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[PMID]:28350850
[Au] Autor:Ramirez-GarciaLuna JL; Chan D; Samberg R; Abou-Rjeili M; Wong TH; Li A; Feyerabend TB; Rodewald HR; Henderson JE; Martineau PA
[Ad] Endereço:Bone Engineering Labs, Research Institute-McGill University Health Centre. Montreal General Hospital C10.160, Cedar Ave., Montreal, QC, Canada.
[Ti] Título:Defective bone repair in mast cell-deficient Cpa3Cre/+ mice.
[So] Source:PLoS One;12(3):e0174396, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the adult skeleton, cells of the immune system interact with those of the skeleton during all phases of bone repair to influence the outcome. Mast cells are immune cells best known for their pathologic role in allergy, and may be involved in chronic inflammatory and fibrotic disorders. Potential roles for mast cells in tissue homeostasis, vascularization and repair remain enigmatic. Previous studies in combined mast cell- and Kit-deficient KitW-sh/W-sh mice (KitW-sh) implicated mast cells in bone repair but KitW-sh mice suffer from additional Kit-dependent hematopoietic and non- hematopoietic deficiencies that could have confounded the outcome. The goal of the current study was to compare bone repair in normal wild type (WT) and Cpa3Cre/+ mice, which lack mast cells in the absence of any other hematopoietic or non- hematopoietic deficiencies. Repair of a femoral window defect was characterized using micro CT imaging and histological analyses from the early inflammatory phase, through soft and hard callus formation, and finally the remodeling phase. The data indicate 1) mast cells appear in healing bone of WT mice but not Cpa3Cre/+ mice, beginning 14 days after surgery; 2) re-vascularization of repair tissue and deposition of mineralized bone was delayed and dis-organised in Cpa3Cre/+ mice compared with WT mice; 3) the defects in Cpa3Cre/+ mice were associated with little change in anabolic activity and biphasic alterations in osteoclast and macrophage activity. The outcome at 56 days postoperative was complete bridging of the defect in most WT mice and fibrous mal-union in most Cpa3Cre/+ mice. The results indicate that mast cells promote bone healing, possibly by recruiting vascular endothelial cells during the inflammatory phase and coordinating anabolic and catabolic activity during tissue remodeling. Taken together the data indicate that mast cells have a positive impact on bone repair.
[Mh] Termos MeSH primário: Regeneração Óssea
Carboxipeptidases A/genética
Fêmur/lesões
Fêmur/patologia
Mastócitos/patologia
[Mh] Termos MeSH secundário: Animais
Feminino
Fêmur/irrigação sanguínea
Fêmur/fisiologia
Deleção de Genes
Masculino
Mastócitos/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.17.1 (Carboxypeptidases A); EC 3.4.17.1 (Cpa3 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174396


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[PMID]:28250021
[Au] Autor:Finlin BS; Zhu B; Confides AL; Westgate PM; Harfmann BD; Dupont-Versteegden EE; Kern PA
[Ad] Endereço:Department of Medicine, Division of Endocrinology, and the Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, KY.
[Ti] Título:Mast Cells Promote Seasonal White Adipose Beiging in Humans.
