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Pesquisa : A05.810.453.736.560 [Categoria DeCS]
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[PMID]:29267498
[Au] Autor:Ni XJ; Xu ZQ; Jin H; Zheng SL; Cai Y; Wang JJ
[Ad] Endereço:Transplantation Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
[Ti] Título:Ginsenoside Rg1 protects human renal tubular epithelial cells from lipopolysaccharide-induced apoptosis and inflammation damage.
[So] Source:Braz J Med Biol Res;51(2):e6611, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Ginsenoside Rg1, one of the most notable active components of Panax ginseng, has been widely reported to exert anti-inflammatory actions. This study aimed to reveal whether ginsenoside Rg1 also exhibits beneficial roles against lipopolysaccharide (LPS)-induced apoptosis and inflammation in human renal tubular epithelial cells, and to evaluate the potential role of the component on tubulointerstitial nephritis treatment. HK-2 cells were treated with various doses of ginsenoside Rg1 (0, 50, 100, 150, and 200 µM) in the absence or presence of 5 µg/mL LPS. Thereafter, CCK-8 assay, flow cytometry, western blot, migration assay, reactive oxygen species (ROS) assay, and ELISA were carried out to respectively assess cell viability, apoptosis, migration, ROS activity, and the release of inflammatory cytokines. As a result, ginsenoside Rg1 protected HK-2 cells from LPS-induced injury, as cell viability was increased, cell apoptosis was decreased, and the release of MCP-1, IL-1ß, IL-6, and TNF-α was reduced. Ginsenoside Rg1 functioned to HK-2 cells in a dose-dependent manner, and the 150 µM dose exhibited the most protective functions. Ginsenoside Rg1 had no significant impact on cell migration and ROS activity, while it alleviated LPS-induced ROS release and migration impairment. Furthermore, the down-regulations of p-PI3K, p-AKT, and up-regulations of PTEN, p-IκBα, p-p65, Bcl-3 induced by LPS were recovered to some extent after ginsenoside Rg1 treatment. In conclusion, ginsenoside Rg1 protects HK-2 cells against LPS-induced inflammation and apoptosis via activation of the PI3K/AKT pathway and suppression of NF-κB pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Apoptose/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Ginsenosídeos/farmacologia
Túbulos Renais/citologia
Lipopolissacarídeos
Nefrite/prevenção & controle
[Mh] Termos MeSH secundário: Análise de Variância
Western Blotting
Linhagem Celular
Ensaios de Migração Celular
Sobrevivência Celular/efeitos dos fármacos
Citocinas/análise
Citocinas/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Túbulos Renais/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/análise
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Proteínas Proto-Oncogênicas c-akt/análise
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Espécies Reativas de Oxigênio/análise
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Ginsenosides); 0 (Lipopolysaccharides); 0 (Protective Agents); 0 (Reactive Oxygen Species); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); PJ788634QY (ginsenoside Rg1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  2 / 20972 MEDLINE  
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[PMID]:29355545
[Au] Autor:Ma YR; Zhou Y; Huang J; Qin HY; Wang P; Wu XA
[Ad] Endereço:Department of Pharmacy, The First Hospital of Lanzhou University, Lanzhou 730000, China.
[Ti] Título:The urinary excretion of metformin, ceftizoxime and ofloxacin in high serum creatinine rats: Can creatinine predict renal tubular elimination?
[So] Source:Life Sci;196:110-117, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The renal excretion of creatinine and most drugs are the net result of glomerular filtration and tubular secretion, and their tubular secretions are mediated by individual transporters. Thus, we hypothesized that the increase of serum creatinine (SCr) levels attributing to inhibiting tubular transporters but not glomerular filtration rate (GFR) could be used to evaluate the tubular excretion of drugs mediated by identical or partial overlap transporter with creatinine. In this work, we firstly developed the creatinine excretion inhibition model with normal GFR by competitively inhibiting tubular transporters, and investigated the renal excretion of metformin, ceftizoxime and ofloxacin in vivo and in vitro. The results showed that the 24-hour urinary excretion of metformin and ceftizoxime in model rats were decreased by 25% and 17% compared to that in control rats, respectively. The uptake amount and urinary excretion of metformin and ceftizoxime could be inhibited by creatinine in renal cortical slices and isolated kidney perfusion. However, the urinary excretion of ofloxacin was not affected by high SCr. These results showed that the inhibition of tubular creatinine transporters by high SCr resulted to the decrease of urinary excretion of metformin and ceftizoxime, but not ofloxacin, which implied that the increase of SCr could also be used to evaluate the tubular excretion of drugs mediated by identical or partial overlap transporter with creatinine in normal GFR rats.
