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Marine Polysaccharides in Pharmaceutical Applications
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Riyasree Paul, Sourav Kabiraj, Sreejan Manna, Sougata Jana
Heparan sulfate is a glycosaminoglycan-based polysaccharide which consists of a linear chain containing repeating units of D-glucuronic acid and iduronic acid in combination with either sulfated or acetylated D-glucosamine residue (Li et al. 2016). The biological activity of heparan sulfate may vary depending on the presence of sulfated residue (Wang, Dhurandhare et al. 2021).
Immunologic Mechanisms in Renal Disease
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Brian D. Schreiber, Gerald C. Groggel
Deregulated growth of mesangial cells may be important in glomerulosclerosis and progressive renal disease (Striker et al., 1991). Recently, heparan sulfate, a component of the GBM and mesangial matrix, has been demonstrated to be a regulator of mesangial cell growth (Groggel et al., 1990). When the glycosaminoglycan form of heparan sulfate is added to mesangial cells in culture, their growth is significantly inhibited (Groggel et al., 1990). The effect is reversible and unique to heparan sulfate since chondroitin sulfate, another glycosaminoglycan found in the glomerulus, had no effect. This inhibitory action of heparan sulfate requires certain structural characteristics, particularly a low degree of sulfation. In both immune and non-immune glomerular injury, the structure of glomerular heparan sulfate is altered (Groggel et al., 1987, 1988). Thus, changes in glomerular heparan sulfate structure produced in immunologic injury of the glomerulus may be important in the development of progressive renal disease.
Heparin and Related Molecules: Antiproliferative and Anti-Inflammatory Effects in the Airways
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
Stephen A. Kilfeather, Clive Page
The presence of other cell types, endothelial, fibroblastic, and inflammatory cells, further complicates the consequences of smooth muscle–GAG interaction. In an initial investigation of local regulation of airway smooth muscle cell proliferation, we have found that bovine airway smooth muscle explants maintained in culture release factors that both reduce and enhance high and low airway smooth muscle cell mitogenic responses, respectively.102 Examination of antithrombin III–binding activity suggested that anticoagulant GAGs were absent from the smooth muscle explant-conditioned media. This excludes the possibility that anticoagulant heparin or related heparan sulphate was responsible for the inhibitory effect. The possibility remains that nonanticoagulant GAGs are released from the smooth muscle mass and that capillary endothelial cells within airway smooth muscle tissue are also a source of antiproliferative GAGs.
Endothelial glycocalyx shedding during active COVID-19 infection and its effect on disease severity
Published in Egyptian Journal of Anaesthesia, 2023
Amr Ragheb Hieba, Emad Abdelmoenam Arida, Hassan Aly Hassan Osman, Salma Alaa El Din Mostafa Imbaby, Heba Abdel Hamid Ahmed Moharem
Regarding the incidence of thrombotic complications, our study showed that there was an association between syndecan-1 and thrombotic complications on day 1 and day 7 (Ps: 0.02, 0.048 respectively). Furthermore, there was an association between the Heparan sulfate levels with thrombotic complications on day 1 and with cardiovascular complications on day 7 (Ps: 0.035, 0.007 respectively). ROC curve analysis demonstrated that the SDC-1 and Heparan sulfate were significantly different between the two groups. Also, according to the ROC curve analysis results, the areas under the curve (AUC) of SDC-1 and Heparan sulfate on day 1 were 0.747 and 0.785, respectively. It revealed an optimal cut-off value of SDC-1 (129.296 ng/ml) and Heparan sulfate (5.419 ng/ml) to distinguish moderate from severe cases. In brief, the ROC result indicated that the SDC-1 with Heparan sulfate might be good candidates to monitor COVID-19 severity.
SARS-CoV-2 Infection Dysregulates Host Iron (Fe)-Redox Homeostasis (Fe-R-H): Role of Fe-Redox Regulators, Ferroptosis Inhibitors, Anticoagulants, and Iron-Chelators in COVID-19 Control
Published in Journal of Dietary Supplements, 2023
Sreus A.G. Naidu, Roger A. Clemens, A. Satyanarayan Naidu
Heparin elicits anti-inflammatory effects on the vasculature as well as in the respiratory airways to alleviate cytokine response in COVID-19/ARDS. The anti-inflammatory spectrum of heparin and its constituent heparan sulfate GAG fragments fall into two mechanisms: i) down-regulate inflammation via interactions with proinflammatory cytokines, and ii) prevent adhesion and influx of inflammatory cells into the diseased area (290). Accordingly, heparin regulates several inflammatory mediators including IL-6, IL-8, platelet growth factor 4 (PGF4), stromal-derived factor 1a, neutrophil elastase, P- and L-selectin, CD11b/CD18, major basic protein (MBP), and eosinophil cationic protein (ECP) (292,293). Heparin also down-regulates NF-κB signaling in human endothelial cells and monocytes (294). Anti-inflammatory therapies that alleviate the cytokine responses, especially IL-6, may alleviate severe symptoms and decrease the CFR in COVID-19 patients. Heparin binding to integrin adhesion molecules inhibits activation and adhesion of leukocytes to the endothelium. Such heparin-mediated low recruitment of immune cells could suppress the subsequent immune activation and cytokine release (295,296). In a retrospective clinical study, treatment of COVID −19 patients with low molecular weight heparin (LMWH) significantly lowered plasma levels of IL −6, a key mediator of CRS (295). Heparin therapy could also relieve hypoxia-mediated clinical manifestations in COVID-19 patients (297).
Advances in the Medical Management of Neurotrophic Keratitis
Published in Seminars in Ophthalmology, 2021
Thomas H. Dohlman, Rohan Bir Singh, Reza Dana
Regenerating agents (RGTAs) represent a novel strategy for promoting corneal re-epithelialization in neurotrophic keratitis. RGTAs are engineered polymers designed to mimic the extracellular matrix, specifically the proteoglycan heparan sulfate. Heparan sulfate is a fundamental component of the extracellular matrix as it plays a critical role in linking various structural proteins such as collagen, elastin, and fibronectin.36 In NK, breakdown of the corneal epithelium predisposes the corneal extracellular matrix to damage. Exogenously administered RGTAs serve to replace damaged heparan-sulfate molecules in order to create a stable matrix microenvironment and stromal bed that resists degradation and facilitates corneal re-epithelialization. In addition to their role in promoting the structural integrity of the cornea, RGTAs have additionally been shown to reduce inflammation and oxidative and proteolytic stress within the cornea.37