[So] Source:Diabetes;66(5):1237-1246, 2017 May.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human subcutaneous (SC) white adipose tissue (WAT) increases the expression of beige adipocyte genes in the winter. Studies in rodents suggest that a number of immune mediators are important in the beiging response. We studied the seasonal beiging response in SC WAT from lean humans. We measured the gene expression of various immune cell markers and performed multivariate analysis of the gene expression data to identify genes that predict UCP1. Interleukin (IL)-4 and, unexpectedly, the mast cell marker CPA3 predicted UCP1 gene expression. Therefore, we investigated the effects of mast cells on UCP1 induction by adipocytes. TIB64 mast cells responded to cold by releasing histamine and IL-4, and this medium stimulated UCP1 expression and lipolysis by 3T3-L1 adipocytes. Pharmacological block of mast cell degranulation potently inhibited histamine release by mast cells and inhibited adipocyte UCP1 mRNA induction by conditioned medium (CM). Consistently, the histamine receptor antagonist chlorpheniramine potently inhibited adipocyte UCP1 mRNA induction by mast cell CM. Together, these data show that mast cells sense colder temperatures, release factors that promote UCP1 expression, and are an important immune cell type in the beiging response of WAT.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Tecido Adiposo Bege/metabolismo
Tecido Adiposo Branco/metabolismo
Mastócitos/metabolismo
RNA Mensageiro/metabolismo
Estações do Ano
Proteína Desacopladora 1/genética
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/efeitos dos fármacos
Adulto
Animais
Carboxipeptidases A/genética
Degranulação Celular
Clorfeniramina/farmacologia
Temperatura Baixa
Feminino
Regulação da Expressão Gênica
Histamina/metabolismo
Antagonistas dos Receptores Histamínicos H1/farmacologia
Seres Humanos
Interleucina-4/genética
Interleucina-4/metabolismo
Lipólise
Masculino
Proteínas de Membrana/genética
Camundongos
Análise Multivariada
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
RNA Mensageiro/efeitos dos fármacos
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Gordura Subcutânea/metabolismo
Coxa da Perna
Proteína Desacopladora 1/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine H1 Antagonists); 0 (IL4 protein, human); 0 (Membrane Proteins); 0 (PPARGC1A protein, human); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (RNA, Messenger); 0 (TMEM26 protein, human); 0 (UCP1 protein, human); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1); 207137-56-2 (Interleukin-4); 3U6IO1965U (Chlorpheniramine); 820484N8I3 (Histamine); EC 3.4.17.1 (CPA3 protein, human); EC 3.4.17.1 (Carboxypeptidases A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1057


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[PMID]:28193842
[Au] Autor:Stevens RL; McNeil HP; Wensing LA; Shin K; Wong GW; Hansbro PM; Krilis SA
[Ad] Endereço:From the Department of Infectious Diseases, Immunology, and Sexual Health, St. George Hospital, and the St. George and Sutherland Clinical School, Faculty of Medicine, University of New South Wales, Sydney, New South Wales 2217, Australia, rstevens@richardstevensphd.org.
[Ti] Título:Experimental Arthritis Is Dependent on Mouse Mast Cell Protease-5.
[So] Source:J Biol Chem;292(13):5392-5404, 2017 Mar 31.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The constitutive heparin (HP) mast cells (MCs) in mice express mouse MC protease (mMCP)-5 and carboxypeptidase A (mMC-CPA). The amino acid sequence of mMCP-5 is most similar to that of human chymase-1, as are the nucleotide sequences of their genes and transcripts. Using a homologous recombination approach, a C57BL/6 mouse line was created that possessed a disrupted gene. The resulting mice were fertile and had no obvious developmental abnormality. Lack of mMCP-5 protein did not alter the granulation of the IL-3/IL-9-dependent mMCP-2 MCs in the jejunal mucosa of -infected mice. In contrast, the constitutive HP MCs in the tongues of mMCP-5-null mice were poorly granulated and lacked mMC-CPA protein. Bone marrow-derived MCs were readily developed from the transgenic mice using IL-3. Although these MCs contained high levels of mMC-CPA mRNA, they also lacked the latter exopeptidase. mMCP-5 protein is therefore needed to target translated mMC-CPA to the secretory granule along with HP-containing serglycin proteoglycans. Alternately, mMCP-5 is needed to protect mMC-CPA from autolysis in the cell's granules. Fibronectin was identified as a target of mMCP-5, and the exocytosis of mMCP-5 from the MCs in the mouse's peritoneal cavity resulted in the expression of metalloproteinase protease-9, which has been implicated in arthritis. In support of the latter finding, experimental arthritis was markedly reduced in mMCP-5-null mice relative to wild-type mice in two disease models.