[Mh] Termos MeSH primário: Ceftizoxima/urina
Creatinina/sangue
Túbulos Renais/metabolismo
Metformina/urina
Ofloxacino/urina
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte/metabolismo
Ceftizoxima/farmacocinética
Taxa de Filtração Glomerular
Técnicas In Vitro
Testes de Função Renal
Masculino
Metformina/farmacocinética
Ofloxacino/farmacocinética
Valor Preditivo dos Testes
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 9100L32L2N (Metformin); A4P49JAZ9H (Ofloxacin); AYI8EX34EU (Creatinine); C43C467DPE (Ceftizoxime)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


  3 / 20972 MEDLINE  
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[PMID]:29185789
[Au] Autor:Mou Y; Zhang Y; Guo C; Zhao J; Zhang Z; Zhou X; Dong J; Liao L
[Ad] Endereço:1 Division of Cardiology, Department of Internal Medicine, Shandong Provincial Hospital Affiliated to Shandong University , Jinan, China .
[Ti] Título:Integrated Treatment of Prostaglandin E1 and Angiotensin-Converting Enzyme Inhibitor in Diabetic Kidney Disease Rats: Possible Role of Antiapoptosis in Renal Tubular Epithelial Cells.
[So] Source:DNA Cell Biol;37(2):133-141, 2018 Feb.
[Is] ISSN:1557-7430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To investigate the therapeutic mechanisms underlying prostaglandin E1 (PGE1) and angiotensin-converting enzyme inhibitor (ACEI) on reducing urinary protein in diabetic kidney disease (DKD). DKD rats were established and randomly divided into four groups: PGE1 (10 µg/kg/day) (P group), ACEI (10 mg/kg/day) (A group), combination of PGE1 with ACEI treatment (P + A group), and saline treatment group (DKD group). Untreated rats were used as normal control (N group). Urinary albumin, endothelin-1 (ET-1), angiotensin II (AngII), TUNEL assay, Masson's trichrome staining, and immunohistochemistry staining for CD68 were evaluated in all groups. Ten days after treatment, urinary albumin was significantly decreased in the P and P + A groups (p < 0.01 vs. the DKD group). At the end of 8 weeks, the albumin was still significantly reduced in the P + A group (p < 0.05 vs. the A group). ET-1 and AngII were also significantly decreased in three treatment groups (p < 0.01 vs. the DKD group), especially in the P + A group. Few cells underwent apoptosis in glomerular regions in DKD rats, while amounts of apoptotic cells were seen in tubules regions. Further, apoptosis and the areas of fibrosis in tubulointerstitial were both decreased most in the P + A group compared with the DKD group. Apoptosis of renal tubular epithelial cells may participate in the development and progression of DKD in rats. Combination of PGE1 with AGEI remarkably protects renal function compared with PGE1 or ACEI monotherapy. The potential therapeutic mechanisms of PGE1 and AGEI might be via multiple targets and, at least in part, through inhibiting the apoptosis of renal tubular epithelial cells.
[Mh] Termos MeSH primário: Alprostadil/farmacologia
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Diabetes Mellitus Experimental/complicações
Nefropatias Diabéticas/tratamento farmacológico
Nefrite Intersticial/tratamento farmacológico
[Mh] Termos MeSH secundário: Angiotensina II/sangue
Animais
Apoptose/efeitos dos fármacos
Diabetes Mellitus Experimental/sangue
Nefropatias Diabéticas/sangue
Nefropatias Diabéticas/etiologia
Avaliação Pré-Clínica de Medicamentos
Endotelina-1/sangue
Células Epiteliais/efeitos dos fármacos
Túbulos Renais/efeitos dos fármacos
Túbulos Renais/patologia
Macrófagos/imunologia
Masculino
Nefrite Intersticial/sangue
Nefrite Intersticial/etiologia
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Endothelin-1); 11128-99-7 (Angiotensin II); F5TD010360 (Alprostadil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1089/dna.2017.3690


  4 / 20972 MEDLINE  
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[PMID]:29326040
[Au] Autor:Noh MR; Jang HS; Song DK; Lee SR; Lipschutz JH; Park KM; Kim JI
[Ad] Endereço:Department of Anatomy and BK21 Plus, Kyungpook National University School of Medicine, Daegu, Republic of Korea.
