Biliary Infection May Exacerbate Biliary Cystogenesis Through the Induction of VEGF in Cholangiocytes of the Polycystic Kidney (PCK) Rat

Abstract

Cholangitis arising from biliary infection dominates the prognosis in Caroli's disease. To clarify the influences of bacterial infection on the biliary cystogenesis, in vivo and in vitro studies were performed using the polycystic kidney (PCK) rat as an animal model of Caroli's disease. Cholangitis became a frequent histological finding in aged PCK rats, and neovascularization around the bile ducts also increased in aged PCK rats. Immunohistochemistry revealed that expression of vascular endothelial growth factor (VEGF) was increased in PCK rat biliary epithelium.

Initial evaluation of hepatic T1 relaxation time as an imaging marker of liver disease associated with autosomal recessive polycystic kidney disease (ARPKD)

“…The PCK rat in the bottom row exhibited cholangitis associated with more severe liver disease, which is also observed periodically in ARPKD patients. cholangitis exhibited more extensive fibrosis staining and increased bile duct dilatation than both the more typical PCK rat and the SD control rat, as previously described in this model (27). The relationship of mean hepatic T 1 relaxation time to bile duct area percent, fibrosis area percent, and hydroxyproline content (μg/mg protein) for each rat (excluding the PCK rat with cholangitis) is shown in Fig.…”

Identification of HSP90 as Potential Biomarker of Biliary Atresia Using Two-Dimensional Electrophoresis and Mass Spectrometry

“…Although the etiology of bile ducts injury in BA in unknown, it is postulated that a pre- or perinatal viral infection initiates cholangiocyte apoptosis and release of antigens that leads to further bile duct injury [27]. When the biliary tract suffers from infection, cholangiocytes secrete vascular endothelial growth factor [28] and serotonin [29], which may contribute to the process of BA [30].…”

Activation of TLR4 induces VEGF expression via Akt pathway in nasal polyps

“…The activation of MAPKs induced by LPS may play a role in the inflammatory responses in NPDFs. Phosphorylation of Akt is a critical step in VEGF production . Treatment with Akt inhibitor decreased the release of VEGF in the NPDF response to LPS.…”