Dermatan disulfate (Intimatan) prevents complement-mediated myocardial injury in the human-plasma-perfused rabbit heart

Hong, Ting-Ting; White, Andrew; Lucchesi, Benedict R.

doi:10.1016/j.intimp.2004.10.013

Cited by 7 publications

(5 citation statements)

References 37 publications

(43 reference statements)

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“…Thus, it was observed that heparin and non-anticoagulant heparin decrease ischemia-reperfusion injury by disrupting multiple levels of the inflammatory cascade, including the novel observation that heparins inhibit activation of the proinflammatory transcription factor NF-êB. That a similar mechanism(s) might apply to sulodexide is suggested by the many studies involving the anti-inflammatory actions attributable to a wide range of glycosaminoglycans (39,63).…”

Section: Prevention Of Reperfusion Injurymentioning

confidence: 99%

Sulodexide: A Renewed Interest in This Glycosaminoglycan

Lauver

Lucchesi

2006

Cardiovascular Drug Reviews

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Glycosaminoglycans (GAGs) are the most abundant group of heteropolysaccharides found in the body. These long unbranched molecules contain a repeating disaccharide unit. GAGs are located primarily in the extracellular matrix or on the surface of cells. These molecules serve as lubricants in the joints while at the same time providing structural rigidity to cells. Sulodexide is a highly purified glycosaminoglycan composed of a fast mobility heparin fraction as well as dermatan sulfate. Sulodexide differs from other glycosaminoglycans, like heparin, by having a longer half-life and a reduced effect on systemic clotting and bleeding. In addition, sulodexide demonstrates a lipolytic activity that is increased in comparison to heparin. Oral administration of sulodexide results in the release of tissue plasminogen activator and an increase in fibrinolytic activities. An increasing body of research has demonstrated the safety and efficacy of sulodexide in a wide range of vascular pathologies.

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Section: Prevention Of Reperfusion Injurymentioning

confidence: 99%

Sulodexide: A Renewed Interest in This Glycosaminoglycan

Lauver

Lucchesi

2006

Cardiovascular Drug Reviews

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“…27,28 Vanhoutte et al 29 demonstrated that syndecan-1, which is a transmembrane (type I) heparan sulfate proteoglycan and is a member of the syndecan proteoglycan family, plays a pivotal role in protection against exaggerated inflammation and adverse infarct healing after myocardial infarction in mice. Moreover, Hong et al 30 showed that supplementation with dermatan sulfate, a glycosaminoglycan, improved cardiac function and maintained viability of cardiac myocytes with complement activation. Based on these observations and the fact that HCII has the ability to inhibit thrombin action by formation of a bimolecular complex with dermatan sulfate, 7,31 the bimolecular complex with HCII and dermatan sulfate might cooperatively have beneficial effects in the heart against cardiac stress, including ischemia and Ang II excess.…”

Section: Discussionmentioning

confidence: 99%

Heparin Cofactor II Protects Against Angiotensin II-Induced Cardiac Remodeling Via Attenuation of Oxidative Stress in Mice