[Mh] Termos MeSH primário: Artrite Experimental/patologia
Quimases/efeitos adversos
Mastócitos/enzimologia
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/enzimologia
Artrite Experimental/etiologia
Carboxipeptidases A/análise
Carboxipeptidases A/deficiência
Carboxipeptidases A/metabolismo
Quimases/deficiência
Quimases/fisiologia
Seres Humanos
Mastócitos/metabolismo
Mastócitos/patologia
Camundongos
Camundongos Endogâmicos C57BL
Vesículas Secretórias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.17.1 (Carboxypeptidases A); EC 3.4.17.1 (Cpa3 protein, mouse); EC 3.4.21.- (Cma1 protein, mouse); EC 3.4.21.39 (Chymases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.773416


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[PMID]:28087198
[Au] Autor:VenkatRao V; Kumar SK; Sridevi P; Muley VY; Chaitanya RK
[Ad] Endereço:Department of Animal Biology, School of Life Sciences, University of Hyderabad, Hyderabad 500046, India.
[Ti] Título:Cloning, characterization and transmission blocking potential of midgut carboxypeptidase A in Anopheles stephensi.
[So] Source:Acta Trop;168:21-28, 2017 Apr.
[Is] ISSN:1873-6254
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Transmission-blocking vaccines (TBV) interrupt malaria parasite transmission and hence form an important component for malaria eradication. Mosquito midgut exopeptidases such as aminopeptidase N & carboxypeptidase B have demonstrated TBV potential. In the present study, we cloned and characterized carboxypeptidase A (CPA) from the midgut of an important malarial vector, Anopheles stephensi. ClustalW amino acid alignment and in silico 3-dimensional structure analysis of CPA predicted the presence of active sites involved in zinc and substrate binding that are conserved among all the known mosquito species. Real-time PCR analysis demonstrated that CPA is predominantly expressed in the midgut throughout the mosquito life cycle and that this gene is significantly elevated in P. berghei-infected mosquitoes compared to uninfected blood-fed controls. The high midgut CPA activity correlated with the prominent mRNA levels observed. Peptide-based anti-CPA antibodies were raised that cross-reacted specifically to ∼48kDa and ∼37kDa bands, which correspond to zymogen and active forms of CPA. Further, the addition of CPA-directed antibodies to P. berghei-containing blood meal significantly reduced the mosquito infection rate in the test group compared to control and blocked the parasite development in the midgut. These results support further development of A. stephensi CPA as a candidate TBV.
[Mh] Termos MeSH primário: Anopheles/enzimologia
Carboxipeptidases A/genética
Clonagem Molecular
Trato Gastrointestinal/enzimologia
Insetos Vetores/enzimologia
Vacinas Antimaláricas
Plasmodium berghei
[Mh] Termos MeSH secundário: Animais
Anopheles/anatomia & histologia
Anopheles/genética
Anopheles/parasitologia
Carboxipeptidases A/química
Carboxipeptidases A/imunologia
Carboxipeptidases A/metabolismo
Feminino
Trato Gastrointestinal/imunologia
Trato Gastrointestinal/parasitologia
Regulação Enzimológica da Expressão Gênica
Seres Humanos
Insetos Vetores/anatomia & histologia
Insetos Vetores/parasitologia
Malária/parasitologia
Malária/prevenção & controle
Malária/transmissão
Masculino
Plasmodium berghei/crescimento & desenvolvimento
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Malaria Vaccines); EC 3.4.17.1 (Carboxypeptidases A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE


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[PMID]:27899481
[Au] Autor:Li L; Bai S; Sheline CT
[Ad] Endereço:Department of Ophthalmology and the Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA.
[Ti] Título:hZnT8 (Slc30a8) Transgenic Mice That Overexpress the R325W Polymorph Have Reduced Islet Zn2+ and Proinsulin Levels, Increased Glucose Tolerance After a High-Fat Diet, and Altered Levels of Pancreatic Zinc Binding Proteins.
