Subendothelial Heparan Sulfate Proteoglycans Become Major L-Selectin and Monocyte Chemoattractant Protein-1 Ligands upon Renal Ischemia/Reperfusion

Celie, Johanna W.A.M.; Rutjes, Niels W.; Keuning, Eelco D.; Soininen, Raija; Heljasvaara, Ritva; Pihlajaniemi, Taina; Dräger, A.M.; Zweegman, Sonja; Kessler, Floortje L.; Beelen, Robert H.J.; Florquin, Sandrine; Aten, Jan; Born, Jacob van den

doi:10.2353/ajpath.2007.070061

Cited by 71 publications

(85 citation statements)

References 51 publications

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“…A functional role for CD62L in monocyte recruitment in kidneys has recently been given by Celie and co workers [29]. In the present paper we demonstrate that an increased CD11b expression is accompanied by a normal level of CD62L.…”

Section: Discussionmentioning

confidence: 55%

Sustained Monocyte Activation in Clinical Remission of Systemic Vasculitis

2008

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Monocytes have been shown to be activated in ANCA-positive systemic vasculitis, but their state of activation in clinical remission is unknown.Fifteen patients with a new diagnosis of systemic vasculitis were included in the study. Blood samples were analysed at diagnosis and at clinical remission after three to six months. The expression of adhesion molecules (CD62L and CD11b) on monocytes and the serum concentration of the endothelium activation factor VEGF and the chemokine MIP-1alpha were determined.We demonstrate an increased expression of CD11b on monocytes from patients with acute vasculitis that is sustained in clinical remission. The increased state of activation in clinical remission was accompanied by a decrease in VEGF and MIP-1alpha levels. This generates the intriguing question whether a treatment targeted to normalize monocyte activation in clinical remission would have an impact on relapse rate and outcome in this group of patients with high risk of systemic and renal complications.

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Section: Discussionmentioning

confidence: 55%

Sustained Monocyte Activation in Clinical Remission of Systemic Vasculitis

2008

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“…The reason remains unclear, but a deficiency in Col 18 may be compensated by other HSPGs such as agrin and perlecan, 37 and additional inflammatory responses in the mesangium may overcome a decrease in renal MCP-1 likely influenced by Col 18-deficiency. 5,39 The second major finding of our study was that Col 18/ endostatin deficiency augmented the glomerular and interstitial capillary loss caused by anti-GBM disease and that supplementation with endostatin had no effect on the progression of anti-GBM disease.…”

Section: Discussionmentioning

confidence: 99%

“…21,24,31,37 In particular, Col 18 plays a role in enhancing renal inflammation because Col 18 bound to locally produced MCP-1 and presented it to infiltrated monocytes, leading to their adhesion to vascular cell adhesion molecule-1. [37][38][39] How- In KO(ϩ) glomeruli, narrowing and loss of capillary lumens were evident with swelling of ECs (S) and loss of fenestra (arrow), and the subendothelial space was expanded with thickening of the GBM (E). Mesangial matrix also accumulated (M) and diffuse effacement of foot process in podocytes was noted (F).…”

Section: Discussionmentioning

confidence: 99%

Lack of Collagen XVIII/Endostatin Exacerbates Immune-Mediated Glomerulonephritis

Hamano

Okude²,

Shirai³

et al. 2010

Journal of the American Society of Nephrology

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Collagen XVIII is a component of the highly specialized extracellular matrix associated with basement membranes of epithelia and endothelia. In the normal kidney, collagen XVIII is distributed throughout glomerular and tubular basement membranes, mesangial matrix, and Bowman's capsule. Proteolytic cleavage within its C-terminal domain releases the fragment endostatin, which has antiangiogenic properties. Because damage to the glomerular basement membrane (GBM) accompanies immune-mediated renal injury, we investigated the role of collagen XVIII/endostatin in this disorder. We induced anti-GBM glomerulonephritis in collagen XVIII ␣1-null and wild-type mice and compared the resulting matrix accumulation, inflammation, and capillary rarefaction. Anti-GBM disease upregulated collagen XVIII/endostatin expression within the GBM and Bowman's capsule of wild-type mice. Collagen XVIII/endostatin-deficient mice developed more severe glomerular and tubulointerstitial injury than wild-type mice. Collagen XVIII/endostatin deficiency altered matrix remodeling, enhanced the inflammatory response, and promoted capillary rarefaction and vascular endothelial cell damage, but did not affect endothelial proliferation. Supplementing collagen XVIII-deficient mice with exogenous endostatin did not affect the progression of anti-GBM disease. Taken together, these results suggest that collagen XVIII/endostatin preserves the integrity of the extracellular matrix and capillaries in the kidney, protecting against progressive glomerulonephritis.

