2024
Renalase peptides reduce pancreatitis severity in mice
Kolodecik T, Guo X, Shugrue C, Guo X, Desir G, Wen L, Gorelick F. Renalase peptides reduce pancreatitis severity in mice. AJP Gastrointestinal And Liver Physiology 2024, 327: g466-g480. PMID: 39010833, PMCID: PMC11427088, DOI: 10.1152/ajpgi.00143.2024.Peer-Reviewed Original ResearchAcute pancreatitisRecombinant renalaseProsurvival propertiesSeverity of acute pancreatitisModel of acute pancreatitisAcute inflammatory injuryClinically relevant modelAnti-inflammatoryHistological tissue injuryPost-ERCPCerulein modelCerulein-inducedInitial dosePancreatitis severityPreclinical modelsImmunohistochemical markersQuantify inflammationInflammatory changesMale micePancreatitisMacrophage populationsTissue injuryCerulein pancreatitisTherapeutic effectRenalaseHas a Hundred Years of Pursuing Proteases Helped to Palliate Pain in Chronic Pancreatitis More Than Placebo?
Singh V, Gorelick F. Has a Hundred Years of Pursuing Proteases Helped to Palliate Pain in Chronic Pancreatitis More Than Placebo? Gastroenterology 2024, 166: 559-561. PMID: 38311123, DOI: 10.1053/j.gastro.2024.01.039.Peer-Reviewed Original ResearchAcute pancreatitis: pathogenesis and emerging therapies
Zaman S, Gorelick F. Acute pancreatitis: pathogenesis and emerging therapies. Journal Of Pancreatology 2024, 7: 10-20. PMID: 38524855, PMCID: PMC10959536, DOI: 10.1097/jp9.0000000000000168.Peer-Reviewed Original ResearchAcute pancreatitisSevere inflammatory disordersLimited treatment optionsLong-term outcomesPotential treatment benefitsPromising new therapyDisease mechanismsPotential therapeutic targetEmerging TherapiesAcute injuryInflammatory disordersPharmacologic interventionsTreatment optionsTreatment benefitPotential therapyNew therapiesSpecific treatmentTherapeutic targetNew treatmentsTherapyPancreatitisTreatmentComplicationsPathogenesisInjury
2023
Clinical predictive value of renalase in post-ERCP pancreatitis
Muniraj T, Desir G, Gorelick F, Guo X, Ciarleglio M, Deng Y, Jamidar P, Farrell J, Aslanian H, Laine L. Clinical predictive value of renalase in post-ERCP pancreatitis. Gastrointestinal Endoscopy 2023, 99: 822-825.e1. PMID: 38103747, DOI: 10.1016/j.gie.2023.12.020.Peer-Reviewed Original ResearchPost-ERCP pancreatitisRenalase levelsPlasma renalase levelsProspective cohort studyPotential clinical roleAcute experimental pancreatitisLongitudinal regression modelsPEP patientsPlasma renalaseCohort studyTertiary hospitalClinical roleExperimental pancreatitisRenalaseAbstractTextERCPPancreatitisFurther studiesAIMSRegression modelsPlasma renalase levels are associated with the development of acute pancreatitis
Wang M, Weiss F, Guo X, Kolodecik T, Bewersdorf J, Laine L, Lerch M, Desir G, Gorelick F. Plasma renalase levels are associated with the development of acute pancreatitis. Pancreatology 2023, 23: 158-162. PMID: 36697349, DOI: 10.1016/j.pan.2023.01.001.Peer-Reviewed Original ResearchConceptsAcute pancreatitisSevere diseasePlasma renalase levelsAcute pancreatitis patientsSevere acute pancreatitisAcute pancreatitis modelPlasma renalaseRenalase levelsSignificant morbidityPancreatitis patientsPlasma levelsHealthy controlsPancreatitis modelPancreatitisPatientsPlasma samplesRenalaseDiseaseNonparametric statistical analysisSecretory proteinsMorbidityStatistical analysisMortalityLevels
2021
Ovariectomy Affects Acute Pancreatitis in Mice
Wang M, Gorelick F. Ovariectomy Affects Acute Pancreatitis in Mice. Digestive Diseases And Sciences 2021, 67: 2971-2980. PMID: 34169436, PMCID: PMC8702581, DOI: 10.1007/s10620-021-07116-w.Peer-Reviewed Original ResearchConceptsOvariectomized mouse modelEffects of estradiolOvariectomized miceAcute pancreatitisEstradiol levelsPancreatitis severityMouse modelPancreatic studiesSevere acute injurySerum estradiol levelsMild acute pancreatitisAcute pancreatitis severityEstradiol conditionsHospital mortalityHourly injectionsAcute injuryOvariectomized modelFemale hormonesEstradiol injectionPancreatitisEstradiol depletionCausative roleDisease severityConclusionsThese findingsMice
