María Carcelén

Instituto de Investigación Marqués de Valdecilla

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José L. Fernández-Luna

Marqués de Valdecilla University Hospital

Olga Gutiérrez

Instituto Nacional de Cancerología

Carlos Velásquez

Instituto de Investigación Marqués de Valdecilla

Mónica Tramullas

Universidad de Cantabria

Emilio Bouza

Hospital General Universitario Gregorio Marañón

Darı́o Garcı́a de Viedma

Hospital General Universitario Gregorio Marañón

Verónica Vidal

Hospital Universitario 12 De Octubre

María A. Hurlé

Universidad de Cantabria

Laura Pérez‐Lago

Hospital General Universitario Gregorio Marañón

Raquel Francés

ESPCI Paris

Cooperative Institutions

Instituto de Investigación Marqués de Valdecilla

Universidad de Cantabria

Instituto de Salud Carlos III

Centro de Investigación Biomédica en Red

Marqués de Valdecilla University Hospital

Hospital General Universitario Gregorio Marañón

Universitat de Barcelona

Universidad Complutense de Madrid

Centro de Investigación Biomédica en Red de Enfermedades Respiratorias

Universitat de València

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Conocimientos actitudes y prácticas que poseen las madres sobre estimulación temprana en niños menores de 2 años con Síndrome de Down que acuden al INNFA de la ciudad de Ibarra en la provincia de Imbabura en le periodo comprendido de diciembre a septiembre del 2012.

María Carcelén Susana Gabriela Acosta Carcelén

En los ultimos anos se ha evidenciado una significativa progresion tanto de naturaleza conceptual como practica de la estimulacion temprana. Este proceso de reflexion y profundizacion sobre el tema pudiera estar dado por el sin numero de programas que se han ido implementando para intervenir, para prevenir minusvalias y aquellos gestados a partir de estudios y practicas psico-socioculturales, lo que ha permitido aportar nuevos elementos a la definicion y al desarrollo practico de la misma, como son aquellos dirigidos a la familia, a grupos especificos, ejemplo a los ninos con Sindrome de Down. En la actualidad, es comun que se incluya a la totalidad de la poblacion infantil, se hace enfasis en que para ello se han creado en diferentes paises una serie de programas con diferentes enfoques y vias: institucionales, comunitarios o de orientacion familiar.

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Amor n'Asturianu / Love in Asturian

mOthertongue (2010)

María Carcelén

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Identification of Epigenetic Interactions between MicroRNA-30c-5p and DNA Methyltransferases in Neuropathic Pain

International Journal of Molecular Sciences (2022)

Raquel Francés Jorge Mata-Garrido Roberto de la Fuente María Carcelén Miguel Lafarga

Neuropathic pain is a prevalent and severe chronic syndrome, often refractory to treatment, whose development and maintenance may involve epigenetic mechanisms. We previously demonstrated a causal relationship between miR-30c-5p upregulation in nociception-related neural structures and neuropathic pain in rats subjected to sciatic nerve injury. Furthermore, a short course of an miR-30c-5p inhibitor administered into the cisterna magna exerts long-lasting antiallodynic effects via a TGF-β1-mediated mechanism. Herein, we show that miR-30c-5p inhibition leads to global DNA hyper-methylation of neurons in the lumbar dorsal root ganglia and spinal dorsal horn in rats subjected to sciatic nerve injury. Specifically, the inhibition of miR-30-5p significantly increased the expression of the novo DNA methyltransferases DNMT3a and DNMT3b in those structures. Furthermore, we identified the mechanism and found that miR-30c-5p targets the mRNAs of DNMT3a and DNMT3b. Quantitative methylation analysis revealed that the promoter region of the antiallodynic cytokine TGF-β1 was hypomethylated in the spinal dorsal horn of nerve-injured rats treated with the miR-30c-5p inhibitor, while the promoter of Nfyc, the host gene of miR-30c-5p, was hypermethylated. These results are consistent with long-term protection against neuropathic pain development after nerve injury. Altogether, our results highlight the key role of miR-30c-5p in the epigenetic mechanisms' underlying neuropathic pain and provide the basis for miR-30c-5p as a therapeutic target.