[Ti] Título:Downregulation of exocyst Sec10 accelerates kidney tubule cell recovery through enhanced cell migration.
[So] Source:Biochem Biophys Res Commun;496(2):309-315, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Migration of surviving kidney tubule cells after sub-lethal injury, for example ischemia/reperfusion (I/R), plays a critical role in recovery. Exocytosis is known to be involved in cell migration, and a key component in exocytosis is the highly-conserved eight-protein exocyst complex. We investigated the expression of a central exocyst complex member, Sec10, in kidneys following I/R injury, as well as the role of Sec10 in wound healing following scratch injury of cultured Madin-Darby canine kidney (MDCK) cells. Sec10 overexpression and knockdown (KD) in MDCK cells were used to investigate the speed of wound healing and the mechanisms underlying recovery. In mice, Sec10 decreased after I/R injury, and increased during the recovery period. In cell culture, Sec10 OE inhibited ruffle formation and wound healing, while Sec10 KD accelerated it. Sec10 OE cells had higher amounts of diacylglycerol kinase (DGK) gamma at the leading edge than did control cells. A DGK inhibitor reversed the inhibition of wound healing and ruffle formation in Sec10 OE cells. Conclusively, downregulation of Sec10 following I/R injury appears to accelerate recovery of kidney tubule cells through activated ruffle formation and enhanced cell migration.
[Mh] Termos MeSH primário: Diacilglicerol Quinase/antagonistas & inibidores
Túbulos Renais/metabolismo
Traumatismo por Reperfusão/prevenção & controle
Proteínas de Transporte Vesicular/genética
[Mh] Termos MeSH secundário: Animais
Bioensaio
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Diacilglicerol Quinase/genética
Diacilglicerol Quinase/metabolismo
Cães
Inibidores Enzimáticos/farmacologia
Exocitose
Regulação da Expressão Gênica
Túbulos Renais/patologia
Células Madin Darby de Rim Canino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Piperidinas/farmacologia
Quinazolinonas/farmacologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Proteínas de Transporte Vesicular/agonistas
Proteínas de Transporte Vesicular/antagonistas & inibidores
Proteínas de Transporte Vesicular/metabolismo
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (EXOC5 protein, mouse); 0 (Enzyme Inhibitors); 0 (Piperidines); 0 (Quinazolinones); 0 (RNA, Small Interfering); 0 (Vesicular Transport Proteins); 120166-69-0 (R 59949); EC 2.7.1.107 (Diacylglycerol Kinase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


  5 / 20972 MEDLINE  
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[PMID]:29277613
[Au] Autor:Liu M; Liu L; Bai M; Zhang L; Ma F; Yang X; Sun S
[Ad] Endereço:Department of Nephrology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China; State Key Laboratory of Cancer Biology, Fourth Military Medical University, Xi'an, Shaanxi, China.
[Ti] Título:Hypoxia-induced activation of Twist/miR-214/E-cadherin axis promotes renal tubular epithelial cell mesenchymal transition and renal fibrosis.
