Estadísticas

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      "titulo" => "Identification of a new therapy for polycystic kidney disease (PKD)"
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      "titulo" => "Bioimpresión 3D de pseudonefronas como un modelo para el estudio de la poliquistosis renal"
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    "titulo" => "New targets for renal and hepatic cystogenesis. The help of proteomic in the understanding of ADPKD"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Introduction&#58;</span> Autosomal Dominant Polycystic Kidney Disease &#40;ADPKD&#41; is the most common monogenic disorder characterized by developing fluid-filled cyst derived from the tubule epithelial cells in kidney&#44; and several extrarenal manifestations as hepatic cysts &#40;Polycystic Liver Disease &#91;PLD&#93;&#41;&#46; Different mechanisms have been related to the pathogenesis of renal and hepatic cystogenesis&#46; The identification of the main cystogenic pathway has not been found&#44; and effective therapeutic approach to block cystogenesis remains undiscovered&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Method&#58;</span> We have recollected kidney and livers from <span class="elsevierStyleItalic">Pkd1</span><span class="elsevierStyleSup"><span class="elsevierStyleItalic">cond&#47;cond</span></span><span class="elsevierStyleItalic">TamCre</span> mice&#46; This model presents a cystogenesis developmental window&#44; because the inactivation of Pkd1 gene in different points of life determines cystic phenotype&#46; We inactivated Pkd1 at postnatal day 10&#47;11 &#40;cystic window&#41; and postnatal day 15&#47;16 &#40;non-cystic window&#41;&#44; which led us to study the differences between wild-type and mutant mice&#46; Finally&#44; we sacrificed them at postnatal day<span class="elsevierStyleHsp" style=""></span>30&#46; Liver and kidney protein were extracted and the proteome was sequenced using mass spectrometry MALDI-TOF&#46; Finally&#44; we used bioinformatics tools to identified the proteins and pathways involved in cystogenesis&#46; By proteomic approaches&#44; we described novel list of proteins implicated in renal and hepatic cystogenesis &#40;up and down regulated&#41;&#44; which are likely to be used as therapeutic targets&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Results&#58;</span> We have identified the renal and hepatic proteome of cysts from a good characterized animal model in the ADPKD field&#44; the <span class="elsevierStyleItalic">Pkd1</span><span class="elsevierStyleSup"><span class="elsevierStyleItalic">cond&#47;cond</span></span><span class="elsevierStyleItalic">TamCre</span> mice&#46; After comparing the different samples &#40;kidney and liver&#41;&#44; cystic and non-cystic&#44; we have identified a list of proteins directly implicated in the process of cystogenesis&#46; Related to liver&#44; we found 26 proteins that appear only on cystic samples and 8 that not appear&#46; However in kidney&#44; we recognized 16 proteins that appear only on cystics and 6 that not appear on them&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Also&#44; we studied the pathways related to these proteins to enlarge the understanding of molecular basis of renal and hepatic cystogenesis&#46; We found that&#44; in both cases&#44; main altered pathways are immune system&#44; signal transduction&#44; metabolism and metabolism of proteins&#46; Moreover&#44; there are more specific pathways&#59; vesicle-mediated transport and cell cycle in liver&#44; in contrast to developmental biology and extracellular matrix organization in kidney&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Conclusion&#58;</span> Our results described a list of new possible targets which could be used as future and more specific therapeutic approaches for renal and hepatic phenotype of ADPKD&#46; Furthermore&#44; and given that the key factor or pathways of cystogenesis in still unknown&#44; our data helps to a better understanding of molecular basis of the disease&#46;</p></span>"
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