Pentraxin 3 and complement cascade activation in the failure of arteriovenous fistula
| Autor: | Giovanni Pertosa, Giuseppe Grandaliano, Daniela Marrone, Antonia Loverre, Giuseppe Castellano, Giuseppe Dalfino, Angela Di Vittorio, Simona Simone, Francesco Paolo Schena |
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| Předmět: |
Male
Pathology medicine.medical_treatment Endothelial cells Messenger Complement Membrane Attack Complex Constriction Pathologic Pentraxin 3 Pathogenesis Kidney Failure Smooth Muscle Leukocytes Settore MED/14 - NEFROLOGIA Treatment Failure Chronic Complement Activation Arterovenous fistula Arteriovenous malformation PTX3 Middle Aged Constriction Serum Amyloid P-Component C-Reactive Protein Female Hemodialysis Cardiology and Cardiovascular Medicine Adult congenital hereditary and neonatal diseases and abnormalities medicine.medical_specialty Mononuclear Myocytes Smooth Muscle Complement Arteriovenous fistula End stage renal disease Emodialysis Renal Dialysis Vascular medicine Humans cardiovascular diseases Endothelium RNA Messenger Aged Pathologic Myocytes business.industry Vascular disease Arteriovenous Anastomosis medicine.disease Stenosis Leukocytes Mononuclear RNA Kidney Failure Chronic Endothelium Vascular business Biomarkers |
| Zdroj: | Università degli studi di Foggia-IRIS Università degli Studi di Milano-IRIS |
| Popis: | Objective Pentraxin-3 (PTX3) has been suggested to play a role in the development of vascular pathology. Stenosis of arteriovenous fistula (AVF) leading to its failure is the major cause of morbidity in hemodialysis patients. To date, little is known on the pathogenesis of AVF stenosis. The aim of the present study was to investigate the potential role of PTX3 in this setting. Methods and results A sample of venous wall was collected at the time of AVF formation in 44 patients with end stage renal disease. Ten patients developed AVF stenosis and from these patients a second portion of the venous wall was obtained during surgical revision of the AVF. Confocal laser scanning microscopy demonstrated that PTX3 immunostaining, hardly detectable in native AVF, was significantly increased in failed AVF, showing a specific co-localization with endothelial cell markers. Circulating mononuclear cells isolated at the time of AVF revision presented a significantly higher PTX3 mRNA expression than those collected during AVF creation. Interestingly, a significant deposition of C5b-9 on endothelial cells, co-localizing with PTX3, was observed in stenotic AVF. Conclusion The present study demonstrates for the first time a close association between PTX3 deposition and complement activation at the endothelial cell level in failed AVF and suggests a role for PTX3 in modulating innate immunity in the pathogenesis of AVF stenosis. |
| Databáze: | OpenAIRE |
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