[So] Source:Biochem Biophys Res Commun;495(3):2324-2330, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The epithelial-to-mesenchymal transition (EMT) induced by chronic hypoxia is one of the critical causes of renal fibrosis. Previous work reported that the transcription factors Twist plays an important role in hypoxia-induced EMT and renal fibrosis. Recent evidence indicates that miR-214 was regulated by Twist in many fibrotic diseases, but their role in hypoxia-induced EMT and renal fibrosis remains unknown. Here, we found that hypoxia significantly upregulated the expression of miR-214-3p in HK-2 cells, unilateral ureteral obstruction (UUO) nephropathy and patients with chronic kidney disease. Knockdown of miR-214-3p reversed the EMT of renal tubular epithelial cells (TECs) and alleviated fibrosis in the UUO mouse in vivo, while the overexpression of miR-214-3p promoted EMT phenotype and expression of fibrotic factors in TECs under hypoxic condition. In addition, Twist was also observed increased gradually with the prolongation of hypoxia, and it positively correlated with the expression of miR-214-3p in HK-2 cells transfected with Twist-overexpression or Twist-siRNA plasmid. Moreover, miR-214-3p negatively regulated the expression of epithelial cadherin (E-cadherin) by binding the E-cadherin 3' UTR under hypoxic condition. Overall, hypoxia-induced activation of Twist/miR-214/E-cadherin axis is involved in the EMT of TECs, and anti-miR-214 may be an attractive strategy to ameliorate the progression of renal fibrosis.
[Mh] Termos MeSH primário: Caderinas/metabolismo
Hipóxia Celular
Transição Epitelial-Mesenquimal
Túbulos Renais/metabolismo
Túbulos Renais/patologia
MicroRNAs/metabolismo
Proteína 1 Relacionada a Twist/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Fibrose/metabolismo
Fibrose/patologia
Seres Humanos
Masculino
Redes e Vias Metabólicas
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cadherins); 0 (MicroRNAs); 0 (Mirn214 microRNA, mouse); 0 (Twist-Related Protein 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


  6 / 20972 MEDLINE  
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[PMID]:29198839
[Au] Autor:Ma Q; Wang Y; Zhang T; Zuo W
[Ad] Endereço:School of Medicine, Tongji University, Shanghai 200433, China.
[Ti] Título:Notch-mediated Sox9 cell activation contributes to kidney repair after partial nephrectomy.
[So] Source:Life Sci;193:104-109, 2018 Jan 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Partial nephrectomy is a surgical technique as an alternative for traditional radical nephrectomy. The advantage of partial nephrectomy technique is nephron-sparing, however, whether the remaining kidney tissue could regenerate the lost nephron is still unknown. The current work is to investigate the kidney tissue repair process and the related cellular and molecular mechanism. MAIN METHODS: We used a novel unilateral partial nephrectomy mouse model to study kidney repair, and focused on a population of Sox9 progenitor cells to study their pivotal role in the regenerative process. Kidney function after nephrectomy was measured using creatinine and urea nitrogen assay kit. Wound healing was assessed by Masson Trichrome Staining. Tissue regeneration was tested by Sox9 cells immunofluorescence staining. The differentiation potential of Sox9 cells were assessed by immunoanalysis with various tubular cell markers. Notch activation was determined by qPCR and Western blotting. KEY FINDINGS: After partial nephrectomy, we found that massive Sox9 cells emerged one day after the surgery and lasted for up to 20days. The Sox9 cells had proliferative capacity and could give rise to epithelial cells of proximal tubule, Henle's loop, distal tubule, collecting duct, and the parietal layer of glomerulus. We also found that the activation of Sox9 cells was mediated by Notch signaling pathway. SIGNIFICANCE: The current study reveals that Notch-mediated Sox9 cell activation can contribute to kidney tubule regeneration after unilateral partial nephrectomy in mice.
[Mh] Termos MeSH primário: Rim/metabolismo
Nefrectomia/métodos
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Creatinina/metabolismo
Células Epiteliais/metabolismo
Rim/fisiologia
Túbulos Renais
Túbulos Renais Proximais/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Nefrectomia/reabilitação
Néfrons
Receptores Notch/metabolismo
Regeneração/fisiologia
Fatores de Transcrição SOX9/genética
Fatores de Transcrição SOX9/metabolismo
Transdução de Sinais
Cicatrização/genética
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Notch); 0 (SOX9 Transcription Factor); 0 (SOX9 protein, human); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  7 / 20972 MEDLINE  
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[PMID]:29190833
[Au] Autor:Horvei KD; Pedersen HL; Fismen S; Thiyagarajan D; Schneider A; Rekvig OP; Winkler TH; Seredkina N
[Ad] Endereço:RNA and Molecular Pathology Research Group, Department of Medical Biology, Faculty of Health Sciences, UIT-The Arctic University of Norway, Tromsø, Norway.
