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.
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.
Authors: Nicholas F Parchim; Wei Wang; Takayuki Iriyama; Olaide A Ashimi; Athar H Siddiqui; Sean Blackwell; Baha Sibai; Rodney E Kellems; Yang Xia Journal: Hypertension Date: 2014-12-01 Impact factor: 10.190
Authors: Gloria C Chi; Annette L Fitzpatrick; Monisha Sharma; Nancy S Jenny; Oscar L Lopez; Steven T DeKosky Journal: J Gerontol A Biol Sci Med Sci Date: 2017-06-01 Impact factor: 6.053
Authors: Giovanni Stallone; Giuseppe Stefano Netti; Luigi Cormio; Giuseppe Castellano; Barbara Infante; Paola Pontrelli; Chiara Divella; Oscar Selvaggio; Federica Spadaccino; Elena Ranieri; Francesca Sanguedolce; Antonio Pennella; Loreto Gesualdo; Giuseppe Carrieri; Giuseppe Grandaliano Journal: Sci Rep Date: 2020-10-27 Impact factor: 4.379