DNMT3B

Nerve Injury

10.3390/ijms232213994

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A novel strategy based on genomics and specific PCR reveals how a multidrug-resistant Mycobacterium tuberculosis strain became prevalent in Equatorial Guinea 15 years after its emergence

Clinical Microbiology and Infection (2016)

Laura Pérez‐Lago Santiago Izco M. Herranz Griselda Tudó María Carcelén

GeneXpert MTB/RIF

Strain (injury)

Molecular Epidemiology

10.1016/j.cmi.2016.10.006

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The Invasion Factor ODZ1 Is Upregulated through an Epidermal Growth Factor-Induced Pathway in Primary Glioblastoma Cells

Carlos Velásquez Olga Gutiérrez María Carcelén José L. Fernández-Luna

We have previously shown that the transmembrane protein ODZ1 promotes cytoskeletal remodelling of glioblastoma (GBM) cells and invasion of the surrounding parenchyma through activation of a RhoA-ROCK pathway. We also described that GBM cells can control the expression of ODZ1 through transcriptional mechanisms triggered by binding of IL-6 to its receptor and a hypoxic environment. Epidermal growth factor (EGF) plays a key role in the invasive capacity of GBM. However, the molecular mechanisms that enable tumor cells to acquire the morphological changes to migrate out from the tumor core have not been fully characterized. Here we show that EGF is able to induce the expression of ODZ1 in primary GBM cells. We analysed the levels of EGF receptor (EGFR) in 20 GBM primary cell lines and found expression in 19 of them by flow cytometry. We selected two cell lines that do or do not express EGFR and found that EGFR-expressing cells responded to EGF ligand by increasing ODZ1 at the mRNA and protein level. Moreover, blockade of EGF-EGFR binding by Cetuximab, inhibition of the p38 MAPK pathway or siRNA-mediated knockdown of MAPK11 (p38 MAPK) reduced the induction of ODZ1 in response to EGF. Overall, we show that EGF may activate an EGFR-mediated signalling pathway through p38 MAPK, to upregulate the invasion factor ODZ1, which may initiate morphological changes for tumor cells to invade the surrounding parenchyma. These data identify a new candidate of the EGF-EGFR pathway for novel therapeutic approaches.

Factor (programming language)

Primary (astronomy)

10.20944/preprints202403.0806.v1

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BMP-7 protects male and female rodents against neuropathic pain induced by nerve injury through a mechanism mediated by endogenous opioids

Pharmacological Research (2019)

Rosmarí de la Puerta María Carcelén Raquel Francés Roberto de la Fuente María A. Hurlé

SNi

Endogenous opioid

Allodynia

Nerve Injury

Sciatic nerve injury

10.1016/j.phrs.2019.104470

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Optimizing and accelerating the assignation of lineages in Mycobacterium tuberculosis using novel alternative single-tube assays

PLoS ONE (2017)

María Carcelén Estefanía Abascal Marta Herránz Sheila Santantón Roberto Zenteno‐Cuevas

The assignation of lineages in Mycobacterium tuberculosis (MTB) provides valuable information for evolutionary and phylogeographic studies and makes for more accurate knowledge of the distribution of this pathogen worldwide. Differences in virulence have also been found for certain lineages. MTB isolates were initially assigned to lineages based on data obtained from genotyping techniques, such as spoligotyping or MIRU-VNTR analysis, some of which are more suitable for molecular epidemiology studies. However, since these methods are subject to a certain degree of homoplasy, other criteria have been chosen to assign lineages. These are based on targeting robust and specific SNPs for each lineage. Here, we propose two newly designed multiplex targeting methods-both of which are single-tube tests-to optimize the assignation of the six main lineages in MTB. The first method is based on ASO-PCR and offers an inexpensive and easy-to-implement assay for laboratories with limited resources. The other, which is based on SNaPshot, enables more refined standardized assignation of lineages for laboratories with better resources. Both methods performed well when assigning lineages from cultured isolates from a control panel, a test panel, and a problem panel from an unrelated population, Mexico, which included isolates in which standard genotyping was not able to classify lineages. Both tests were also able to assign lineages from stored isolates, without the need for subculture or purification of DNA, and even directly from clinical specimens with a medium-high bacilli burden. Our assays could broaden the contexts where information on lineages can be acquired, thus enabling us to quickly update data from retrospective collections and to merge data with those obtained at the time of diagnosis of a new TB case.

Lineage (genetic)

Multiplex

10.1371/journal.pone.0186956

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HIF2α Upregulates the Migration Factor ODZ1 under Hypoxia in Glioblastoma Stem Cells

International Journal of Molecular Sciences (2022)

María Carcelén Carlos Velásquez Verónica Vidal Olga Gutiérrez José L. Fernández-Luna