[Ti] Título:Lupus nephritis progression in FcγRIIB-/-yaa mice is associated with early development of glomerular electron dense deposits and loss of renal DNase I in severe disease.
[So] Source:PLoS One;12(11):e0188863, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FcγRIIB-/-yaa mice develop severe lupus glomerulonephritis due to lack of an inhibitory immune cell receptor combined with a Y-chromosome linked autoimmune accelerator mutation. In the present study, we have investigated nephritis development and progression in FcγRIIB-/-yaa mice to find shared features with NZB/NZW F1 lupus prone mice and human disease. We sacrificed 25 male FcγRIIB-/-yaa mice at various disease stages, and grouped them according to activity and chronicity indices for lupus nephritis. Glomerular morphology and localization of electron dense deposits containing IgG were further determined by immune electron microscopy. Renal DNase I and pro-inflammatory cytokine mRNA levels were measured by real-time quantitative PCR. DNase I protein levels was assessed by immunohistochemistry and zymography. Our results demonstrate early development of electron dense deposits containing IgG in FcγRIIB-/-yaa mice, before detectable levels of serum anti-dsDNA antibodies. Similar to NZB/NZW F1, electron dense deposits in FcγRIIB-/-yaa progressed from being confined to the mesangium in the early stage of lupus nephritis to be present also in capillary glomerular basement membranes. In the advanced stage of lupus nephritis, renal DNase I was lost on both transcriptional and protein levels, which has previously been shown in NZB/NZW F1 mice and in human disease. Although lupus nephritis appears on different genetic backgrounds, our findings suggest similar processes when comparing different murine models and human lupus nephritis.
[Mh] Termos MeSH primário: Desoxirribonuclease I/metabolismo
Glomérulos Renais/patologia
Nefrite Lúpica/patologia
Receptores de IgG/genética
[Mh] Termos MeSH secundário: Animais
Progressão da Doença
Imunoglobulina G/metabolismo
Glomérulos Renais/enzimologia
Glomérulos Renais/metabolismo
Túbulos Renais/metabolismo
Nefrite Lúpica/metabolismo
Masculino
Glicoproteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Receptor 7 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fcgr2b protein, mouse); 0 (Immunoglobulin G); 0 (Membrane Glycoproteins); 0 (Receptors, IgG); 0 (Tlr7 protein, mouse); 0 (Toll-Like Receptor 7); EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188863


  8 / 20972 MEDLINE  
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[PMID]:28747315
[Au] Autor:Dominguez JH; Liu Y; Gao H; Dominguez JM; Xie D; Kelly KJ
[Ad] Endereço:Nephrology Division, Department of Medicine, and.
[Ti] Título:Renal Tubular Cell-Derived Extracellular Vesicles Accelerate the Recovery of Established Renal Ischemia Reperfusion Injury.
[So] Source:J Am Soc Nephrol;28(12):3533-3544, 2017 Dec.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ischemic renal injury is a complex syndrome; multiple cellular abnormalities cause accelerating cycles of inflammation, cellular damage, and sustained local ischemia. There is no single therapy that effectively resolves the renal damage after ischemia. However, infusions of normal adult rat renal cells have been a successful therapy in several rat renal failure models. The sustained broad renal benefit achieved by relatively few donor cells led to the hypothesis that extracellular vesicles (EV, largely exosomes) derived from these cells are the therapeutic effector We now show that EV from adult rat renal tubular cells significantly improved renal function when administered intravenously 24 and 48 hours after renal ischemia in rats. Additionally, EV treatment significantly improved renal tubular damage, 4-hydroxynanoneal adduct formation, neutrophil infiltration, fibrosis, and microvascular pruning. EV therapy also markedly reduced the large renal transcriptome drift observed after ischemia. These data show the potential utility of EV to limit severe renal ischemic injury after the occurrence.