2020
Zinc: Roles in pancreatic physiology and disease
Wang M, Phadke M, Packard D, Yadav D, Gorelick F. Zinc: Roles in pancreatic physiology and disease. Pancreatology 2020, 20: 1413-1420. PMID: 32917512, PMCID: PMC7572834, DOI: 10.1016/j.pan.2020.08.016.Peer-Reviewed Original ResearchConceptsZinc deficiencyReduced zinc levelsPancreatic injuryChronic pancreatitisAcute pancreatitisIL-1βInflammatory cytokinesGastrointestinal diseasesPancreatic diseaseIntestinal absorptionAnimal modelsMacrophage activationCalcium homeostasisNutritional deficienciesBiologic effectsPancreatic physiologyZinc levelsCellular changesDiseasePreliminary dataPancreatitisInflammationEssential trace elementDeficiencyCytokines
2018
Cigarette toxin 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces experimental pancreatitis through α7 nicotinic acetylcholine receptors (nAChRs) in mice
Alahmari AA, Sreekumar B, Patel V, Ashat M, Alexandre M, Uduman AK, Akinbiyi EO, Ceplenski A, Shugrue CA, Kolodecik TR, Tashkandi N, Messenger SW, Groblewski GE, Gorelick FS, Thrower EC. Cigarette toxin 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces experimental pancreatitis through α7 nicotinic acetylcholine receptors (nAChRs) in mice. PLOS ONE 2018, 13: e0197362. PMID: 29870540, PMCID: PMC5988302, DOI: 10.1371/journal.pone.0197362.Peer-Reviewed Original ResearchConceptsNNK treatmentHuman acinar cellsNicotinic acetylcholine receptorsTrypsinogen activationAcetylcholine receptorsΑ7 nicotinic acetylcholine receptorIndependent risk factorMarkers of inflammationAcinar cellsΑ7nAChR knockout miceΑ7nAChR activationNeutrophil infiltrationWT miceAcute pancreatitisC57BL/6 miceCigarette smokingPancreatic edemaRisk factorsClinical studiesPancreatitisCigarette smokeKnockout miceExperimental pancreatitisΑ7 isoformPyknotic nucleiAnatomy, Histology, and Fine Structure of the Pancreas
Longnecker D, Gorelick F, Thompson E. Anatomy, Histology, and Fine Structure of the Pancreas. 2018, 10-23. DOI: 10.1002/9781119188421.ch2.Peer-Reviewed Original ResearchPancreatic stellate cellsStellate cellsPrevention of pancreatitisPancreatic surgeryChronic pancreatitisMajor cell typesBlood supplyPancreatic fibrosisPancreatic anatomyClinical experienceEndocrine componentUltrastructural anatomyPancreatitisPancreasDuct systemCell typesAnatomyCellsSurgeryFibrosisHistologicHistologyCancerNew findingsExocrine
2017
The serum protein renalase reduces injury in experimental pancreatitis
Kolodecik TR, Reed AM, Date K, Shugrue C, Patel V, Chung SL, Desir GV, Gorelick FS. The serum protein renalase reduces injury in experimental pancreatitis. Journal Of Biological Chemistry 2017, 292: 21047-21059. PMID: 29042438, PMCID: PMC5743078, DOI: 10.1074/jbc.m117.789776.Peer-Reviewed Original ResearchMeSH KeywordsAcinar CellsAnimalsAnti-Inflammatory Agents, Non-SteroidalBiomarkersCalcium SignalingCarbacholCell LineCeruletideEnzyme ActivationFluorescent Antibody Technique, IndirectGene Expression Regulation, EnzymologicHumansHypertensionLigandsMembrane Transport ModulatorsMiceMice, KnockoutMonoamine OxidasePancreasPancreatitisPlasma Membrane Calcium-Transporting ATPasesRecombinant Fusion ProteinsTaurolithocholic AcidConceptsRecombinant human renalaseAcute pancreatitisAcute injuryCell injuryAcinar cell injuryHuman acinar cellsCytosolic calcium levelsPlasma membrane calcium ATPasePancreatitis onsetIschemic injuryWT micePathological increaseHistological changesProtective effectSevere diseaseMurine modelMembrane calcium ATPasePancreatitisCalcium levelsExperimental pancreatitisBile acidsTissue damageRenalaseInjuryCerulein modelDo Animal Models of Acute Pancreatitis Reproduce Human Disease?
