Health science Research Institute Germans Trias i Pujol IGTP

Barcelona, Spain

Health science Research Institute Germans Trias i Pujol IGTP

Barcelona, Spain

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Roura S.,Health science Research Institute Germans Trias i Pujol IGTP | Pujal J.-M.,Health science Research Institute Germans Trias i Pujol IGTP | Bayes-Genis A.,Health science Research Institute Germans Trias i Pujol IGTP | Bayes-Genis A.,University of Barcelona | And 2 more authors.
Annals of the New York Academy of Sciences | Year: 2012

Endothelial recovery and cell replacement are therapeutic challenges for cardiovascular medicine. Initially employed in the treatment of blood malignancies due to its high concentration of hematological precursors, umbilical cord blood (UCB) is now a non-controversial and accepted source of both hematopoietic and non-hematopoietic progenitors for a variety of emerging cell therapies in clinical trials. Here, we review the current therapeutic potential of UCB, focusing in recent evidence demonstrating the ability of UCB-derived mesenchymal stem cells to differentiate into the endothelial lineage and to develop new vasculature in vivo. © 2012 New York Academy of Sciences.


Pujal J.-M.,Health science Research Institute Germans Trias i Pujol IGTP | Roura S.,Health science Research Institute Germans Trias i Pujol IGTP | Munoz-Marmol A.M.,Hospital Universitari Germans Trias i Pujol | Mate J.-L.,Hospital Universitari Germans Trias i Pujol | And 3 more authors.
Chimerism | Year: 2012

The existence of allogeneic cells within an individual has been demonstrated in multiple fields such as hematopoietic stem cell or solid organ transplantation, non-depleted blood transfusions and the most common form which is bidirectional maternal-fetal cell trafficking, whereby cells from the fetus pass through the placental barrier. In order to graphically illustrate this early natural phenomenon that initiates the journey of a child's cells within the mother's blood and other tissues, we used a new procedure in microscopy imaging generating Large Scale Panoramic Pictures (LSPP). This technique can also be extended to explore a broad diversity of experimental models. © 2012 Landes Bioscience.


Sanjurjo L.,Health science Research Institute Germans Trias i Pujol IGTP | Amezaga N.,Health science Research Institute Germans Trias i Pujol IGTP | Aran G.,Health science Research Institute Germans Trias i Pujol IGTP | Naranjo-Gomez M.,Health science Research Institute Germans Trias i Pujol IGTP | And 7 more authors.
Autophagy | Year: 2015

CD5L (CD5 molecule-like) is a secreted glycoprotein that participates in host response to bacterial infection. CD5L influences the monocyte inflammatory response to the bacterial surface molecules lipopolysaccharide (LPS) and lipoteichoic acid (LTA) by inhibiting TNF secretion. Here we studied the intracellular events that lead to macrophage TNF inhibition by human CD5L. To accomplish this goal, we performed functional analyses with human monocytic THP1 macrophages, as well as with peripheral blood monocytes. Inhibition of phosphatidylinositol 3-kinase (PtdIns3K) reversed the inhibitory effect of CD5L on TNF secretion. Among the various PtdIns3K isoforms, our results indicated that CD5L activates PtdIns3K (whose catalytic subunit is termed PIK3C3), a key modulator involved in autophagy. Further analysis revealed a concomitant enhancement of autophagy markers such as cellular LC3-II content, increased LC3 puncta, as well as LC3-LysoTracker Red colocalization. Moreover, electron microscopy showed an increased presence of cytosolic autophagosomes in THP1 macrophages overexpressing CD5L. Besides preventing TNF secretion, CD5L also inhibited IL1B and enhanced IL10 secretion. This macrophage anti-inflammatory pattern of CD5L was reverted upon silencing of autophagy protein ATG7 by siRNA transfection. Additional siRNA experiments in THP1 macrophages indicated that the induction of autophagy mechanisms by CD5L was achieved through cell-surface scavenger receptor CD36, a multiligand receptor expressed in a wide variety of cell types. Our data represent the first evidence that CD36 is involved in autophagy and point to a significant contribution of the CD5L-CD36 axis to the induction of macrophage autophagy. © 2015, Sanjurjo, Núria Amézaga, Gemma Aran, Mar Naranjo-Gómez, Lilibeth Arias, Carolina Armengol, Francesc E Borrás, and Maria-Rosa Sarrias.


