Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 9 de 9
Filter
Add more filters










Publication year range
1.
Investig. desar. ; 29(1): 69-98, ene.-jun. 2021.
Article in Spanish | LILACS, COLNAL | ID: biblio-1346389

ABSTRACT

RESUMEN La responsabilidad social, como una de las respuestas a los actuales conflictos socioambientales, implica esfuerzos adicionales de las organizaciones para fortalecer su capacidad de gestión. Esto sucede, de manera especial, en las compañías mineras, cuyas actividades comprometen el uso de recursos de comunidades, entre ellos los naturales. Esta investigación analizó los aportes que la gestión de comunicaciones hace al relacionamiento con las comunidades en el marco de dos programas de responsabilidad social de los proyectos mineros Quebradona y Gramalote (ubicados en Antioquia, Colombia), adscritos a la compañía Anglogold Ashanti y ganadores del Premio Sello Social a la Minería en Antioquia, siendo dos de los proyectos con mayor exigencia y veeduría ciudadana en la región. Desde una mirada con predominancia interpretativa, y acudiendo a la revisión de documentos y entrevistas a jefes de áreas sociales, comunicadores, beneficiarios y líderes ambientales, se concluyó que el análisis del entorno, la visibilización de los programas y la mediación en los conflictos socioambientales son los principales aportes de los comunicadores en los proyectos mineros.


ABSTRACT Social responsibility, as one of the responses to current sock-environmental conflicts, implies additional efforts by organizations to strengthen their management capacity. This happens, especially, in mining companies, our activities compromise the use of community resources, including natural resources. This research analyzed the contributions that communications management makes to relations with communities within the framework of two social responsibility programs of the Quebradona and Gramalote mining projects (located in Antioquia, Colombia), attached to the company Anglogold Ashanti and winners of the Premio Sello Social a la Minería en Antioquia, being two of the projects with the highest demand and citizen oversight in the region. From an interpretive perspective and going to the review of documents and interviews with heads of social areas, communicators, beneficiaries, and environmental leaders, it was concluded that the analysis of the environment, the visibility of the programs and mediation in socio-environmental conflicts are the main contributions of communicators in mining projects.


Subject(s)
Humans , Social Responsibility , Communication , Natural Resources , Miners , Mining , Organization and Administration , Records , Negotiating , Environment , Community Resources
2.
Int J Dev Biol ; 65(4-5-6): 365-376, 2021.
Article in English | MEDLINE | ID: mdl-32930373

ABSTRACT

The amount of proteins of the regulatory pluripotency network can be determinant for somatic cell reprogramming into induced pluripotent stem cells (iPSCs) as well as for the maintenance of pluripotent stem cells (PSCs). Here, we report a transposon-based reprogramming system (PB-Booster) that allowed high expression levels of a polycistronic transgene containing Myc, Klf4, Oct4 and Sox2 (MKOS) and showed increased reprogramming efficiency of fresh mouse embryonic fibroblasts (MEFs) into iPSCs under low, but not under high, MKOS expression levels. In contrast, MEFs after 2 passages derived into a similar number of iPSC colonies as fresh MEFs at a high MKOS dose, but this number was reduced at a low MKOS dose. Timing of reprogramming was not affected by MKOS expression levels but, importantly, exogenous MKOS expression in established PSCs caused a significant cell loss. At high but not at low MKOS expression levels, MEFs of the CD1 strain produced more initial cell clusters than iPSCs and, although reprogrammed at a similar efficiency as MEFs of the 129/Sv strain, iPSCs could not be maintained in the absence of exogenous MKOS. In CD1-iPSCs, Oct4, Nanog, Rex1 and Esrrb expression levels were reduced when compared with the levels in PSCs derived from the 129/Sv strain. Culture of CD1-iPSCs in medium with MEK and GSK3ß inhibitors allowed their self-renewal in the absence of exogenous MKOS, but the expression levels of Oct4, Nanog, Rex1 and Esrrb were only partially increased. Despite the reduced levels of those pluripotency factors, CD1-iPSC kept high capacity for contribution to chimeric mouse embryos. Therefore, levels of regulatory pluripotency factors influence reprogramming initiation and PSC maintenance in vitro without affecting their differentiation potential in vivo.