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“…Changes in mRNAs encoding several enzymes involved in heparan sulfate biosynthesis have been noted after cytokine stimulation of endothelial cells, 46 which may result in cleavage of the chains or structural changes that result in altered binding of chemokines and cell adhesion molecules. 47,48 Whether these changes are beneficial to the host or merely reflect a pathophysiologic response is unknown.…”

Section: Discussionmentioning

confidence: 99%

Inactivation of heparan sulfate 2-O-sulfotransferase accentuates neutrophil infiltration during acute inflammation in mice

Axelsson

Kang

et al. 2012

Blood

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Neutrophil recruitment and extravasation at sites of inflammation provide a mechanism for host defense. We showed previously that heparan sulfate, a type of sulfated glycosaminoglycan, facilitates neutrophil recruitment based on the reduction of neutrophil infiltration in mice in which the overall sulfation of the chains was reduced by selective inactivation of IntroductionThe inflammatory response, initiated by injury or infection, begins by release of cytokines, such as TNF-␣ and IL-1, from resident macrophages. These effectors stimulate endothelial cells, resulting in the secretion of von Willebrand factor, which aids in platelet recruitment and thrombus formation, and the rapid appearance of P-selectin on the apical (lumenal) face of endothelial cells. P-selectin interacts with its primary ligand, P-selectin glycoprotein ligand-1 expressed on neutrophils, enabling rolling of the cells under blood flow. Chemokines released by resident inflammatory and stromal cells transcytose across the endothelium and bind to the apical surface. Their presentation to rolling leukocytes then activates G-protein-coupled receptors, which in turn activates integrins and causes firm adhesion of the leukocytes to the endothelium. Changes in cell shape and spreading occur followed by transcellular and paracellular extravasation. After entry into tissues, neutrophils release proteases and reactive oxygen species that kill foreign pathogens and prepare the tissue for repair.A large body of evidence suggests the importance of heparan sulfate in inflammation. Cytokines (TNF-␣, IL-1, and others), Land P-selectins, and chemokines bind to therapeutic heparin and purified heparan sulfate. Furthermore, heparin blocks L-and P-selectin in vivo in mice, 1,2 which may explain in part its anti-inflammatory activity in humans. 3 Recently, we showed that mice bearing an endothelial-specific mutation of the biosynthetic enzyme, N-acetylglucosamine N-deacetylase-N-sulfotransferase-1 (Ndst1) exhibit reduced neutrophil extravasation in vivo in several acute inflammatory models. 4 Decreased neutrophil infiltration was partially the result of enhanced rolling velocity in vitro, which correlated with weaker binding of L-selectin to endothelial cells. Inactivation of Ndst1 also resulted in reduced chemokine transcytosis across endothelial cells and reduced presentation on the cell surface. Ndst1-deficient mice exhibit decreased allergen-induced airway hyper-responsiveness and inflammation characterized by a significant reduction in airway recruitment of inflammatory cells (eosinophils, macrophages, neutrophils, and lymphocytes). 5 Heparan sulfate has a complex structure, consisting of variably sulfated disaccharides arranged in clusters, which make up the binding sites for ligands. 6 Ndst1 and other Ndst isoforms catalyze the initial sulfation of subsets of glucosamine residues, creating the substrates for 2-O-sulfation of adjacent uronic acid residues and 6-O-sulfation (and more rarely 3-O-sulfation) of N-sulfoglucosamine units. 7 Thus, inactivation of...

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Subendothelial Heparan Sulfate Proteoglycans Become Major L-Selectin and Monocyte Chemoattractant Protein-1 Ligands upon Renal Ischemia/Reperfusion

Cited by 71 publications

References 51 publications

Sustained Monocyte Activation in Clinical Remission of Systemic Vasculitis

Sustained Monocyte Activation in Clinical Remission of Systemic Vasculitis

Lack of Collagen XVIII/Endostatin Exacerbates Immune-Mediated Glomerulonephritis

Inactivation of heparan sulfate 2-O-sulfotransferase accentuates neutrophil infiltration during acute inflammation in mice

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