{"id":19,"date":"2020-09-15T20:56:38","date_gmt":"2020-09-15T20:56:38","guid":{"rendered":"https:\/\/www.renalphysiopathology.com\/?page_id=19"},"modified":"2023-01-30T22:39:39","modified_gmt":"2023-01-30T22:39:39","slug":"research","status":"publish","type":"page","link":"https:\/\/www.renalphysiopathology.com\/research\/","title":{"rendered":"Research"},"content":{"rendered":"\n<p><\/p>\n\n\n<div id=\"pl-gb19-663b6a758a08e\"  class=\"panel-layout\" ><div id=\"pg-gb19-663b6a758a08e-0\"  class=\"panel-grid panel-no-style\" ><div id=\"pgc-gb19-663b6a758a08e-0-0\"  class=\"panel-grid-cell\" ><div id=\"panel-gb19-663b6a758a08e-0-0-0\" class=\"so-panel widget widget_sow-hero panel-first-child panel-last-child\" data-index=\"0\" ><div class=\"panel-widget-style panel-widget-style-for-gb19-663b6a758a08e-0-0-0\" ><div class=\"so-widget-sow-hero so-widget-sow-hero-default-d5ea886990e3 so-widget-fittext-wrapper\" data-fit-text-compressor=\"1\"><div class=\"sow-slider-base \" style=\"display: none\"><ul class=\"sow-slider-images\" data-settings=\"{&quot;pagination&quot;:true,&quot;speed&quot;:800,&quot;timeout&quot;:8000,&quot;paused&quot;:false,&quot;pause_on_hover&quot;:false,&quot;swipe&quot;:true,&quot;nav_always_show_mobile&quot;:&quot;&quot;,&quot;breakpoint&quot;:&quot;780px&quot;}\">\t\t<li class=\"sow-slider-image  sow-slider-image-cover\" style=\"background-color: #efefef\" >\n\t\t\t\t\t<div class=\"sow-slider-image-container\">\n\t\t\t<div class=\"sow-slider-image-wrapper\">\n\t\t\t\t<h5><\/h5>\n<h2 style=\"text-align: center\">Research Interest<\/h2>\n<p><!--more--><\/p>\n<p><!--more--><!--more--><!--more--><\/p>\n<h5 style=\"text-align: center\">Our main interest is to understand the immune modulation during early stages of\u00a0chronic kidney disease, hypertension and renal rejection in transplant.<\/h5>\n<h5 style=\"text-align: center\">We integrate molecular, cellular, and physiologic aspects in order to develop\u00a0strategies that will permit prevention or early diagnose of these conditions.<\/h5>\n\t\t\t<\/div>\n\t\t<\/div>\n\t\t<div class=\"sow-slider-image-overlay sow-slider-image-cover\" style=\"background-image: url(https:\/\/www.renalphysiopathology.com\/wp-content\/uploads\/2020\/10\/Research-1.jpg);opacity: 0.59\"  ><\/div>\t\t<\/li>\n\t\t<\/ul>\t\t\t\t<ol class=\"sow-slider-pagination\">\n\t\t\t\t\t\t\t\t\t\t\t<li><a href=\"#\" data-goto=\"0\" aria-label=\"display slide 1\"><\/a><\/li>\n\t\t\t\t\t\t\t\t\t<\/ol>\n\n\t\t\t\t<div class=\"sow-slide-nav sow-slide-nav-next\">\n\t\t\t\t\t<a href=\"#\" data-goto=\"next\" aria-label=\"next slide\" data-action=\"next\">\n\t\t\t\t\t\t<em class=\"sow-sld-icon-thin-right\"><\/em>\n\t\t\t\t\t<\/a>\n\t\t\t\t<\/div>\n\n\t\t\t\t<div class=\"sow-slide-nav sow-slide-nav-prev\">\n\t\t\t\t\t<a href=\"#\" data-goto=\"previous\" aria-label=\"previous slide\" data-action=\"prev\">\n\t\t\t\t\t\t<em class=\"sow-sld-icon-thin-left\"><\/em>\n\t\t\t\t\t<\/a>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div><\/div><\/div><\/div><\/div><\/div><div id=\"pg-gb19-663b6a758a08e-1\"  class=\"panel-grid panel-no-style\" ><div id=\"pgc-gb19-663b6a758a08e-1-0\"  class=\"panel-grid-cell panel-grid-cell-empty\" ><\/div><\/div><div id=\"pg-gb19-663b6a758a08e-2\"  class=\"panel-grid panel-no-style\" ><div id=\"pgc-gb19-663b6a758a08e-2-0\"  class=\"panel-grid-cell panel-grid-cell-empty\" ><\/div><\/div><div id=\"pg-gb19-663b6a758a08e-3\"  class=\"panel-grid panel-no-style\" ><div id=\"pgc-gb19-663b6a758a08e-3-0\"  class=\"panel-grid-cell\" ><div id=\"panel-gb19-663b6a758a08e-3-0-0\" class=\"so-panel widget widget_sow-headline panel-first-child panel-last-child\" data-index=\"1\" ><div class=\"so-widget-sow-headline so-widget-sow-headline-default-126af80fd6f0\"><div class=\"sow-headline-container \">\n\t<h2 class='sow-headline'>Our Projects<\/h2>\t\t\t\t\t<div class=\"decoration\">\n\t\t\t\t\t\t<div class=\"decoration-inside\"><\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t\t<\/div><\/div><\/div><\/div><\/div><div id=\"pg-gb19-663b6a758a08e-4\"  class=\"panel-grid panel-no-style\" ><div id=\"pgc-gb19-663b6a758a08e-4-0\"  class=\"panel-grid-cell\" ><div id=\"panel-gb19-663b6a758a08e-4-0-0\" class=\"so-panel widget widget_sow-editor panel-first-child panel-last-child\" data-index=\"2\" ><div class=\"so-widget-sow-editor so-widget-sow-editor-base\">\n<div class=\"siteorigin-widget-tinymce textwidget\">\n\t<h3>Evaluating