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Introduction and Review of Biological Background
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Three small PGs have been recently identified.79,83 Decorin and biglycan consist of one GAG chain (usually chondroitin sulfate or dermatan sulfate) bound to a single protein. Fibromodulin has four keratan sulfate chains and a heavily glycosylated protein chain. These PGs are about 45,000 Da total and comprise about 5% of all PGs in cartilage. Small PGs are found in all connective tissues. Their roles are suspected to be as cross-linking agents between PG subunits, between cells and PGs, or between collagen fibrils and PGs. Thus, small PGs play a key role in the structure of cartilage and other connective tissues.
Structure and Function of Cartilage
Published in Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi, Articular Cartilage, 2017
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi
Decorin and biglycan belong to the Class I SLRPs. Decorin, the most abundant SLRP in cartilage, is localized to the interterritorial matrix, with concentrations of decorin increasing with age (Roughley et al. 1994). The structure of decorin is semicircular with one dermatan or chondroitin sulfate attached. This concave structure supports its proposed function in associating with the collagen triple helix during fibril formation and regulating fibril spacing, as decorin has been observed “decorating” type II collagen fibrils. Interestingly, although decorin knockout mice have reduced tendon and skin tensile properties, resulting in skin fragility, the articular cartilage in adult mice appears normal (Reed and Iozzo 2002). Biglycan is localized to the pericellular matrix, with two dermatan or chondroitin sulfates attached. It is a regulator of bone formation, as biglycan knockout mice experience retarded skeletal growth (Young et al. 2002). Interestingly, both decorin and biglycan bind TGF-β. Fibromodulin, lumican, and prolargin belong to the Class II SLRPs, with both fibromodulin and lumican increasing in concentration with age. All three SLRPs bind to collagens. Fibromodulin has been linked to regulation of collagen fibril diameter (Hedbom and Heinegard 1989; Hedlund et al. 1994). The Class III SLRP epiphycan is found in the growth plate (Johnson et al. 1997).
Wound care
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
The ability to repair is also age-dependent. In humans, scarring of cutaneous wounds will begin from about 24 weeks gestation, depending in part on the size of the wound. The exact reasons for this are unclear, though some have postulated on the significance of various findings including the following: Environment – sterile intrauterine environment, amniotic fluid rich in HA and growth factors. However, early studies have shown that the intrauterine environment is neither necessary nor sufficient for scarless repair, i.e. it is a property intrinsic to foetal skin.Lorenz (Development, 1992) showed that foetal skin transplanted into adult athymic mice healed scarlessly.Wounds are conspicuous by an absence of inflammation and angiogenesis; healing is largely controlled by fibroblasts rather than macrophages. It is not true regeneration per se, but it is well-organised healing.Rapid increase in HA and receptors on fibroblasts.Type III collagen deposition is more organised.Reduced levels of TGF-β, PDGF, bFGF.More fibromodulin (inhibits TGF-β), less decorin.More adhesion proteins, e.g. fibronectin and tenascin (modulator of cell growth and migration in foetal wounds).
Beyond the amyloid hypothesis: how current research implicates autoimmunity in Alzheimer’s disease pathogenesis
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Miyo K. Chatanaka, Dorsa Sohaei, Eleftherios P. Diamandis, Ioannis Prassas
A study that has only focused on CSF samples is that of Lim et al. [231], where they used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to perform an unbiased, untargeted shotgun analysis, to identify novel autoantibody candidates in patients with AD. They discovered 16 candidate autoantibodies. These results should be viewed with caution, since this was a pilot study with a limited number of samples [AD = 10, Parkinson’s Disease (PD) = 10, Headache control = 10], and it was primarily qualitative. The candidate autoantibodies found were not confirmed with alternative techniques or independent sets of samples. Some of the more promising autoantibody hits include glia-derived nexin (SERPINE2), fibromodulin (FMOD), and quinone oxidoreductase (CRYZ). SERPINE2 is a serine protease inhibitor, and it plays a crucial role in synaptic plasticity in the CNS [272]. Its levels are associated with tau-positive dystrophic neurites and amyloid processing [273]; so autoantibodies to it could indicate dysfunctional CNS neurons.
Regulatory T Cells in Bioactive Peptides-Induced Oral Tolerance; a Two-Edged Sword Related to the Risk of Chronic Diseases: A Systematic Review
Published in Nutrition and Cancer, 2021
Meisam Barati, Masoumeh Jabbari, Hamid Nickho, Mojgan Esparvarinha, Amirreza Javadi Mamaghani, Hasan Majdi, Anwar Fathollahi, Sayed Hossein Davoodi
OA is a deteriorating disease of articular cartilage and subchondral bones. In the recent decades, the growing bodies of evidences indicate the important role of the immune system in the pathogenesis of this disease (53, 54). Collagen IX, Fibromodulin and Hyaluronan, the cartilage specific antigens, release due to the primary injury of articular cartilage caused by mechanical factors. These antigens can play as triggers for immune response activation in susceptible persons (55–58). Immune cells including macrophages, T cells and B cells infiltrate into the joint tissue and chemokines and cytokines release to the synovial fluid from various cell types in the joint. Complement system also activates and collectively, the inflammatory milieu induces production of cartilage degrading factors mostly from chondrocytes. These processes result in more and more damage to the articular cartilage. Based on the evidences from recent studies, it has been shown that there are substantial inflammatory components in the pathogenesis and development of OA (59–61).
CD43 in the malignant flow cytometry laboratory in 2020
Published in Expert Review of Hematology, 2021
One study suggested that CD43 may be particularly useful in identifying borderline LPDs, a group of disorders with a ‘CLL-adjacent’ phenotype, and which constitutes its most challenging differential diagnosis (Figure 2) [16,36]. These disorders, which are still molecularly ill-characterized, seem to have a higher percentage of MYD88 L265P mutations (10–20% vs. about 1–2% in CLL) and a (1–2 log) lower expression of fibromodulin (FMOD) than CLL, which has characteristically high FMOD gene expression [16,36,39,40]. Because CD43 is negative or dimly expressed in a majority of borderline LPD, it is the most clear-cut antigenic difference between CLL and borderline LPD. It is worth noting that the use of CD43 to classify B-LPD has grown over the inclusion period, with no studies published between 2010 and 2016 and 12 since 2017.