Journal of Cardiothoracic-Renal Research最新文献

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Breaking the barrier of chronic allograft nephropathy (CAN)—Transplant's next major challenge 打破慢性移植物肾病(CAN)的屏障——移植的下一个主要挑战
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 Epub Date: 2006-02-22 DOI: 10.1016/j.jccr.2005.12.007
Edward S. Kraus
{"title":"Breaking the barrier of chronic allograft nephropathy (CAN)—Transplant's next major challenge","authors":"Edward S. Kraus","doi":"10.1016/j.jccr.2005.12.007","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.12.007","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 89-90"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.12.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72242099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Angiotensin II stimulates a novel angiotensin II type 1 receptor-associated protein, GLP gene expression in rat kidney proximal tubular cells 血管紧张素II刺激大鼠肾近端小管细胞中新型血管紧张素Ⅱ1型受体相关蛋白GLP基因表达
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 Epub Date: 2006-02-22 DOI: 10.1016/j.jccr.2005.12.005
Deng-Fu Guo , Valerie Tardif , Isabelle Chenier , John S.D. Chan , Julie R. Ingelfinger , Xiang Mei Chen , Tadashi Inagami
{"title":"Angiotensin II stimulates a novel angiotensin II type 1 receptor-associated protein, GLP gene expression in rat kidney proximal tubular cells","authors":"Deng-Fu Guo ,&nbsp;Valerie Tardif ,&nbsp;Isabelle Chenier ,&nbsp;John S.D. Chan ,&nbsp;Julie R. Ingelfinger ,&nbsp;Xiang Mei Chen ,&nbsp;Tadashi Inagami","doi":"10.1016/j.jccr.2005.12.005","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.12.005","url":null,"abstract":"<div><p><span>We have recently demonstrated that a novel angiotensin II (Ang II) type 1 receptor-associated protein, GLP induces cellular hypertrophy and Ang II stimulated GLP mRNA expression in a time-, dose-, and AT</span><sub>1</sub><span><span><span><span> receptor-dependent manner in rat immortalized renal proximal tubular cells (IRPTCs). The present studies investigated which signaling pathways are involved in Ang II stimulated GLP mRNA expression in IRPTCs. Cellular GLP mRNA expression was determined by </span>reverse transcription polymerase chain reaction. The effect of Ang II was blocked by </span>epidermal growth factor receptor inhibitor, </span>AG1478<span>, PKC<span><span><span><span><span><span> inhibitor, GF109203X, MAPK kinase inhibitor, </span>PD98059<span>, antioxidants, taurine and tiron, and NADH/NADPH oxidase inhibitor, DPI, whereas, no effects were observed on Ang II-induced GLP mRNA expression with </span></span>p38 MAPK inhibitors, </span>SB203580<span><span> and PD169316, and Janus kinase 2 inhibitor, </span>AG490. IRPTCs stably expressing GLP gene significantly increased reactive oxygen species (ROS) generation compared to control IRPTCs analyzed by </span></span>lucigenin<span> assay. Furthermore, NADH/NADPH oxidase inhibitor, DPI, and antioxidants taurine and tiron inhibited GLP-induced total protein content and de novo protein synthesis. These studies demonstrated that the stimulatory action of Ang II on GLP mRNA expression in IRPTCs is mediated by multiple signal mechanisms, </span></span>transactivation of EGF receptor and subsequent MAPK activation, PKC activation and ROS generation. Furthermore, the cellular hypertrophic effect of GLP gene in IRPTCs is mediated at least in part via ROS generation.</span></span></span></p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 91-100"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.12.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72277082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cyclosporine reduction causes decreasing of angiotensin II and transforming growth factor-beta expression in chronic allograft nephropathy 环孢菌素减少导致慢性移植物肾病血管紧张素II和转化生长因子β表达降低
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 Epub Date: 2006-02-22 DOI: 10.1016/j.jccr.2005.11.005
Matthew R. Weir , John C. Papadimitriou , Cinthia I. Drachenberg , Hong Song , Stephen T. Bartlett , Chiming Wei
