example, the results of research by Liu et al. showed that exposure to air pollutants, including PM, can increase the concentration of elements in the body, which has a negative effect on bone density and may decrease BMD in people. A cohort study of 10-year-old children in Germany showed a significant association between increasing PM10 and PM2.5–10 levels in the air and increasing serum osteocalcin and C-terminal telopeptide type I collagen (CTx) concentrations in blood that has a negative effect on BMD (Liu et al. 2015). On the other hand, atmospheric pollution-induced cellular oxidative stress has been described as an effective pathogenic mechanism in osteoporosis caused through exposure to PM (Qiao et al. 2020). In addition, the increased bone mineral loss through systemic oxidative stress or inflammation due to exposure to PM was reported (Ranzani et al. 2020). Bones are targets of inflammation, as systemic bone loss may be occurred due to bone resorption. A probable bone detrimental effect of inflammation related to environmental pollution is taken place through osteoclastic synergistic action. Such action was observed for the children exposed to significant concentrations of lipopolysaccharides associated with PM in Mexico City. By the way, researchers emphasized on defining up-regulated critical mediators of bone loss and associated bone responses during children growing up in polluted environment (Calderón-Garcidueñas et al. 2013). However, mediators between PM and osteoporosis can be considered to find the mechanism of action in research, the most important of which are pro-inflammatory markers including interleukin, tumor necrosis factor alpha, and C-reactive protein, chronic inflammation (Qiao et al. 2020).