Matilla-Duenas A.,Health science Research Institute Germans Trias I Pujol IGTP | Matilla-Duenas A.,Autonomous University of Barcelona | Ashizawa T.,University of Florida | Brice A.,Institute Du Cerveau Et Of La Moelle Epiniere | And 16 more authors.
Cerebellum | Year: 2014

Intensive scientific research devoted in the recent years to understand the molecular mechanisms or neurodegeneration in spinocerebellar ataxias (SCAs) are identifying new pathways and targets providing new insights and a better understanding of the molecular pathogenesis in these diseases. In this consensus manuscript, the authors discuss their current views on the identified molecular processes causing or modulating the neurodegenerative phenotype in spinocerebellar ataxias with the common opinion of translating the new knowledge acquired into candidate targets for therapy. The following topics are discussed: transcription dysregulation, protein aggregation, autophagy, ion channels, the role of mitochondria, RNA toxicity, modulators of neurodegeneration and current therapeutic approaches. Overall point of consensus includes the common vision of neurodegeneration in SCAs as a multifactorial, progressive and reversible process, at least in early stages. Specific points of consensus include the role of the dysregulation of protein folding, transcription, bioenergetics, calcium handling and eventual cell death with apoptotic features of neurons during SCA disease progression. Unresolved questions include how the dysregulation of these pathways triggers the onset of symptoms and mediates disease progression since this understanding may allow effective treatments of SCAs within the window of reversibility to prevent early neuronal damage. Common opinions also include the need for clinical detection of early neuronal dysfunction, for more basic research to decipher the early neurodegenerative process in SCAs in order to give rise to new concepts for treatment strategies and for the translation of the results to preclinical studies and, thereafter, in clinical practice. © 2013 Springer Science+Business Media.


PubMed | Health science Research Institute Germans Trias i Pujol IGTP
Type: Consensus Development Conference | Journal: Cerebellum (London, England) | Year: 2014

Intensive scientific research devoted in the recent years to understand the molecular mechanisms or neurodegeneration in spinocerebellar ataxias (SCAs) are identifying new pathways and targets providing new insights and a better understanding of the molecular pathogenesis in these diseases. In this consensus manuscript, the authors discuss their current views on the identified molecular processes causing or modulating the neurodegenerative phenotype in spinocerebellar ataxias with the common opinion of translating the new knowledge acquired into candidate targets for therapy. The following topics are discussed: transcription dysregulation, protein aggregation, autophagy, ion channels, the role of mitochondria, RNA toxicity, modulators of neurodegeneration and current therapeutic approaches. Overall point of consensus includes the common vision of neurodegeneration in SCAs as a multifactorial, progressive and reversible process, at least in early stages. Specific points of consensus include the role of the dysregulation of protein folding, transcription, bioenergetics, calcium handling and eventual cell death with apoptotic features of neurons during SCA disease progression. Unresolved questions include how the dysregulation of these pathways triggers the onset of symptoms and mediates disease progression since this understanding may allow effective treatments of SCAs within the window of reversibility to prevent early neuronal damage. Common opinions also include the need for clinical detection of early neuronal dysfunction, for more basic research to decipher the early neurodegenerative process in SCAs in order to give rise to new concepts for treatment strategies and for the translation of the results to preclinical studies and, thereafter, in clinical practice.


PubMed | Health science Research Institute Germans Trias i Pujol IGTP
Type: | Journal: Annals of the New York Academy of Sciences | Year: 2012

Endothelial recovery and cell replacement are therapeutic challenges for cardiovascular medicine. Initially employed in the treatment of blood malignancies due to its high concentration of hematological precursors, umbilical cord blood (UCB) is now a non-controversial and accepted source of both hematopoietic and non-hematopoietic progenitors for a variety of emerging cell therapies in clinical trials. Here, we review the current therapeutic potential of UCB, focusing in recent evidence demonstrating the ability of UCB-derived mesenchymal stem cells to differentiate into the endothelial lineage and to develop new vasculature in vivo.


PubMed | Health science Research Institute Germans Trias i Pujol IGTP
Type: Journal Article | Journal: Autophagy | Year: 2015

CD5L (CD5 molecule-like) is a secreted glycoprotein that participates in host response to bacterial infection. CD5L influences the monocyte inflammatory response to the bacterial surface molecules lipopolysaccharide (LPS) and lipoteichoic acid (LTA) by inhibiting TNF secretion. Here we studied the intracellular events that lead to macrophage TNF inhibition by human CD5L. To accomplish this goal, we performed functional analyses with human monocytic THP1 macrophages, as well as with peripheral blood monocytes. Inhibition of phosphatidylinositol 3-kinase (PtdIns3K) reversed the inhibitory effect of CD5L on TNF secretion. Among the various PtdIns3K isoforms, our results indicated that CD5L activates PtdIns3K (whose catalytic subunit is termed PIK3C3), a key modulator involved in autophagy. Further analysis revealed a concomitant enhancement of autophagy markers such as cellular LC3-II content, increased LC3 puncta, as well as LC3-LysoTracker Red colocalization. Moreover, electron microscopy showed an increased presence of cytosolic autophagosomes in THP1 macrophages overexpressing CD5L. Besides preventing TNF secretion, CD5L also inhibited IL1B and enhanced IL10 secretion. This macrophage anti-inflammatory pattern of CD5L was reverted upon silencing of autophagy protein ATG7 by siRNA transfection. Additional siRNA experiments in THP1 macrophages indicated that the induction of autophagy mechanisms by CD5L was achieved through cell-surface scavenger receptor CD36, a multiligand receptor expressed in a wide variety of cell types. Our data represent the first evidence that CD36 is involved in autophagy and point to a significant contribution of the CD5L-CD36 axis to the induction of macrophage autophagy.

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