{"title":"Cyclosporine reduction causes decreasing of angiotensin II and transforming growth factor-beta expression in chronic allograft nephropathy","authors":"Matthew R. Weir ,&nbsp;John C. Papadimitriou ,&nbsp;Cinthia I. Drachenberg ,&nbsp;Hong Song ,&nbsp;Stephen T. Bartlett ,&nbsp;Chiming Wei","doi":"10.1016/j.jccr.2005.11.005","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.11.005","url":null,"abstract":"<div><h3>Background</h3><p>High cyclosporine<span><span> (CsA) levels might lead to nephrotoxicity due to increasing </span>angiotensin II<span> (AII) and transforming growth factor-beta (TGF-β) production. We hypothesized that a chronic reduction in CsA levels would decrease local renal AII and TGF-β expression and result in improvement of renal function and renal pathological changes in renal transplant recipients.</span></span></p></div><div><h3>Methods</h3><p><span>We determined the AII and TGF-β expression by immunohistochemical staining (IHCS) in sequential human renal biopsy<span> specimens in patients with chronic allograft nephropathies (time between biopsies: 15.9</span></span> <!-->±<!--> <span>0.8 months) after they had their CsA levels reduced by 50%. Pathological evaluation included percentage expression (%) of interstitial fibrosis<span><span> and tubular atrophy (FIB), vascular sclerosis (VS), </span>transplant glomerulopathy<span> (TG), and vascular hyalinosis (VH). Serum creatinine (CR, mg/dl) and BUN (mg/dl) levels were also investigated.</span></span></span></p></div><div><h3>Results</h3><p>Renal pathological score significantly improved with chronic reduction in CsA blood levels (FIB: from 52 to 26%, <em>p</em> <!-->&lt;<!--> <!-->0.05; VS: from 22 to 5%, <em>p</em> <!-->&lt;<!--> <!-->0.05; TG: from 40 to 13%, <em>p</em> <!-->&lt;<!--> <!-->0.05; VH: from 17 to 1.8%, <em>p</em> <!-->&lt;<!--> <!-->0.05, respectively). Renal function also significantly improved with chronic reduction of CsA blood level (BUN: from 84<!--> <!-->±<!--> <!-->14 to 40<!--> <!-->±<!--> <!-->3<!--> <!-->mg/dl, <em>p</em> <!-->&lt;<!--> <!-->0.05; CR: from 3.4<!--> <!-->±<!--> <!-->0.4 to 2.2<!--> <!-->±<!--> <!-->0.1<!--> <!-->mg/dl, <em>p</em> <!-->&lt;<!--> <!-->0.05, respectively). AII and TGF-β IHCS score (0–4) and positive staining area (%) were significantly decreased in patients with chronic reduction in CsA levels.</p></div><div><h3>Conclusion</h3><p>These data indicate that chronic reduction in CsA diminishes production of renal tissue AII and AT1<span> receptor expression, and results in decreased fibrosis and improvement of renal function in patients with chronic allograft nephropathy.</span></p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 81-88"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.11.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72277083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
DMNQ S-53 induces apoptosis and inhibits the growth of Lewis lung carcinoma cells in vitro and in vivo DMNQ S-53在体外和体内诱导Lewis肺癌细胞凋亡并抑制其生长
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 Epub Date: 2006-02-22 DOI: 10.1016/j.jccr.2005.12.004
Jae-Ho Lee , Eun-Ok Lee , Hyo-Jung Lee , Kwan-Hyun Kim , Kyoo-Seok Ahn , Sung-Joon Lee , Ji-Young Kim , Sung-Hoon Kim
{"title":"DMNQ S-53 induces apoptosis and inhibits the growth of Lewis lung carcinoma cells in vitro and in vivo","authors":"Jae-Ho Lee ,&nbsp;Eun-Ok Lee ,&nbsp;Hyo-Jung Lee ,&nbsp;Kwan-Hyun Kim ,&nbsp;Kyoo-Seok Ahn ,&nbsp;Sung-Joon Lee ,&nbsp;Ji-Young Kim ,&nbsp;Sung-Hoon Kim","doi":"10.1016/j.jccr.2005.12.004","DOIUrl":"https://doi.org/10.1016/j.jccr.2005.12.004","url":null,"abstract":"<div><p><em>Background:</em> 6-(1-Proproxyiminomethyl)-5,8-dimethoxy-1,4-naphthoquinone S-53 (DMNQ S-53) was synthesized to develop a novel anti-tumor agent against lung cancer. <em>Methods:</em><span> Cytotoxicity assay, DNA fragmentation assay<span><span>, cell cycle analysis<span>, mitochondrial potential measurement and Western blotting were employed in vitro and also </span></span>Lewis lung carcinoma (LLC) animal model was used for evaluating the anti-tumor of DMNQ S53 in vivo. </span></span><em>Results and conclusions:</em><span> DMNQ S-53 exerted cytotoxicity against LLC cells with IC</span><sub>50</sub> of ∼5<!--> <span><span>μM. DMNQ S-53 also increased the sub G1 cell population stained by propidium iodide (PI) as well as ladder-like </span>DNA fragmentation<span> in a concentration dependent manner. Western blot analysis revealed that DMNQ S-53 induced apoptosis<span> was associated with the activation of caspase-9 and -3, cleavage of poly (ADP-ribose) polymerase (PARP) and the increased ratio of Bax to Bcl-2 expression in LLC cells in a concentration dependent manner. In addition, DMNQ S-53 reduced mitochondrial potential suggesting the involvement of the mitochondrial intrinsic pathway. Furthermore, intraperitoneally injection of DMNQ S-53 resulted in the inhibition of the tumor volume/weight of LLC cells inoculated on the flank of C57BL6 mice up to ∼50%. Taken together, these results strongly indicate that DMNQ S-53 may inhibit LLC tumor growth in vitro and in vivo via apoptosis induction through the mitochondria-mediated caspase activation pathway.</span></span></span></p></div>","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"1 1","pages":"Pages 73-79"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jccr.2005.12.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72285115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Angiotensin II stimulates a novel angiotensin II type 1 receptor-associated protein, GLP gene expression in rat kidney proximal tubular cells 血管紧张素II刺激大鼠肾近端小管细胞中一种新的血管紧张素II型1受体相关蛋白GLP基因的表达