[So] Source:Diabetes;66(2):551-559, 2017 Feb.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Zinc (Zn ) is involved in both type 1 diabetes (T1DM) and type 2 diabetes (T2DM). The wild-type (WT) form of the ß-cell-specific Zn transporter, ZNT8, is linked to T2DM susceptibility. ZnT8 null mice have a mild phenotype with a slight decrease in glucose tolerance, whereas patients with the ZnT8 R325W polymorphism (rs13266634) have decreased proinsulin staining and susceptibility to T2DM. We measured Zn , insulin, and proinsulin stainings and performed intraperitoneal glucose tolerance testing in transgenic mice overexpressing hZnT8 WT or hZnT8 R325W fed a normal or high-fat diet. The hZnT8 R325W transgenic line had lower pancreatic [Zn ] and proinsulin and higher insulin and glucose tolerance compared with control littermates after 10 weeks of a high-fat diet in male mice. The converse was true for the hZnT8 WT transgenic line, and dietary Zn supplementation also induced glucose intolerance. Finally, pancreatic zinc binding proteins were identified by Zn -affinity chromatography and proteomics. Increasing pancreatic Zn (hZnT8WT) induced nucleoside diphosphate kinase B, and Zn reduction (hZnT8RW) induced carboxypeptidase A1. These data suggest that pancreatic Zn and proinsulin levels covary but are inversely variant with insulin or glucose tolerance in the HFD model of T2DM suggesting novel therapeutic targets.
[Mh] Termos MeSH primário: Proteínas de Transporte/metabolismo
Proteínas de Transporte de Cátions/genética
Dieta Hiperlipídica
Intolerância à Glucose/genética
Pâncreas/metabolismo
Proinsulina/metabolismo
Zinco/metabolismo
[Mh] Termos MeSH secundário: Animais
Carboxipeptidases A/metabolismo
Suplementos Nutricionais
Intolerância à Glucose/metabolismo
Teste de Tolerância a Glucose
Seres Humanos
Imuno-Histoquímica
Masculino
Camundongos
Camundongos Transgênicos
Nucleosídeo NM23 Difosfato Quinases/metabolismo
Pâncreas/efeitos dos fármacos
Polimorfismo Genético
Zinco/farmacologia
Transportador 8 de Zinco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Cation Transport Proteins); 0 (NM23 Nucleoside Diphosphate Kinases); 0 (SLC30A8 protein, human); 0 (Zinc Transporter 8); 9035-68-1 (Proinsulin); EC 2.7.4.6 (Nme2 protein, mouse); EC 3.4.17.1 (Carboxypeptidases A); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE
[do] DOI:10.2337/db16-0323


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[PMID]:27381924
[Au] Autor:Reitz M; Brunn ML; Rodewald HR; Feyerabend TB; Roers A; Dudeck A; Voehringer D; Jönsson F; Kühl AA; Breloer M
[Ad] Endereço:Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.
[Ti] Título:Mucosal mast cells are indispensable for the timely termination of Strongyloides ratti infection.
[So] Source:Mucosal Immunol;10(2):481-492, 2017 Mar.
[Is] ISSN:1935-3456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mast cells and basophils are innate immune cells with overlapping functions that contribute to anti-helminth immunity. Mast cell function during helminth infection was previously studied using mast cell-deficient Kit-mutant mice that display additional mast cell-unrelated immune deficiencies. Here, we use mice that lack basophils or mucosal and connective tissue mast cells in a Kit-independent manner to re-evaluate the impact of each cell type during helminth infection. Neither mast cells nor basophils participated in the immune response to tissue-migrating Strongyloides ratti third-stage larvae, but both cell types contributed to the early expulsion of parasitic adults from the intestine. The termination of S. ratti infection required the presence of mucosal mast cells: Cpa3 mice, which lack mucosal and connective tissue mast cells, remained infected for more than 150 days. Mcpt5 R-DTA mice, which lack connective tissue mast cells only, and basophil-deficient Mcpt8 mice terminated the infection after 1 month with wild-type kinetics despite their initial increase in intestinal parasite burden. Because Cpa3 mice showed intact Th2 polarization and efficiently developed protective immunity after vaccination, we hypothesize that mucosal mast cells are non-redundant terminal effector cells in the intestinal epithelium that execute anti-helminth immunity but do not orchestrate it.
