Browsing by Author "Romero, Diego"

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    Breast lesions with atypia in percutaneous biopsies, managed with surgery in the last 10 years
    (2019) Carrillo, Mitzy; Maturana, Gregorio; Maiz, Cristobal; Romero, Diego; Dominguez, Francisco; Oddo, David; Villarroel, Alejandra; Razmilic, Dravna; Elena Navarro, Maria; Leon, Augusto; Sanchez, Cesar; Camus, Mauricio
    Introduction: The optimal management of breast lesions with atypia (BLA), detected in percutaneous biopsies after screening mammograms, is a controversial issue. The aim of this paper is to compare histological diagnosis by percutaneous biopsy with the results of the surgical biopsy of these lesions and to analyse the changes to clinical approach this would imply.
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    Fibroblast Primary Cilia Are Required for Cardiac Fibrosis
    (2019) Villalobos, Elisa; Criollo, Alfredo; Schiattarella, Gabriele G.; Altamirano, Francisco; French, Kristin M.; May, Herman, I; Jiang, Nan; Ngoc Uyen Nhi Nguyen; Romero, Diego; Carlos Roa, Juan; Garcia, Lorena; Diaz-Araya, Guillermo; Morselli, Eugenia; Ferdous, Anwarul; Conway, Simon J.; Sadek, Hesham A.; Gillette, Thomas G.; Lavandero, Sergio; Hill, Joseph A.
    BACKGROUND: The primary cilium is a singular cellular structure that extends from the surface of many cell types and plays crucial roles in vertebrate development, including that of the heart. Whereas ciliated cells have been described in developing heart, a role for primary cilia in adult heart has not been reported. This, coupled with the fact that mutations in genes coding for multiple ciliary proteins underlie polycystic kidney disease, a disorder with numerous cardiovascular manifestations, prompted us to identify cells in adult heart harboring a primary cilium and to determine whether primary cilia play a role in disease-related remodeling.
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    Galectin-8 induces partial epithelial–mesenchymal transition with invasive tumorigenic capabilities involving a FAK/EGFR/proteasome pathway in Madin–Darby canine kidney cells
    (2018) Oyanadel, Claudia; Holmes Videla, Christopher Edward; Pardo Huguet, Evelyn Cristina; Retamal Villarroel, Claudio Enrique; Shaughnessy, Ronan Patrick; Smith, Patricio C.; Cortés Martínez, Priscilla Rocío; Bravo Zehnder, Marcela; Metz Baer, Claudia Andrea; Feuerhake, Teo; Romero, Diego; Roa Strauch, Juan Carlos Enrique; Montecinos, Viviana; Soza Gajardo, Andrea; González, Alfonso
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    Interleukin 33/ST2 Axis Components Are Associated to Desmoplasia, a Metastasis-Related Factor in Colorectal Cancer
    (2019) Landskron, Glauben; De la Fuente Lopez, Marjorie; Dubois-Camacho, Karen; Diaz-Jimenez, David; Orellana-Serradell, Octavio; Romero, Diego; Sepulveda, Santiago A.; Salazar, Christian; Parada-Venegas, Daniela; Quera, Rodrigo; Simian, Daniela; Gonzalez, Maria-Julieta; Kronberg, Udo; Abedrapo, Mario; Gallegos, Ivan; Contreras, Hector R.; Pena, Cristina; Diaz-Araya, Guillermo; Carlos Roa, Juan; Hermoso, Marcela A.
    In colorectal cancer (CRC), cancer-associated fibroblasts (CAFs) are the most abundant component from the tumor microenvironment (TM). CAFs facilitate tumor progression by inducing angiogenesis, immune suppression and invasion, thus altering the organization/composition of the extracellular matrix (i.e., desmoplasia) and/or activating epithelial-mesenchymal transition (EMT). Soluble factors from the TM can also contribute to cell invasion through secretion of cytokines and recently, IL-33/ST2 pathway has gained huge interest as a protumor alarmin, promoting progression to metastasis by inducing changes in TM. Hence, we analyzed IL-33 and ST2 content in tumor and healthy tissue lysates and plasma from CRC patients. Tissue localization and distribution of these molecules was evaluated by immunohistochemistry (using localization reference markers a-smooth muscle actin or alpha-SMA and E-cadherin), and clinical/histopathological information was obtained from CRC patients. In vitro experiments were conducted in primary cultures of CAFs and normal fibroblasts (NFs) isolated from tumor and healthy tissue taken from CRC patients. Additionally, migration and proliferation analysis were performed in HT29 and HCT116 cell lines. It was found that IL-33 content increases in left-sided CRC patients with lymphatic metastasis, with localization in tumor epithelia associated with abundant desmoplasia. Although ST2 content showed similarities between tumor and healthy tissue, a decreased immunoreactivity was observed in left-sided tumor stroma, associated to metastasis related factors (advanced stages, abundant desmoplasia, and presence of tumor budding). A principal component analysis (including stromal and epithelial IL-33/ST2 and alpha-SMA immunoreactivity with extent of desmoplasia) allowed us to distinguish clusters of low, intermediate and abundant desmoplasia, with potential to develop a diagnostic signature with benefits for further therapeutic targets. IL-33 transcript levels from CAFs directly correlated with CRC cell line migration induced by CAFs conditioned media, with rhlL-33 inducing a mesenchymal phenotype in HT29 cells. These results indicate a role of IL-33/ST2 in tumor microenvironment, specifically in the interaction between CAFs and epithelial tumor cells, thus contributing to invasion and metastasis in left-sided CRC, most likely by activating desmoplasia.
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    Transcriptomic profiles reveal differences in zinc metabolism, inflammation, and tight junction proteins in duodenum from cholesterol gallstone subjects
    (2020) Riveras Hernández, Eleodoro Javier; Azócar, Lorena; Moyano, Tomás C.; Ocares, Marcia; Molina, Héctor; Romero, Diego; Roa Strauch, Juan Carlos Enrique; Valbuena Mora, José Rafael; Gutiérrez, Rodrigo A.; Miquel P., Juan Francisco
    Cholesterol Gallstone Disease (GSD) is a common multifactorial disorder characterized by crystallization and aggregation of biliary cholesterol in the gallbladder. The global prevalence of GSD is similar to 10-20% in the adult population but rises to 28% in Chile (17% among men and 30% among women). The small intestine may play a role in GSD pathogenesis, but the molecular mechanisms have not been clarified. Our aim was to identify the role of the small intestine in GSD pathogenesis. Duodenal biopsy samples were obtained from patients with GSD and healthy volunteers. GSD status was defined by abdominal ultrasonography. We performed a transcriptome study in a discovery cohort using Illumina HiSeq. 2500, and qPCR, immunohistochemistry and immunofluorescence were used to validate differentially expressed genes among additional case-control cohorts. 548 differentially expressed genes between GSD and control subjects were identified. Enriched biological processes related to cellular response to zinc, and immune and antimicrobial responses were observed in GSD patients. We validated lower transcript levels of metallothionein, NPC1L1 and tight junction genes and higher transcript levels of genes involved in immune and antimicrobial pathways in GSD patients. Interestingly, serum zinc and phytosterol to cholesterol precursor ratios were lower in GSD patients. A significant association was observed between serum zinc and phytosterol levels. Our results support a model where proximal small intestine plays a key role in GSD pathogenesis. Zinc supplementation, modulation of proximal microbiota and/or intestinal barrier may be novel targets for strategies to prevent GSD.