Background: Glioblastoma (GBM) remains a major clinical challenge due to its invasive capacity, resistance to treatment, and recurrence. We have previously shown that ODZ1 contributes to glioblastoma invasion and that ODZ1 mRNA levels can be upregulated by epigenetic mechanisms in response to hypoxia. Herein, we have further studied the transcriptional regulation of ODZ1 in GBM stem cells (GSCs) under hypoxic conditions and analyzed whether HIF2α has any role in this regulation. Methods: We performed the experiments in three primary GSC cell lines established from tumor specimens. GSCs were cultured under hypoxia, treated with HIF regulators (DMOG, chetomin), or transfected with specific siRNAs, and the expression levels of ODZ1 and HIF2α were analyzed. In addition, the response of the ODZ1 promoter cloned into a luciferase reporter plasmid to the activation of HIF was also studied. Results: The upregulation of both mRNA and protein levels of HIF2α under hypoxia conditions correlated with the expression of ODZ1 mRNA. Moreover, the knockdown of HIF2α by siRNAs downregulated the expression of ODZ1. We found, in the ODZ1 promoter, a HIF consensus binding site (GCGTG) 1358 bp from the transcription start site (TSS) and a HIF-like site (CCGTG) 826 bp from the TSS. Luciferase assays revealed that the stabilization of HIF by DMOG resulted in the increased activity of the ODZ1 promoter. Conclusions: Our data indicate that the HIF2α-mediated upregulation of ODZ1 helps strengthen the transcriptional control of this migration factor under hypoxia in glioblastoma stem cells. The discovery of this novel transcriptional pathway identifies new targets to develop strategies that may avoid GBM tumor invasion and recurrence.

Hypoxia-Inducible Factors

10.3390/ijms23020741

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Plasmonic Biosensing for Label-Free Detection of Two Hallmarks of Cancer Cells: Cell-Matrix Interaction and Cell Division

Biosensors (2022)

María Carcelén Verónica Vidal Alfredo Franco Marcos Gómez Fernando Moreno

Two key features of cancer cells are sustained proliferation and invasion, which is preceded by a modification of the adhesion properties to the extracellular matrix. Currently, fluorescence-based techniques are mainly used to detect these processes, including flow cytometry and fluorescence resonance energy transfer (FRET) microscopy. We have previously described a simple, fast and label-free method based on a gold nanohole array biosensor to detect the spectral response of single cells, which is highly dependent on the actin cortex. Here we used this biosensor to study two cellular processes where configuration of the actin cortex plays an essential role: cell cycle and cell-matrix adhesion. Colorectal cancer cells were maintained in culture under different conditions to obtain cells stopped either in G0/G1 (resting cells/cells at the initial steps of cell growth) or G2 (cells undergoing division) phases of the cell cycle. Data from the nanohole array biosensor showed an ability to discriminate between both cell populations. Additionally, cancer cells were monitored with the biosensor during the first 60 min after cells were deposited onto a biosensor coated with fibronectin, an extracellular matrix protein. Spectral changes were detected in the first 20 min and increased over time as the cell-biosensor contact surface increased. Our data show that the nanohole array biosensor provides a label-free and real-time procedure to detect cells undergoing division or changes in cell-matrix interaction in both clinical and research settings.

Matrix (chemical analysis)

10.3390/bios12090674

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Treatment of multiple sclerosis with rituximab: A Spanish multicenter experience

Frontiers in Neurology (2023)

Francisco Gascón Carmen Alcalá Lluís Ramió‐Torrentà Paloma Montero Jorge Matías‐Guiu

Rituximab (RTX) is considered a potential therapeutic option for relapsing-remitting (RRMS) and progressive forms (PMS) of multiple sclerosis (MS). The main objective of this work was to investigate the effectiveness and safety of rituximab in MS.Observational multicenter study of clinical and radiological effectiveness and safety of rituximab in RRMS and PMS.A total of 479 rituximab-treated patients were included in 12 Spanish centers, 188 RRMS (39.3%) and 291 (60.7%) PMS. Despite standard treatment, the annualized relapse rate (ARR) the year before RTX was 0.63 (SD: 0.8) and 156 patients (41%) had at least one gadolinium-enhanced lesion (GEL) on baseline MRI. Mean EDSS had increased from 4.3 (SD: 1.9) to 4.8 (SD: 1.7) and almost half of the patients (41%) had worsened at least one point. After a median follow-up of 14.2 months (IQR: 6.5-27.2), ARR decreased by 85.7% (p < 0.001) and GEL by 82.9%, from 0.41 to 0.07 (p < 0.001). A significant decrease in EDSS to 4.7 (p = 0.046) was observed after 1 year of treatment and this variable remained stable during the second year of therapy. There was no evidence of disease activity in 68% of patients. Infusion-related symptoms were the most frequent side effect (19.6%) and most were mild. Relevant infections were reported only in 18 patients (including one case of probable progressive multifocal leukoencephalopathy).Rituximab could be an effective and safe treatment in RRMS, including aggressive forms of the disease. Some selected PMS patients could also benefit from this treatment.

Relapsing remitting

Clinical endpoint

Natalizumab

10.3389/fneur.2023.1060696

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