[Mh] Termos MeSH primário: Intestino Delgado/imunologia
Mastócitos/imunologia
Strongyloides ratti/imunologia
Estrongiloidíase/imunologia
Células Th2/imunologia
[Mh] Termos MeSH secundário: Animais
Carboxipeptidases A/genética
Quimases/genética
Imunidade nas Mucosas
Intestino Delgado/parasitologia
Larva
Mastócitos/parasitologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Carga Parasitária
Ratos
Ratos Wistar
Triptases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.17.1 (Carboxypeptidases A); EC 3.4.17.1 (Cpa3 protein, mouse); EC 3.4.21.- (Cma1 protein, mouse); EC 3.4.21.39 (Chymases); EC 3.4.21.59 (Mcpt8 protein, mouse); EC 3.4.21.59 (Tryptases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160707
[St] Status:MEDLINE
[do] DOI:10.1038/mi.2016.56


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[PMID]:27603351
[Au] Autor:Dai LN; Chen YW; Yan WH; Lu LN; Tao YJ; Cai W
[Ad] Endereço:aDepartment of Pediatric Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine bShanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
[Ti] Título:Hereditary pancreatitis of 3 Chinese children: Case report and literature review.
[So] Source:Medicine (Baltimore);95(36):e4604, 2016 Sep.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hereditary pancreatitis (HP) is quite rare and is distinguished by incomplete penetrance presentation as early-onset relapsing pancreatitis, usually beginning in childhood. HP is now known to be commonly relevant to mutations in the PRSS1 (gene-encoding cationic trypsinogen), SPINK1 (serine protease inhibitor, Kazal type 1), CFTR (cystic fibrosis), carboxypeptidase A1 (CPA1), and chymotrypsin C (CTRC) genes as reported in some Caucasian studies. HP has a variable spectrum of severity and may develop complications. METHODS & RESULTS: We describe the clinical course of 3 preschool children, hospitalized with postprandial abdominal pain, whose laboratory tests showed high serum amylase. Similar episodes of abdominal pain led to readmission, and the patients recovered quickly after using symptomatic therapy. The condition of the first boy, who developed a pancreatic tail pseudocyst and splenic infarction, was especially complicated. The boy underwent 2 endoscopic retrograde cholangiopancreatographies and stenting, along with a surgical procedure that completely relieved his symptoms for 3 months. The 3 patients and their parents were given genetic testing. All of the patients carried 1 or more gene mutations inherited from their mothers, fathers, or both parents; however, none of the parents were affected. CONCLUSION: For children with repeated pancreatitis, clinicians should consider HP in the differential diagnosis. It is reliable to perform gene sequencing on suspicious patients and their parents. Multidisciplinary and comprehensive treatment should be recommended to manage HP and its complications. Cholangiopancreatography and stenting is a relatively minimally invasive approach when compared with surgery and can be tried as an early intervention. Surgical procedures should be reserved for patients with complications.
[Mh] Termos MeSH primário: Carboxipeptidases A/genética
Proteínas de Transporte/genética
Pancreatite Crônica/genética
Tripsina/genética
[Mh] Termos MeSH secundário: Pré-Escolar
Seres Humanos
Masculino
Inibidor da Tripsina Pancreática de Kazal
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (SPINK1 protein, human); 50936-63-5 (Trypsin Inhibitor, Kazal Pancreatic); EC 3.4.17.1 (Carboxypeptidases A); EC 3.4.21.4 (PRSS1 protein, human); EC 3.4.21.4 (Trypsin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160908
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000004604


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[PMID]:27358403
[Au] Autor:Szabó A; Pilsak C; Bence M; Witt H; Sahin-Tóth M
[Ad] Endereço:From the Department of Molecular and Cell Biology and.