the Pro-Inflammatory Role of NGAL Receptor in the Progression of Proteinuric Chronic Kidney Disease &#8211; Fondecyt 1231909<\/h3>\n<p style=\"text-align-last: start; text-align: justify;\">Chronic kidney disease (CKD) is characterized by reduced glomerular filtration rate (GFR), albuminuria, glomerulosclerosis and tubulointerstitial fibrosis. Clinical data and experimental studies support that inflammation is a relevant mechanism for the development of CKD that occurs in early stages of renal damage. In this context, we have demonstrated that Neutrophil Gelatinase-Associated Lipocalin (NGAL), a glycoprotein expressed in kidney and immune cells, promotes the pro-inflammatory phenotype characterized by the induction of Monocyte Chemokine Protein-1 (MCP-1) and by the recruitment of macrophages (Mo) at the renal level. On the other hand, albumin has been shown to induce proinflammatory damage in tubular cells (MCP-1 induction and Mo infiltration), which has been suggested as a mechanism of damage during proteinuric CKD. Interestingly, albumin can bind to the 24p3R protein, which is also the receptor for NGAL. However, it has not been established whether 24p3R contributes to renal dysfunction and inflammatory processes leading to fibrosis during CKD progression.<\/p>\n<p>&nbsp;<\/p>\n<h3>Role of Connexin 43 in the Activation of Antigen-Presenting Cells During Chronic Kidney Disease Progression &#8211; ECOS210024<\/h3>\n<p style=\"text-align-last: start; text-align: justify;\">In inflammatory kidney disease, renal (CD11c<sup>+<\/sup>) antigen-presenting cells (APCs) mediate not only T-cell migration by intravascular processes, but are also essential for immune tolerance to self-destruction. Moreover, connexin 43 (Cx43) has been shown to participate in the formation of junctional channels between neighboring cells, allowing direct communication through the exchange of small molecules such as ions or second messengers. However, it has been shown that this protein can be upregulated after induction of kidney disease in rodents and humans, preventing inflammatory cell infiltration and interstitial fibrosis during chronic kidney disease (CKD) progression. Given that inflammation is a critical factor for the onset and progression of CKD, we propose that Cx43 in (CD11c<sup>+<\/sup>) APCs could be essential for these inflammatory processes; which could provide new relevant data on the progression of renal inflammation to fibrosis and its consolidation in CKD.<\/p>\n<p>&nbsp;<\/p>\n<h3>Role of Renal CD11c+ Antigen Presenting Cells in Experimental Arterial Hypertension &#8211; FONDECYT 3201016<\/h3>\n<p style=\"text-align-last: start; text-align: justify;\">Hypertension (HTA) is a critical factor for cardiovascular (CV) risk, where its prevalence is continuously augmenting. Classical studies have suggested that kidney presents a &#8220;memory&#8221; to transfer the hypertensive phenotype to other subject, however, has not been determined which cell-type from kidney is responsible for this condition. We propose that a subtype of renal CD11c<sup>+<\/sup> Antigen Presenting Cells could be modulating the hypertensive phenotype in patients and in experimental models.<\/p>\n<p>&nbsp;<\/p>\n<h3>The Studying NGAL Production from Antigen-Presenting Cells for Determining its Role in Chronic Kidney Disease Progression &#8211; FONDECYT 1201251<\/h3>\n<p style=\"text-align-last: start; text-align: justify;\">The Chronic Kidney Disease (CKD) progression drives to the End-Stage Renal Disease (ESRD), which increases dramatically the risk of cardiovascular (CV) mortality. Nevertheless, at this moment there is no treatment able to prevent the CKD progression. Renal inflammation is a relevant mechanism for the CKD development that occurs at early stages of renal damage. We have demonstrated that Neutrophil Gelatinase-associated Lipocalin (NGAL) production from CD11c+ Antigen Presenting Cells (APCs) modulates the release of cytokines relating to the CV inflammation and tissue remodeling. However, whether CD11c<sup>+<\/sup> APCs and their NGAL production are crucial for renal dysfunction and kidney damage remain unknown. Our objective is to determine the role of NGAL and CD11c<sup>+<\/sup> APCs during early CKD progression.