et al. 2010

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Abstract-Heparin cofactor II (HCII), a serine protease inhibitor, inhibits tissue thrombin action after binding with dermatan sulfate proteoglycans in the extracellular matrix of the vascular system. We previously reported that heterozygous HCII-deficient (HCII ϩ/Ϫ ) humans and mice demonstrate acceleration of vascular remodeling, including atherosclerosis. However, the action of HCII on cardiac remodeling never has been determined. HCII ϩ/ϩ and HCII ϩ/Ϫ mice at age 25 weeks were infused with angiotensin II (Ang II; 2.0 mg/kg/d) for 2 weeks by an osmotic mini-pump. Echocardiography revealed acceleration of cardiac concentric remodeling in HCII ϩ/Ϫ mice and larger left atrial volume in HCII ϩ/Ϫ mice than in HCII ϩ/ϩ mice. Histopathologic studies showed more prominent interstitial fibrosis in both the left atrium and left ventricle in HCII ϩ/Ϫ mice than in HCII ϩ/ϩ mice. Daily urinary excretion of 8-hydroxy-2Ј-deoxyguanosine, a parameter of oxidative stress, and dihydroethidium-positive spots, indicating superoxide production in the myocardium, were markedly increased in Ang II-treated HCII ϩ/Ϫ mice compared to those in HCII ϩ/ϩ mice. Cardiac gene expression levels of atrial natriuretic peptides and brain natriuretic peptides, members of the natriuretic peptide family, Nox 4, Rac-1, and p67 phox as components of NAD(P)H oxidase, and transforming growth factor-␤1 and procollagen III were more augmented in HCII ϩ/Ϫ mice than in HCII ϩ/ϩ mice. However, administration of human HCII protein attenuated all of those abnormalities in Ang II-treated HCII ϩ/Ϫ mice. Moreover, human HCII protein supplementation almost abolished cardiac fibrosis in Ang II-treated HCII ϩ/ϩ mice. The results indicate that HCII has a protective role against Ang II-induced cardiac remodeling through suppression of the NAD(P)H oxidase-transforming growth factor-␤1 pathway. (Hypertension. 2010;56:430-436.)

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“…51 Pathological changes in the composition of speci c CS/DS isomers is also reported in other disease states, including Alzheimer's dementia, spinal cord injury, and cardiac reperfusion injury. 28, [52][53][54] We therefore sought to determine whether the CS/DS-GAG sulfation signature is altered in association with mucosal IBD lesions. Relative to healthy control tissue, we found marked differences in the CS/DS-GAG pro le of mucosal biopsies taken from individuals with both active IBD symptoms at diagnosis and evidence of endoscopic and histologic in ammation.…”

Section: Discussionmentioning

confidence: 99%

Characterizing the intestinal chondroitin sulfate glycosaminoglycan sulfation signature in inflammatory bowel disease

Francis,

Zheng,

Suskind

et al. 2024

Preprint

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The intestinal extracellular matrix (ECM) helps maintain intestinal homeostasis, and pathologic ECM remodeling is implicated in inflammatory bowel disease (IBD). Chondroitin sulfate and dermatan sulfate glycosaminoglycans (CS/DS-GAGs) are integral components of the ECM, and alterations in CS/DS-GAGs significantly influence its function. However, it is unknown whether changes in CS/DS-GAG composition are linked to IBD. Our aim was to characterize the intestinal ECM CS/DS-GAG composition in active IBD using mass spectrometry to analyze intestinal biopsy samples. We characterized the intestinal CS/DS-GAG composition in 50 pediatric and young adult patients (n = 13 control, n = 37 IBD; age 7–23) and 6 adult patients (n = 6 control, age 24–67). The abundance of isomers associated with matrix stability (CS-A and DS) was significantly decreased in patients with IBD compared to controls, while isomers implicated in inflammation (CS-C and CS-E) were significantly increased. This imbalance of intestinal CS/DS isomers was restored among patients achieving clinical remission. Across the entire cohort, the abundance of pro-stabilizing CS/DS isomers negatively correlated with clinical disease activity scores, whereas both CS-C and CS-E content positively correlated with disease activity scores. Thus, pediatric patients with active IBD exhibited increased pro-inflammatory and decreased pro-stabilizing CS/DS isomer composition, and future studies are needed to determine whether changes in the CS/DS-GAG composition play a pathogenic role in IBD.

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Dermatan disulfate (Intimatan) prevents complement-mediated myocardial injury in the human-plasma-perfused rabbit heart

Cited by 7 publications

References 37 publications

Sulodexide: A Renewed Interest in This Glycosaminoglycan

Sulodexide: A Renewed Interest in This Glycosaminoglycan

Heparin Cofactor II Protects Against Angiotensin II-Induced Cardiac Remodeling Via Attenuation of Oxidative Stress in Mice

Characterizing the intestinal chondroitin sulfate glycosaminoglycan sulfation signature in inflammatory bowel disease

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