Roles of vascular endothelial growth factor in acute rejection reaction following liver transplantation

2011 ◽  
Vol 25 (4) ◽  
pp. 207-209 ◽  
Author(s):  
Tian-Bao Zhou ◽  
Guang-Shun Yang
2019 ◽  
Vol 63 (2) ◽  
Author(s):  
Antonio Franchitto ◽  
Diletta Overi ◽  
Romina Mancinelli ◽  
Anna Paola Mitterhofer ◽  
Paolo Muiesan ◽  
...  

Extrahepatic bile ducts are characterized by the presence of peribiliary glands (PBGs), which represent stem cell niches implicated in biliary regeneration. Orthotopic liver transplantation may be complicated by non-anastomotic strictures (NAS) of the bile ducts, which have been associated with ischemic injury of PBGs and occur more frequently in livers obtained from donors after circulatory death than in those from brain-dead donors. The aims of the present study were to investigate the PBG phenotype in bile ducts after transplantation, the integrity of the peribiliary vascular plexus (PVP) around PBGs, and the expression of vascular endothelial growth factor-A (VEGF-A) by PBGs. Transplanted ducts obtained from patients who underwent liver transplantation were studied (N=62). Controls included explanted bile duct samples not used for transplantation (N=10) with normal histology. Samples were processed for histology, immunohistochemistry and immunofluorescence. Surface epithelium is severely injured in transplanted ducts; PBGs are diffusely damaged, particularly in ducts obtained from circulatory-dead compared to brain-dead donors. PVP is reduced in transplanted compared to controls. PBGs in transplanted ducts contain more numerous progenitor and proliferating cells compared to controls, show higher positivity for VEGF-A compared to controls, and express VEGF receptor-2. In conclusion, PBGs and associated PVP are damaged in transplanted extrahepatic bile ducts; however, an activation of the PBG niche takes place and is characterized by proliferation and VEGF-A expression. This response could have a relevant role in reconstituting biliary epithelium and vascular plexus and could be implicated in the genesis of non-anastomotic strictures.


2002 ◽  
Vol 13 (1) ◽  
pp. 260-264
Author(s):  
Majid Shahbazi ◽  
Anthony A. Fryer ◽  
Vera Pravica ◽  
Iain J. Brogan ◽  
Helen M. Ramsay ◽  
...  

ABSTRACT. Acute rejection is a major cause of reduced survival of renal allografts. Vascular endothelial growth factor (VEGF) is a mitogen for endothelial cells and is expressed widely by renal tissue and T cells. VEGF influences adhesion and migration of leukocytes across the endothelium. This study investigates whether genetically determined variation in VEGF expression influences the development of renal allograft rejection. VEGF promoter polymorphisms were examined by using sequence-specific primer–PCR in 173 renal transplant recipients. Acute rejection occurred in 38.7%; median time to first rejection episode was 14 d. VEGF in vitro expression was investigated in stimulated leukocytes from 30 controls. The −1154*G and −2578*C alleles were associated with higher VEGF production. VEGF −1154 GG and GA genotypes were significantly associated with acute rejection risk at 3 mo (P = 0.004, odds ration [OR] = 6.8, 95% CI = 1.8 to 25 and P = 0.035, OR = 4.1, 95% CI = 1.1 to 15, respectively). Furthermore, VEGF −2578 CC and CA genotypes were associated with increased rejection risk (P = 0.005, OR = 4.1, 95% CI = 1.5 to 11.3 and P = 0.035, OR = 2.7, 95% CI = 1.1 to 7, respectively). These polymorphisms demonstrate linkage disequilibrium (P = 0.001). These data indicate that the −1154*G and −2578*C containing genotypes, encoding higher VEGF production, are strongly associated with acute rejection and may be useful markers of rejection risk.


2007 ◽  
Vol 35 (4) ◽  
pp. 442-449 ◽  
Author(s):  
W Peng ◽  
J Chen ◽  
Y Jiang ◽  
Z Shou ◽  
Y Chen ◽  
...  

Urinary vascular endothelial growth factor (VEGF) was determined by enzyme-linked immunosorbent assay in 199 renal allograft recipients and 80 healthy controls. Urinary VEGF level did not change significantly during the first 8 weeks after transplantation in 119 patients with stable renal function and there were no abnormal histological findings (No-AR). In 67 patients with acute rejection, urinary VEGF was significantly higher (28.57 ± 6.21 pg/μmol creatinine) than in the No-AR patients (3.05 ± 0.45 pg/μmol creatinine) and healthy controls (2.87 ± 0.35 pg/μmol creatinine). At a cut-off point of 3.26 pg/μmol creatinine, sensitivity and specificity for diagnosis of acute rejection were 86.6 and 71.4%, respectively. The 13 patients with subclinical rejection excreted urinary VEGF (16.14 ± 4.09 pg/μmol creatinine) at a significantly higher level than No-AR patients (3.05 ± 0.45 pg/μmol creatinine). At a cut-off point of 4.69 pg/μmol creatinine, sensitivity and specificity for diagnosis of subclinical rejection were 84.6 and 79.8%, respectively. In conclusion, monitoring VEGF in urine might offer a new non-invasive way to detect acute and subclinical rejection in renal transplant recipients.


Sign in / Sign up

Export Citation Format

Share Document