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.005
D. Guo, Valérie Tardif, I. Chénier, J. Chan, J. Ingelfinger, X. Chen, T. Inagami
{"title":"Angiotensin II stimulates a novel angiotensin II type 1 receptor-associated protein, GLP gene expression in rat kidney proximal tubular cells","authors":"D. Guo, Valérie Tardif, I. Chénier, J. Chan, J. Ingelfinger, X. Chen, T. Inagami","doi":"10.1016/J.JCCR.2005.12.005","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.12.005","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"90 1","pages":"91-100"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75695059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
New sniper assignment for a celebrity—role of endothelin-1 in diabetic cardiomyopathy 内皮素-1在糖尿病性心肌病中的作用
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.11.006
Jun Ren, Chiming Wei
{"title":"New sniper assignment for a celebrity—role of endothelin-1 in diabetic cardiomyopathy","authors":"Jun Ren, Chiming Wei","doi":"10.1016/J.JCCR.2005.11.006","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.11.006","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"227 1","pages":"30-32"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72903384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Outcomes of surgical ventricular restoration following recent myocardial infarction 近期心肌梗死后手术心室修复的结果
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.001
J. Williams, N. Patel, Lois U. Nwakanma, J. Conte
{"title":"Outcomes of surgical ventricular restoration following recent myocardial infarction","authors":"J. Williams, N. Patel, Lois U. Nwakanma, J. Conte","doi":"10.1016/J.JCCR.2005.12.001","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.12.001","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"42 1","pages":"51-58"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82639475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Outcomes of surgical ventricular restoration following recent myocardial infarction 近期心肌梗死后手术心室修复的结果
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.006
I. Kron
{"title":"Outcomes of surgical ventricular restoration following recent myocardial infarction","authors":"I. Kron","doi":"10.1016/J.JCCR.2005.12.006","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.12.006","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"91 1 Pt 2 1","pages":"58"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89430643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Oxidative DNA damage and DNA mismatch repair pathway play an important role in failing human myocardium DNA氧化损伤和DNA错配修复途径在心肌衰竭中起重要作用
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.11.004
R. Lin, Daqing Gao, Yesong Gu, P. Bonde, Torin P. Fitton, J. Hare, J. Conte, G. Williams, Chiming Wei
{"title":"Oxidative DNA damage and DNA mismatch repair pathway play an important role in failing human myocardium","authors":"R. Lin, Daqing Gao, Yesong Gu, P. Bonde, Torin P. Fitton, J. Hare, J. Conte, G. Williams, Chiming Wei","doi":"10.1016/J.JCCR.2005.11.004","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.11.004","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"61 2 1","pages":"41-49"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78078184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Hope or hype: The obsession for tetrahydrobiopterin and GTP cyclohydrolase I (GTPCH I) in cardiovascular medicine 希望还是炒作:心血管医学对四氢生物蝶呤和GTP环水解酶I (GTPCH I)的痴迷
Journal of Cardiothoracic-Renal Research Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.11.002
Jun Ren
{"title":"Hope or hype: The obsession for tetrahydrobiopterin and GTP cyclohydrolase I (GTPCH I) in cardiovascular medicine","authors":"Jun Ren","doi":"10.1016/J.JCCR.2005.11.002","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.11.002","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"102 1","pages":"15-21"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80527272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
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