2019
O-GlcNAc transferase suppresses necroptosis and liver fibrosis
Zhang B, Li MD, Yin R, Liu Y, Yang Y, Mitchell-Richards KA, Nam JH, Li R, Wang L, Iwakiri Y, Chung D, Robert ME, Ehrlich BE, Bennett AM, Yu J, Nathanson MH, Yang X. O-GlcNAc transferase suppresses necroptosis and liver fibrosis. JCI Insight 2019, 4: e127709. PMID: 31672932, PMCID: PMC6948774, DOI: 10.1172/jci.insight.127709.Peer-Reviewed Original ResearchConceptsReceptor-interacting protein kinase 3Liver fibrosisLiver diseaseHepatocyte necroptosisEthanol-induced liver injuryAlcoholic liver cirrhosisChronic liver diseaseMultiple liver diseasesWeeks of ageProtein expression levelsPortal inflammationLiver cirrhosisLiver injuryBallooning degenerationElevated protein expression levelsSpontaneous genetic modelFibrosisKey suppressorKey mediatorMiceProtein kinase 3CirrhosisExpression levelsGlcNAc levelsMixed lineage kinase
2017
Novel application and serial evaluation of tissue-engineered portal vein grafts in a murine model
Maxfield MW, Stacy MR, Kurobe H, Tara S, Yi T, Cleary MA, Zhuang ZW, Rodriguez-Davalos MI, Emre SH, Iwakiri Y, Shinoka T, Breuer CK. Novel application and serial evaluation of tissue-engineered portal vein grafts in a murine model. Regenerative Medicine 2017, 12: 929-938. PMID: 29215317, PMCID: PMC5827823, DOI: 10.2217/rme-2017-0021.Peer-Reviewed Original Research
2015
Development of Small Diameter Nanofiber Tissue Engineered Arterial Grafts
Kurobe H, Maxfield MW, Tara S, Rocco KA, Bagi PS, Yi T, Udelsman B, Zhuang ZW, Cleary M, Iwakiri Y, Breuer CK, Shinoka T. Development of Small Diameter Nanofiber Tissue Engineered Arterial Grafts. PLOS ONE 2015, 10: e0120328. PMID: 25830942, PMCID: PMC4382213, DOI: 10.1371/journal.pone.0120328.Peer-Reviewed Original ResearchConceptsSmooth muscle cellsSmall-diameter arteriesSynthetic graftsDiameter arteriesSurvival of miceLarge-sized arteriesF4/80-positive macrophagesInner luminal diameterMatrix metalloproteinases 2Smooth muscle actinAneurysmal dilatationGraft stenosisSurgical repairPatency ratesSham groupArterial graftsSized arteriesVascular diseaseSham operationBg miceLuminal diameterDoppler ultrasoundHistologic analysisInterposition conduitsMuscle actinHepatic congestion leads to fibrosis: Findings in a newly developed murine model
Hidaka H, Iwakiri Y. Hepatic congestion leads to fibrosis: Findings in a newly developed murine model. Hepatology 2015, 61: 428-430. PMID: 25283276, PMCID: PMC4303496, DOI: 10.1002/hep.27550.Commentaries, Editorials and LettersCan hypersplenism secondary to portal hypertension be treated by non-selective beta blockers?
Kim MY, Iwakiri Y. Can hypersplenism secondary to portal hypertension be treated by non-selective beta blockers? Hepatology International 2015, 9: 337-338. PMID: 25788189, PMCID: PMC5046185, DOI: 10.1007/s12072-014-9601-1.Commentaries, Editorials and Letters
2010
The type III inositol 1,4,5-trisphosphate receptor is associated with aggressiveness of colorectal carcinoma
Shibao K, Fiedler MJ, Nagata J, Minagawa N, Hirata K, Nakayama Y, Iwakiri Y, Nathanson MH, Yamaguchi K. The type III inositol 1,4,5-trisphosphate receptor is associated with aggressiveness of colorectal carcinoma. Cell Calcium 2010, 48: 315-323. PMID: 21075448, PMCID: PMC3572849, DOI: 10.1016/j.ceca.2010.09.005.Peer-Reviewed Original ResearchConceptsTrisphosphate receptorCaco-2 colon cancer cellsGain of expressionColorectal cancerColorectal carcinomaColon cancer cellsColon cancerType IIICellular functionsInhibition of apoptosisType III inositolLymph node metastasisDepth of invasionNormal colorectal mucosaShRNA knockdownMargin of tumorDevelopment of diseaseExpression levelsLiver metastasesCell proliferationNode metastasisTNM stageApoptosisColorectal mucosaIsoforms
2007
Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease
Fernández-Hernando C, Ackah E, Yu J, Suárez Y, Murata T, Iwakiri Y, Prendergast J, Miao RQ, Birnbaum MJ, Sessa WC. Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease. Cell Metabolism 2007, 6: 446-457. PMID: 18054314, PMCID: PMC3621848, DOI: 10.1016/j.cmet.2007.10.007.Peer-Reviewed Original ResearchMeSH KeywordsAcute Coronary SyndromeAnimalsApolipoproteins EApoptosisAtherosclerosisBone Marrow TransplantationCoronary OcclusionDisease Models, AnimalEndothelial CellsFemaleHumansInflammation MediatorsMacrophagesMaleMiceMice, KnockoutNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktConceptsLoss of Akt1Apolipoprotein E knockout backgroundOcclusive coronary artery diseaseBone marrow transfer experimentsAcute coronary syndromeCoronary artery diseaseLesion expansionCoronary syndromeCoronary atherosclerosisSevere atherosclerosisArtery diseaseInflammatory mediatorsCoronary lesionsVascular protectionVascular originProinflammatory genesENOS phosphorylationCardiovascular systemLesion formationGenetic ablationEndothelial cellsAtherogenesisEnhanced expressionKnockout backgroundVessel wall