<\/p>\n<p>&nbsp;<\/p>\n<h3>Study of the role of Antigen Presenting Cells in the early stages of Chronic Kidney Disease &#8211; DIUA 157\/2018<\/h3>\n<p style=\"text-align-last: start; text-align: justify;\">Clinical studies and experimental evidence obtained from our recently Fondecyt project, propose that inflammation is a critical mechanism for Chronic Kidney Disease (CKD) development, which occur in early stages of kidney damage. The myeloid Antigen Presenting Cells (APCs) represent an immunological sentinel at renal level that mediates the migration of T-cells, in an antigen-dependent manner, promoting a pro-inflammatory phenotype and interstitial fibrosis in CKD. Previous studies carried out in collaboration by our group, indicate that APCs elimination prevents kidney damage and T-cells infiltration in an experimental model of hypertension. However, whether APCs have a relevant role in renal function and in inflammatory processes that leads to fibrosis during the early stages of CKD, remain unknown. Our objective is to determine the role of APCs in early stages of CKD progression.<\/p>\n<p>&nbsp;<\/p>\n<h3>The role of NGAL in the inflammation during the early stages of chronic kidney disease progression &#8211; Fondecyt 11150542.<\/h3>\n<p style=\"text-align-last: start; text-align: justify;\">Chronic Kidney Disease (CKD) is a worldwide public health problem, difficult to diagnose and that dramatically increases the risk of cardiovascular death in patients with hypertension and diabetes mellitus. Renal inflammation is a relevant mechanism in the development of CKD, which starts early and prior to tissue remodeling. Studies in patients and experimental animals have shown that the Neutrophil Gelatinase-associated Lipocalin protein (NGAL) is elevated in early stages of CKD. However, it is unknown if NGAL participates in immune activation during CKD. Our objective is to analyze the renal pro-inflammatory status and characterize the NGAL kinetics in different compartments of mice with CKD.<\/p>\n<p>&nbsp;<\/p>\n<h3>Kidney Transplant Network in Experimental Animals: Preclinical Models for the Study of Renal Rejection in Chile &#8211; REDI170633.<\/h3>\n<p style=\"text-align-last: start; text-align: justify;\">The development of this network in kidney transplant will not only allows the establishment of national and international interdisciplinary collaborations and the formation of advanced human capital (postgraduate students, surgical internships, etc.), but it will also enable the generation of scientific projects related to the study of renal rejection through the use of this experimental model. In this way, it is sought that the accumulation of pre-clinical evidence lead to the generation of clinical studies related to the function of the transplanted organ, the pre- and post-transplant procedures and renal rejection, and with them, improve the quality of life of patients with chronic end-stage renal disease who require a kidney transplant.<\/p>\n<p>&nbsp;<\/p>\n<h3>Validation of a urinary biomarkers panel that predicts post-transplant renal rejection in adult and pediatric patients.<\/h3>\n<p style=\"text-align-last: start; text-align: justify;\">Since there is no standardized methodology for multiple, rapid and non-invasive detection that allows frequent monitoring of renal function, and thus, facilitate the diagnosis\/prognosis of rejection after kidney transplant (Tx) in adult and pediatric patients, we propose to analyze different urinary biomarkers in order to provide a new integrated and low-cost methodology that allows frequent monitoring of the functioning of the Tx, in order to generate changes in their treatment and avoid rejection of the transplanted kidney.<\/p>\n<\/div>\n<\/div><\/div><\/div><\/div><\/div>","protected":false},"excerpt":{"rendered":"","protected":false},"author":1,"featured_media":561,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":[],"_links":{"self":[{"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/pages\/19"}],"collection":[{"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/comments?post=19"}],"version-history":[{"count":43,"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/pages\/19\/revisions"}],"predecessor-version":[{"id":1178,"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/pages\/19\/revisions\/1178"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/media\/561"}],"wp:attachment":[{"href":"https:\/\/www.renalphysiopathology.com\/wp-json\/wp\/v2\/media?parent=19"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}