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      Taurocholate Feeding to Bile Duct Ligated Rats Prevents Caffeic Acid-Induced Bile Duct Damage by Changes in Cholangiocyte VEGF Expression

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          Abstract

          Cholangiocytes are the target cells in cholestatic models of ductal hyperplasia including bile duct ligation (BDL). We have shown that: (i) cholangiocytes express VEGFR-2 and VEGFR-3; (ii) VEGF-A and VEGF-C stimulate cholangiocyte proliferation via an autocrine mechanism; and (iii) chronic administration of VEGF-A prevents cholangiocyte damage induced by hepatic artery ligation. Caffeic acid phenethyl ester (CAPE) induces growth inhibition in different cells. Taurocholic acid (TC) protects cholangiocytes against injury induced by parasympathetic or sympathetic denervation. The aims of this study were to determine if: (i) CAPE induces bile duct damage; and (ii) TC prevents CAPE-induced bile duct damage by increasing cholangiocyte VEGF expression.

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          Novel and therapeutic effect of caffeic acid and caffeic acid phenyl ester on hepatocarcinoma cells: complete regression of hepatoma growth and metastasis by dual mechanism.

          Tae-Wook Chung, Sung-Kwon Moon, Young-Chae Chang … (2004)
          Our previous studies have clearly shown that the angiogenic enzymes, matrix metalloproteinase (MMP) -2/9, are directly involved in human hepatic tumorigenesis and metastasis and suggest that the MMP-2/9 inhibitors, which have dual inhibitory activities on enzyme activity and transcription, represent the best candidates for achieving tumor regression. Many anti-cancer drugs have strong cellular cytotoxicity and side effects, indicating that strong anti-cancer drugs that have no or minimal cytotoxicity and side effects need to be developed. The specific aim of the present study was to develop powerful anti-cancer drugs with specific tumor regression and anti-metastatic potential having the dual inhibitory activities of specific MMP-2 and -9 enzyme activities and gene transcription at the molecular level. Caffeic acid (CA), a strong and selective MMP-9 activity and transcription inhibitor, was isolated from the plant Euonymus alatus and its derivative, caffeic acid phenethyl ester (CAPE), was synthesized. CA and CAPE selectively inhibited MMP-2 and -9 but not -1, -3, -7, or cathepsin K. Treatment of HepG2 cells with CA (100 microg/mL) and CAPE (5 microg/mL) suppressed phorbol 12-myristate 13-acetate (PMA) -induced MMP-9 expression by inhibiting the function of NF-kappaB, but not AP-1. We confirmed that CA and CAPE suppressed the growth of HepG2 tumor xenografts in nude mice in vivo. The subcutaneous and oral administrations of CA and CAPE significantly reduced the liver metastasis. These results confirm the therapeutic potential of the compounds and suggest that the anti-metastatic and anti-tumor effects of CA and CAPE are mediated through the selective suppression of MMP-9 enzyme activity and transcriptional down-regulation by the dual inhibition of NF-kappaB as well as MMP-9 catalytic activity.
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            The cholangiopathies: disorders of biliary epithelia.

            Mario Strazzabosco, N F LaRusso, Konstantinos Lazaridis (2004)
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              Proliferating cholangiocytes: a neuroendocrine compartment in the diseased liver.

              Shannon Glaser, Maria Mancino, Domenico Alvaro … (2006)
              In the last 15 years, the intrahepatic biliary tree has become the object of extensive studies, which highlighted the extraordinary biologic properties of cholangiocytes involved in bile formation, proliferation, injury repair, fibrosis, angiogenesis, and regulation of blood flow. Proliferation is a "typical" property of cholangiocytes and is key as a mechanism of repair responsible for maintaining the integrity of the biliary tree. Cholangiocyte proliferation occurs virtually in all pathologic conditions of liver injury where it is associated with inflammation, regeneration, and repair, thus conditioning the evolution of liver damage. Interestingly, proliferating cholangiocytes acquire the phenotype of neuroendocrine cells, and secrete different cytokines, growth factors, neuropeptides, and hormones, which represent potential mechanisms for cross talk with other liver cells. Many studies suggest the generation of a neuroendocrine compartment in the injured liver, mostly constituted by cells with cholangiocyte features, which functionally conditions the progression of liver disease. These insights on cholangiocyte pathophysiology will provide new potential strategies for the management of chronic liver diseases. The purpose of this review is to summarize the recent findings on the mechanisms regulating cholangiocyte proliferation and the significance of the neuroendocrine regulation of cholangiocyte biology.
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                Author and article information

                Journal
                Title: Experimental Biology and Medicine
                Abbreviated Title: Exp Biol Med (Maywood)
                ISSN (Print): 1535-3702
                ISSN (Electronic): 1535-3699
                Publication date Created: April 2009
                Publication date Created: April 2009
                Publication date (Electronic): April 2009
                Publication date (Print): April 2009
                Volume: 234
                Issue: 4
                Pages: 462-474
                Affiliations
                [1 ]Department of Medicine, Scott & White and Texas A&M Health Science Center, College of Medicine, Temple, Texas 76504; Department of Human Anatomy, University of Rome, “La Sapienza", I-00185 Rome, Italy; Department of Experimental Medicine, State University of L’Aquila, I-67100 L’Aquila, Italy; Department of Health Science, IUSM University of Rome, I-00185 Rome, Italy; Division of Gastroenterology, Tohoku University Hospital, Aobaku, Sendai 980-8574, Japan; Division Gastroenterology Polo Pontino,...
                Article
                DOI: 10.3181/0808-RM-255
                PMC ID: 2668715
                PubMed ID: 19234059
                SO-VID: 3e2c4432-a759-4af4-86ac-d26f2afd19f2
                Copyright © © 2009
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                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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