[Ti] Título:Complex Formation of Human Proelastases with Procarboxypeptidases A1 and A2.
[So] Source:J Biol Chem;291(34):17706-16, 2016 08 19.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pancreas secretes digestive proenzymes typically in their monomeric form. A notable exception is the ternary complex formed by proproteinase E, chymotrypsinogen C, and procarboxypeptidase A (proCPA) in cattle and other ruminants. In the human and pig pancreas binary complexes of proCPA with proelastases were found. To characterize complex formation among human pancreatic protease zymogens in a systematic manner, we performed binding experiments using recombinant proelastases CELA2A, CELA3A, and CELA3B; chymotrypsinogens CTRB1, CTRB2, CTRC, and CTRL1; and procarboxypeptidases CPA1, CPA2, and CPB1. We found that proCELA3B bound not only to proCPA1 (KD 43 nm) but even more tightly to proCPA2 (KD 18 nm), whereas proCELA2A bound weakly to proCPA1 only (KD 152 nm). Surprisingly, proCELA3A, which shares 92% identity with proCELA3B, did not form stable complexes due to the evolutionary replacement of Ala(241) with Gly. The polymorphic nature of position 241 in both CELA3A (∼4% Ala(241) alleles) and CELA3B (∼2% Gly(241) alleles) points to individual variations in complex formation. The functional effect of complex formation was delayed procarboxypeptidase activation due to increased affinity of the inhibitory activation peptide, whereas proelastase activation was unchanged. We conclude that complex formation among human pancreatic protease zymogens is limited to a subset of proelastases and procarboxypeptidases. Complex formation stabilizes the inhibitory activation peptide of procarboxypeptidases and thereby increases zymogen stability and controls activation.
[Mh] Termos MeSH primário: Carboxipeptidases A/metabolismo
Precursores Enzimáticos/metabolismo
Elastase Pancreática/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Carboxipeptidase B/genética
Carboxipeptidase B/metabolismo
Carboxipeptidases A/genética
Bovinos
Linhagem Celular
Ativação Enzimática/fisiologia
Precursores Enzimáticos/genética
Seres Humanos
Mutação de Sentido Incorreto
Elastase Pancreática/genética
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CPB1 protein, human); 0 (Enzyme Precursors); EC 3.4.17.1 (Carboxypeptidases A); EC 3.4.17.2 (Carboxypeptidase B); EC 3.4.21.36 (Pancreatic Elastase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160701
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.743237


  9 / 823 MEDLINE  
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[PMID]:27353089
[Au] Autor:Ngkelo A; Richart A; Kirk JA; Bonnin P; Vilar J; Lemitre M; Marck P; Branchereau M; Le Gall S; Renault N; Guerin C; Ranek MJ; Kervadec A; Danelli L; Gautier G; Blank U; Launay P; Camerer E; Bruneval P; Menasche P; Heymes C; Luche E; Casteilla L; Cousin B; Rodewald HR; Kass DA; Silvestre JS
[Ad] Endereço:Institut National de la Santé et de la Recherche Médicale (INSERM), UMRS-970, Centre de Recherche Cardiovasculaire, Université Paris Descartes, Sorbonne Paris Cité, F-75015 Paris, France.
[Ti] Título:Mast cells regulate myofilament calcium sensitization and heart function after myocardial infarction.