Gorelick FS, Lerch MM. Do Animal Models of Acute Pancreatitis Reproduce Human Disease? Cellular And Molecular Gastroenterology And Hepatology 2017, 4: 251-262. PMID: 28752114, PMCID: PMC5518169, DOI: 10.1016/j.jcmgh.2017.05.007.Peer-Reviewed Original ResearchAcute pancreatitisBiological disease mechanismsNonmalignant gastrointestinal diseasesPathophysiological disease mechanismsDisease mechanismsPotential therapeutic targetPaucity of dataHospital admissionCommon causeExperimental pancreatitis modelGastrointestinal diseasesPancreatitis modelTherapeutic targetAnimal modelsNatural historySpecific causesDiseaseDisease modelsPancreatitisDisease developmentUnderlying cellMolecular mechanismsHuman diseasesCauseLimited informationAcademic Pancreas Centers of Excellence: Guidance from a multidisciplinary chronic pancreatitis working group at PancreasFest
Sheth SG, Conwell DL, Whitcomb DC, Alsante M, Anderson MA, Barkin J, Brand R, Cote GA, Freedman SD, Gelrud A, Gorelick F, Lee LS, Morgan K, Pandol S, Singh VK, Yadav D, Wilcox CM, Hart PA. Academic Pancreas Centers of Excellence: Guidance from a multidisciplinary chronic pancreatitis working group at PancreasFest. Pancreatology 2017, 17: 419-430. PMID: 28268158, PMCID: PMC5525332, DOI: 10.1016/j.pan.2017.02.015.Peer-Reviewed Original ResearchConceptsChronic pancreatitisPancreas centerManagement of CPDisease-related morbidityProgressive inflammatory diseaseMultidisciplinary managementSurgical treatmentPancreatic functionInflammatory diseasesMedical treatmentGuidance statementsConsensus opinionPancreatitisAcademic physiciansTreatmentWorking GroupLiterature reviewMorbidityGroupEpidemiologyDiseasePhysiciansDiagnosis
2014
Low pH enhances connexin32 degradation in the pancreatic acinar cell
Reed AM, Kolodecik T, Husain SZ, Gorelick FS. Low pH enhances connexin32 degradation in the pancreatic acinar cell. AJP Gastrointestinal And Liver Physiology 2014, 307: g24-g32. PMID: 24812055, PMCID: PMC4080162, DOI: 10.1152/ajpgi.00010.2014.Peer-Reviewed Original ResearchConceptsPancreatic acinar cellsAcinar cellsGap junctionsGap junctional intercellular communicationIntercellular communicationRat pancreatic acinar cellsPredominant gap junction proteinExtracellular pHAcute pancreatitisJunctional intercellular communicationClinical conditionsGap junction proteinJunction proteinsGap junctional intracellular communicationAutophagic pathwayFirst evidenceCellsIntracellular communicationConnexin32Pancreatitis
2013
Models of Acute and Chronic Pancreatitis
Lerch MM, Gorelick FS. Models of Acute and Chronic Pancreatitis. Gastroenterology 2013, 144: 1180-1193. PMID: 23622127, DOI: 10.1053/j.gastro.2012.12.043.Peer-Reviewed Original ResearchConceptsChronic pancreatitisModels of AcuteInfluence of inflammationAutoimmune chronic pancreatitisChronic ethanol feedingCombination of lipopolysaccharideMechanisms of pathogenesisAcinar cell responsesHuman diseasesPancreatic cancerSevere diseaseRodent modelsEthanol feedingSupraphysiologic concentrationsPancreatitisPancreatitis modelAnimal modelsTherapeutic interventionsCell responsesDiseaseFurther characterizationEarly stagesAcuteInflammationCholecystokinin
2012
Tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone initiates and enhances pancreatitis responses
Alexandre M, Uduman AK, Minervini S, Raoof A, Shugrue CA, Akinbiyi EO, Patel V, Shitia M, Kolodecik TR, Patton R, Gorelick FS, Thrower EC. Tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone initiates and enhances pancreatitis responses. AJP Gastrointestinal And Liver Physiology 2012, 303: g696-g704. PMID: 22837343, PMCID: PMC3468532, DOI: 10.1152/ajpgi.00138.2012.Peer-Reviewed Original ResearchConceptsNicotinic acetylcholine receptorsAcetylcholine receptorsCigarette smoke toxinsParameters of pancreatitisPancreatitis responsesTobacco carcinogen 4Acinar cell responsesRat pancreatic aciniSmoke toxinsAcute pancreatitisCigarette smokingIntraperitoneal injectionAcinar cell preparationsClinical studiesLong-term effectsCarcinogen 4Pancreatitis modelAdrenergic receptorsReceptor typesCell responsesTobacco toxinsPyknotic nucleiNNKPancreatic aciniPancreatitis