[Mh] Termos MeSH primário: Vesículas Extracelulares
Túbulos Renais/metabolismo
Rim/metabolismo
Traumatismo por Reperfusão/patologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/patologia
Aldeídos/química
Animais
Comunicação Celular
Modelos Animais de Doenças
Exossomos/metabolismo
Feminino
Perfilação da Expressão Gênica
Genótipo
Hipóxia/patologia
Rim/patologia
Microcirculação
Neutrófilos/metabolismo
Fenótipo
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Insuficiência Renal
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aldehydes); 0 (RNA, Messenger); K1CVM13F96 (4-hydroxy-2-nonenal)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016121278


  9 / 20972 MEDLINE  
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[PMID]:27772637
[Au] Autor:Fogo AB; Lusco MA; Najafian B; Alpers CE
[Ad] Endereço:Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, TN. Electronic address: agnes.fogo@vanderbilt.edu.
[Ti] Título:AJKD Atlas of Renal Pathology: Pauci-immune Necrotizing Crescentic Glomerulonephritis.
[So] Source:Am J Kidney Dis;68(5):e31-e32, 2016 Nov.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/patologia
Glomerulonefrite/patologia
Rim/patologia
[Mh] Termos MeSH secundário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/metabolismo
Membrana Basal Glomerular/metabolismo
Membrana Basal Glomerular/patologia
Membrana Basal Glomerular/ultraestrutura
Glomerulonefrite/metabolismo
Granuloma/patologia
Seres Humanos
Rim/metabolismo
Rim/ultraestrutura
Túbulos Renais/metabolismo
Túbulos Renais/patologia
Túbulos Renais/ultraestrutura
Microscopia
Microscopia Eletrônica
Microscopia de Fluorescência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28916336
[Au] Autor:De Jonghe S; Johnson MD; Mamidi RNVS; Vinken P; Feyen B; Lammens G; Proctor J
[Ad] Endereço:Janssen Research & Development, A Division of Janssen Pharmaceutica NV, Turnhoutseweg 30, B-2340 Beerse, Belgium. Electronic address: sdjonghe@its.jnj.com.
[Ti] Título:Renal tubular and adrenal medullary tumors in the 2-year rat study with canagliflozin confirmed to be secondary to carbohydrate (glucose) malabsorption in the 15-month mechanistic rat study.
[So] Source:Chem Biol Interact;277:85-90, 2017 Nov 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:During preclinical development of canagliflozin, an SGLT2 inhibitor, treatment-related pheochromocytomas, renal tubular tumors (RTT), and testicular Leydig cell tumors were reported in the 2-year rat toxicology study. In a previous 6-month rat mechanistic study, feeding a glucose free diet prevented canagliflozin effects on carbohydrate malabsorption as well as the increase in cell proliferation in adrenal medulla and kidneys, implicating carbohydrate malabsorption as the mechanism for tumor formation. In this chronic study male Sprague-Dawley rats were dosed orally with canagliflozin at high dose-levels (65 or 100 mg/kg/day) for 15 months and received either a standard diet or a glucose-free diet. Canagliflozin-dosed rats on standard diet showed presence of basophilic renal tubular tumors (6/90) and an increased incidence of adrenal medullary hyperplasia (35/90), which was fully prevented by feeding a glucose-free diet (no RTT's; adrenal medullary hyperplasia in ≤5/90). These data further confirm that kidney and adrenal medullary tumors in the 2-year rat study were secondary to carbohydrate (glucose) malabsorption and were not due to a direct effect of canagliflozin on these target tissues.
[Mh] Termos MeSH primário: Neoplasias das Glândulas Suprarrenais/tratamento farmacológico
Canagliflozina/uso terapêutico
Glucose/metabolismo
Hipoglicemiantes/uso terapêutico
Neoplasias Renais/tratamento farmacológico
Túbulos Renais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Neoplasias das Glândulas Suprarrenais/metabolismo
Neoplasias das Glândulas Suprarrenais/patologia
Animais
Sacarose na Dieta/metabolismo
Neoplasias Renais/metabolismo
Neoplasias Renais/patologia
Túbulos Renais/metabolismo
Túbulos Renais/patologia
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Sucrose); 0 (Hypoglycemic Agents); 0SAC974Z85 (Canagliflozin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE



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