Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11800
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dc.contributor.authorWen, Shu Wenen
dc.contributor.authorAger, Eleanor Ien
dc.contributor.authorNeo, Jaclynen
dc.contributor.authorChristophi, Christopheren
dc.date.accessioned2015-05-16T01:25:42Z
dc.date.available2015-05-16T01:25:42Z
dc.date.issued2013-06-17en
dc.identifier.citationCancer Biology & Therapy 2013; 14(8): 720-7en
dc.identifier.govdoc23792575en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11800en
dc.description.abstractBlockade of the renin angiotensin system (RAS) can inhibit tumor growth and this may be mediated via undefined immunomodulatory actions. This study investigated the effects of RAS blockade on liver macrophages (Kupffer cells; KCs) in an orthotopic murine model of colorectal cancer (CRC) liver metastases. Here we showed that pharmacological targeting of the RAS [ANG II (31.25 µg/kg/h i.p.), ANG-(1-7) (24 µg/kg/h i.p.) or the ACE inhibitor; captopril (750 mg/kg/d i.p.)] altered endogenous KC numbers in the tumor-bearing liver throughout metastatic growth. Captopril, and to a lesser extent ANG-(1-7), increased KC numbers in the liver but not tumor. KCs were found to express the key RAS components: ACE and AT1R. Treatment with captopril and ANG II increased the number of AT1R-expressing KCs, although total KC numbers were not affected by ANG II. Captopril (0.1 µM) also increased macrophage invasion in vitro. Additionally, captopril was administered with KC depletion before tumor induction (day 0) or at established metastatic growth (day 18) using gadolinium chloride (GdCl 3; 20 mg/kg). Livers were collected at day 21 and quantitative stereology used as a measure of tumor burden. Captopril reduced growth of CRC liver metastases. However, when captopril was combined with early KC depletion (day 0) tumor growth was significantly increased compared with captopril alone. In contrast, late KC depletion (day 18) failed to influence the anti-tumor effects of captopril. The result of these studies suggests that manipulation of the RAS can alter KC numbers and may subsequently influence progression of CRC liver metastases.en
dc.language.isoenen
dc.subject.otherACE inhibitoren
dc.subject.otherKupffer cellen
dc.subject.othercaptoprilen
dc.subject.othercolorectal canceren
dc.subject.othermacrophageen
dc.subject.otherAngiotensin I.pharmacologyen
dc.subject.otherAngiotensin II.pharmacologyen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherCaptopril.pharmacologyen
dc.subject.otherColorectal Neoplasms.drug therapy.metabolism.pathologyen
dc.subject.otherDisease Models, Animalen
dc.subject.otherGadolinium.pharmacologyen
dc.subject.otherKupffer Cells.drug effects.pathologyen
dc.subject.otherLiver Neoplasms.drug therapy.metabolism.secondaryen
dc.subject.otherMacrophages.drug effects.pathologyen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred CBAen
dc.subject.otherPeptide Fragments.pharmacologyen
dc.subject.otherRenin-Angiotensin System.drug effects.physiologyen
dc.titleThe renin angiotensin system regulates Kupffer cells in colorectal liver metastases.en
dc.typeJournal Articleen
dc.identifier.journaltitleCancer biology & therapyen
dc.identifier.affiliationDepartment of Surgery, The University of Melbourne, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationShuWen.Wen@qimr.edu.auen
dc.identifier.doi10.4161/cbt.25092en
dc.description.pages720-7en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/23792575en
dc.type.austinJournal Articleen
local.name.researcherChristophi, Christopher
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptSurgery-
crisitem.author.deptHepatopancreatobiliary Surgery-
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