2019
Early trypsin activation develops independently of autophagy in caerulein-induced pancreatitis in mice
Malla SR, Krueger B, Wartmann T, Sendler M, Mahajan UM, Weiss FU, Thiel FG, De Boni C, Gorelick FS, Halangk W, Aghdassi AA, Reinheckel T, Gukovskaya AS, Lerch MM, Mayerle J. Early trypsin activation develops independently of autophagy in caerulein-induced pancreatitis in mice. Cellular And Molecular Life Sciences 2019, 77: 1811-1825. PMID: 31363815, PMCID: PMC8221268, DOI: 10.1007/s00018-019-03254-7.Peer-Reviewed Original Research
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 nuclei
2013
Impaired autophagic flux mediates acinar cell vacuole formation and trypsinogen activation in rodent models of acute pancreatitis
Mareninova O, Hermann K, French S, O’Konski M, Pandol S, Webster P, Erickson A, Katunuma N, Gorelick F, Gukovsky I, Gukovskaya A. Impaired autophagic flux mediates acinar cell vacuole formation and trypsinogen activation in rodent models of acute pancreatitis. Journal Of Clinical Investigation 2013, 123: 1844-1844. PMCID: PMC3613939, DOI: 10.1172/jci69660.Peer-Reviewed Original Research
2010
Molecular 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 proteins
2009
The Acinar Cell and Early Pancreatitis Responses
Gorelick FS, Thrower E. The Acinar Cell and Early Pancreatitis Responses. Clinical Gastroenterology And Hepatology 2009, 7: s10-s14. PMID: 19896090, PMCID: PMC3073378, DOI: 10.1016/j.cgh.2009.07.036.Peer-Reviewed Original ResearchConceptsAcinar cellsAcid loadForms of pancreatitisAcute acid loadSpecific calcium channelsInhibition of secretionPathologic responseAcute pancreatitisPancreatic acinar cellsPathological elevationAbnormal calciumPancreatitis eventsCalcium-dependent phosphataseAlcohol abuseCalcium channelsHarmful stimuliSmall intestineCalcium releasePancreatitisTrypsinogen activationPancreatitis responsesCalcium occursSpecific intracellular signalsActivationIntracellular signalsReducing Extracellular pH Sensitizes the Acinar Cell to Secretagogue-Induced Pancreatitis Responses in Rats
Bhoomagoud M, Jung T, Atladottir J, Kolodecik TR, Shugrue C, Chaudhuri A, Thrower EC, Gorelick FS. Reducing Extracellular pH Sensitizes the Acinar Cell to Secretagogue-Induced Pancreatitis Responses in Rats. Gastroenterology 2009, 137: 1083-1092. PMID: 19454288, PMCID: PMC2736307, DOI: 10.1053/j.gastro.2009.05.041.Peer-Reviewed Original ResearchConceptsAcinar cellsAcute pancreatitisPancreatic acinar cellsSecretagogue-induced pancreatitisAcid loadAcid challengeAcute acid loadKey early eventPancreatic edemaClinical studiesCell injuryPancreatitisAmylase secretionIsolated aciniAbstractTextPhe effectTrypsinogen activationInjuryPancreatitis responsesZymogen activationAIMSEarly eventsRatsActivationRelevant concentrations
2000
EARLY TRYPSINOGEN ACTIVATION IN ACUTE PANCREATITIS
Lerch M, Gorelick F. EARLY TRYPSINOGEN ACTIVATION IN ACUTE PANCREATITIS. Medical Clinics Of North America 2000, 84: 549-563. PMID: 10872413, DOI: 10.1016/s0025-7125(05)70239-x.Peer-Reviewed Original Research
1999
Mechanisms of intracellular zymogen activation
Gorelick F, Otani T. Mechanisms of intracellular zymogen activation. Best Practice & Research Clinical Gastroenterology 1999, 13: 227-240. PMID: 11030603, DOI: 10.1053/bega.1999.0021.Peer-Reviewed Original ResearchConceptsTrypsinogen activation peptideAcinar cellsZymogen processingDistinct subcellular compartmentsZymogen activationSerine proteasesIntracellular serine proteaseIntracellular zymogen activationCaerulein-induced pancreatitisAcinar cell compartmentPancreatic acinar cellsAcute pancreatitisSubcellular compartmentsHuman pancreatitisPancreatitisExperimental pancreatitisSupramaximal concentrationsHereditary pancreatitisLow-pH compartmentsPancreatic aciniTrypsinogen activationTrypsinogen processingGenetic diseasesCell pathwaysIntracellular activation