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2篇 您的检索式：作者名="Ellis D Avner"

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		题名	作者	年代	出处	被引量
	1	Unique interstitial miRNA signature drives fibrosis in a murine model of autosomal dominant polycystic kidney disease显示文摘AIM To delineate changes in miRNA expression localized to the peri-cystic local microenvironment(PLM) in an orthologous mouse model of autosomal dominant polycystic kidney disease(ADPKD)(mcwPkd1^(nl/nl)).METHODS We profiled miRNA expression in the whole kidney and laser captured microdissection(LCM) samples from PLM in mcwPkd1^(nl/nl)kidneys with Qiagen miScript 384 HC miRNA PCR arrays. The three times points used are:(1) post-natal(PN) day 21, before the development of trichrome-positive areas;(2) PN28, the earliest sign of trichrome staining; and(3) PN42 following the development of progressive fibrosis. PN21 served as appropriate controls and as the reference time point for comparison of miRNA expression profiles.RESULTS LCM samples revealed three temporally upregulated miRNAs [2 to 2.75-fold at PN28 and 2.5 to 4-fold(P ≤ 0.05) at PN42] and four temporally downregulated miRNAs [2 to 2.75 fold at PN28 and 2.75 to 5-fold(P ≤ 0.05) at PN42]. Expression of twenty-six miRNAs showed no change until PN42 [six decreased(2.25 to 3.5-fold)(P ≤ 0.05) and 20 increased(2 to 4-fold)(P ≤ 0.05)]. Many critical miRNA changes seen in the LCM samples from PLM were not seen in the contralateral whole kidney.CONCLUSION Precise sampling with LCM identifies miRNA changes that occur with the initiation and progression of renal interstitial fibrosis(RIF). Identification of the target proteins regulated by these miRNAs will provide new insight into the process of fibrosis and identify unique therapeutic targets to prevent or slow the development and progression of RIF in ADPKD.	Ameya Patil William E Sweeney Jr Cynthia G Pan Ellis D Avner	2018	World Journal of Nephrology2018，7，5：	1
	2	Tesevatinib ameliorates progression of polycystic kidney disease in rodent models of autosomal recessive polycystic kidney disease显示文摘AIM To investigate the therapeutic potential of tesevatinib(TSV),a unique multi-kinase inhibitor currently in Phase Ⅱ clinical trials for autosomal dominant polycystic kidney disease(ADPKD),in well-defined rodent models of autosomal recessive polycystic kidney disease(ARPKD).METHODS We administered TSV in daily doses of 7.5 and 15 mg/kg per day by I.P.to the well characterized bpk model of polycystic kidney disease starting at postnatal day(PN) 4 through PN21 to assess efficacy and toxicity in neonatal mice during postnatal development and still undergoing renal maturation.We administered TSV by oral gavage in the same doses to the orthologous PCK model(from PN30 to PN90) to assess efficacy and toxicity in animals where developmental processes are complete.The following parameters were assessed:Body weight,total kidney weight;kidney weight to body weight ratios;and morphometric determination of a cystic index and a measure of hepatic disease.Renal function was assessed by:Serum BUN;creatinine;and a 12 h urinary concentrating ability.Validation of reported targets including the level of angiogenesis and inhibition of angiogenesis(active VEGFR2/KDR) was assessed by Western analysis.RESULTS This study demonstrates that:(1) in vivo pharmacological inhibition of multiple kinase cascades with TSV reduced phosphorylation of key mediators of cystogenesis:EGFR,ErbB 2,c-Src and KDR;and(2) this reduction of kinase activity resulted in significant reduction of renal and biliary disease in both bpk and PCK models of ARPKD.The amelioration of disease by TSV was not associated with any apparent toxicity.CONCLUSION The data supports the hypothesis that this multi-kinase inhibitor TSV may provide an effective clinical therapy for human ARPKD.	William E Sweeney Philip Frost Ellis D Avner	2017	World Journal of Nephrology2017，6，4：	1

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