[So] Source:J Exp Med;213(7):1353-74, 2016 Jun 27.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute myocardial infarction (MI) is a severe ischemic disease responsible for heart failure and sudden death. Inflammatory cells orchestrate postischemic cardiac remodeling after MI. Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key roles for mast cells (MCs) in postischemic cardiac remodeling. Because c-Kit mutations affect multiple cell types of both immune and nonimmune origin, we addressed the impact of MCs on cardiac function after MI, using the c-Kit-independent MC-deficient (Cpa3(Cre/+)) mice. In response to MI, MC progenitors originated primarily from white adipose tissue, infiltrated the heart, and differentiated into mature MCs. MC deficiency led to reduced postischemic cardiac function and depressed cardiomyocyte contractility caused by myofilament Ca(2+) desensitization. This effect correlated with increased protein kinase A (PKA) activity and hyperphosphorylation of its targets, troponin I and myosin-binding protein C. MC-specific tryptase was identified to regulate PKA activity in cardiomyocytes via protease-activated receptor 2 proteolysis. This work reveals a novel function for cardiac MCs modulating cardiomyocyte contractility via alteration of PKA-regulated force-Ca(2+) interactions in response to MI. Identification of this MC-cardiomyocyte cross-talk provides new insights on the cellular and molecular mechanisms regulating the cardiac contractile machinery and a novel platform for therapeutically addressable regulators.
[Mh] Termos MeSH primário: Sinalização do Cálcio
Cálcio/metabolismo
Mastócitos/metabolismo
Infarto do Miocárdio/metabolismo
Miocárdio/metabolismo
Miofibrilas/metabolismo
[Mh] Termos MeSH secundário: Animais
Carboxipeptidases A/genética
Carboxipeptidases A/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/genética
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Camundongos
Camundongos Knockout
Contração Miocárdica/genética
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/patologia
Miofibrilas/patologia
Proteólise
Proteínas Proto-Oncogênicas c-kit/genética
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptor PAR-2/genética
Receptor PAR-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, PAR-2); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.4.17.1 (Carboxypeptidases A); EC 3.4.17.1 (Cpa3 protein, mouse); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160630
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160081


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[PMID]:27316830
[Au] Autor:Kukk K; Samel N
[Ad] Endereço:Department of Chemistry, Tallinn University of Technology, Akadeemia tee 15, 12618 Tallinn, Estonia.
[Ti] Título:Enhanced expression of human prostaglandin H synthase-2 in the yeast Pichia pastoris and removal of the C-terminal tag with bovine carboxypeptidase A.
[So] Source:J Biotechnol;231:224-231, 2016 Aug 10.
[Is] ISSN:1873-4863
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Vertebrate prostaglandin H synthases (PGHSs) are membrane-bound disulphide-containing hemoglycoproteins. Therefore, eukaryotic expression systems are required for the production of recombinant PGHSs. Recently we announced the expression of human PGHS-2 (hPGHS-2) in the yeast Pichia pastoris. Here we report improved production of hPGHS-2 in P. pastoris and a convenient method for the purification and de-tagging of the protein. An affinity tag comprised of a proline, a glycine and eight histidines was introduced into the C-terminal end of hPGHS-2. The tagged hPGHS-2 was expressed intracellularly in P. pastoris under the control of a constitutive or methanol-inducible promoter. Compared to constitutive expression, methanol-induced expression yielded approximately four times more protein. The analysis of high and low gene copy number recombinants revealed a positive correlation between the gene copy number and the expression level of hPGHS-2. The recombinant hPGHS-2 was purified using immobilised metal ion affinity chromatography. A novel elution method, treatment of the affinity resin with bovine carboxypeptidase A, was employed. The yield of pure de-tagged hPGHS-2 from 1l of yeast culture was approximately 3mg. The protein purification process with simultaneous removal of the C-terminal polyhistidine tag could be easily applied for the affinity purification of other proteins.
[Mh] Termos MeSH primário: Carboxipeptidases A/metabolismo
Ciclo-Oxigenase 2/metabolismo
Pichia/genética
Proteínas Recombinantes/metabolismo
[Mh] Termos MeSH secundário: Animais
Bovinos
Cromatografia de Afinidade
Ciclo-Oxigenase 2/química
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/isolamento & purificação
Dosagem de Genes/genética
Seres Humanos
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Recombinant Proteins); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.4.17.1 (Carboxypeptidases A)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160619
[St] Status:MEDLINE



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