2011
Investigating the Pathobiology of Alcoholic Pancreatitis
Pandol SJ, Lugea A, Mareninova OA, Smoot D, Gorelick FS, Gukovskaya AS, Gukovsky I. Investigating the Pathobiology of Alcoholic Pancreatitis. Alcohol Clinical And Experimental Research 2011, 35: 830-837. PMID: 21284675, PMCID: PMC3083481, DOI: 10.1111/j.1530-0277.2010.01408.x.Peer-Reviewed Original ResearchConceptsAlcoholic pancreatitisAlcohol-induced pancreatitisPotential therapeutic strategyDuration of drinkingKey cellular organellesEffects of alcoholCigarette smokingClinical benefitDietary factorsCommon causeEpidemiologic studiesPancreatitisTherapeutic strategiesAlcohol abuseAnimal modelsHeavy drinkersDisease initiationPathobiologic processesAlcohol effectsCellular organellesMolecular mechanismsEndoplasmic reticulumRecent findingsCurrent studySmokingThe Emerging Role of Smoking in the Development of Pancreatitis
Alexandre M, Pandol SJ, Gorelick FS, Thrower EC. The Emerging Role of Smoking in the Development of Pancreatitis. Pancreatology 2011, 11: 469-474. PMID: 21986098, PMCID: PMC3222114, DOI: 10.1159/000332196.Peer-Reviewed Original ResearchConceptsDevelopment of pancreatitisTobacco smokingChronic pancreatitisAcute pancreatitisCigarette smokingPancreatic cancerBACKGROUND/Cigarette smokeElectronic searchSmokingPancreatitisOnly articlesEmerging RolePancreasNicotineOriginal articlesRiskMetabolitesSpecific constituentsPubMedCancerDiseaseDoseProgression
2010
Low Extracellular pH Induces Damage in the Pancreatic Acinar Cell by Enhancing Calcium Signaling*
Reed AM, Husain SZ, Thrower E, Alexandre M, Shah A, Gorelick FS, Nathanson MH. Low Extracellular pH Induces Damage in the Pancreatic Acinar Cell by Enhancing Calcium Signaling*. Journal Of Biological Chemistry 2010, 286: 1919-1926. PMID: 21084290, PMCID: PMC3023488, DOI: 10.1074/jbc.m110.158329.Peer-Reviewed Original ResearchConceptsPathogenesis of pancreatitisAcinar cellsRyR inhibitorsLow pHeDevelopment of pancreatitisRyanodine receptor inhibitorPancreatic acinar cellsReceptor inhibitorsClinical conditionsCellular injuryPancreatitisBasolateral regionExocrine pancreasPancreatitis responsesInjurious effectsCalcium signalingPathogenesisInduces damageInhibitorsCellsRyRsInjuryEarly stepsPancreasSensitizationMolecular and cellular mechanisms of pancreatic injury
Thrower EC, Gorelick FS, Husain SZ. Molecular and cellular mechanisms of pancreatic injury. Current Opinion In Gastroenterology 2010, 26: 484-489. PMID: 20651589, PMCID: PMC3023172, DOI: 10.1097/mog.0b013e32833d119e.Peer-Reviewed Original ResearchConceptsPancreatic injuryCellular mechanismsFibroblast growth factor 21Antiapoptotic effectGrowth factor 21Ameliorate injuryEndoplasmic reticulum stressChronic pancreatitisFactor 21Immune cellsExendin-4Endogenous trypsin inhibitorBile acidsDisease severityInjuryPancreatitisCausative factorsSensitizing factorTrypsinogen activationProtein CReticulum stressTrypsinogen mutationsBcl-2Intracellular eventsUpregulation of proteinsAlcohol Abuse, Endoplasmic Reticulum Stress and Pancreatitis
Pandol SJ, Gorelick FS, Gerloff A, Lugea A. Alcohol Abuse, Endoplasmic Reticulum Stress and Pancreatitis. Digestive Diseases 2010, 28: 776-782. PMID: 21525762, PMCID: PMC3211518, DOI: 10.1159/000327212.Peer-Reviewed Original ResearchConceptsX-box binding protein 1Alcohol abuseChronic pancreatitisEthanol feedingUnfolded protein responseER stressSignificant pathological responseAcinar cellsAfrican American ethnicityEndoplasmic reticulum stressPancreatic manifestationAlcoholic pancreatitisAdaptive unfolded protein responseMinority of individualsChronic inflammationMost individualsPathological responseCommon causePancreatic diseaseApparent diseasePancreatitisBinding protein 1Heavy drinkersExocrine pancreasPancreas