Subject(s)
Cellular Reprogramming , Induced Pluripotent Stem Cells , Animals , Cell Differentiation , Cells, Cultured , Cellular Reprogramming/genetics , Fibroblasts , Mice , Mice, 129 Strain , Transgenes
3.
Stem Cells Dev ; 28(16): 1104-1115, 2019 08 15.
Article in English | MEDLINE | ID: mdl-31140356

ABSTRACT

Transplantation of dopaminergic (DA) cells into the striatum can rescue from dopamine deficiency in a Parkinson's disease condition, but this is not a suitable procedure for regaining the full control of motor activity. The minimal condition toward recovering the nigrostriatal pathway is the proper innervation of transplanted DA neurons or their precursors from the substancia nigra pars compacta (SNpc) to their target areas. However, functional integration of transplanted cells would require first that the host SNpc is suitable for their survival and/or differentiation. We recently reported that the intact adult SNpc holds a strong neurogenic environment, but primed embryonic stem cells (ie, embryoid body cells, EBCs) could not derive into DA neurons. In this study, we transplanted into the intact or lesioned SNpc, EBCs derived from embryonic stem cells that were prompt to differentiate into DA neurons by the forced expression of Lmx1a in neural precursor cells (R1B5/NesE-Lmx1a). We observed that, 6 days posttransplantation (dpt), R1B5 or R1B5/NesE-Lmx1a EBCs gave rise to Nes+ and Dcx+ cells within the host SNpc, but a large number of Th+ cells derived only from EBCs exogenously expressing Lmx1a. In contrast, when transplantation was carried out into the 6-hydroxidopamine-lesioned SNpc, the emergence of Th+ cells from EBCs was independent of exogenous Lmx1a expression, although these cells were not found by 15 dpt. These results suggest that the adult SNpc is not only a permissive niche for initiation of DA differentiation of non-neuralized cells but also releases factors upon damage that promote the acquisition of DA characteristics by transplanted EBCs.


Subject(s)
Cell Differentiation/physiology , Dopamine/metabolism , Embryonic Stem Cells/cytology , Substantia Nigra/cytology , Animals , Cells, Cultured , Corpus Striatum/cytology , Corpus Striatum/metabolism , Dopaminergic Neurons/cytology , Dopaminergic Neurons/metabolism , Doublecortin Protein , Embryonic Stem Cells/metabolism , Mice , Neural Stem Cells/cytology , Neural Stem Cells/metabolism , Neurogenesis/physiology , Parkinson Disease/metabolism , Substantia Nigra/metabolism , Transcription Factors/metabolism
4.
Free Radic Biol Med ; 135: 102-115, 2019 05 01.
Article in English | MEDLINE | ID: mdl-30818059

ABSTRACT

The relationship between the mechanisms that underlie longevity and aging and the metabolic alterations due to feeding conditions has not been completely defined. In the present work, through the deletion of the gene encoding catalase, hydrogen peroxide (H2O2) was uncovered as a relevant regulator of longevity and of liver metabolism. Mice lacking catalase (Cat-/-) fed ad libitum with a regular diet showed a shorter lifespan than wild type mice, which correlated with reduced body weight, blood glucose levels and liver fat accumulation, but not with increased oxidative damage or consistent premature aging. High fat diet (HFD) and fasting increased oxidative damage in the liver of wild type animals but, unexpectedly, this was not the case for that of Cat-/- mice. Interestingly, although HFD feeding similarly increased the body weight of Cat-/- and wild-type mice, hyperglycemia and liver steatosis did not develop in the former. Fat accumulation due to fasting, on the other hand, was diminished in mice lacking catalase, which correlated with increased risk of death and low ketone body blood levels. Alteration in expression of some metabolic genes in livers of catalase deficient mice was consistent with reduced lipogenesis. Specifically, Pparγ2 expression up-regulation in response to a HFD and down-regulation upon fasting was lower and higher, respectively, in livers of Cat-/- than of wild type mice, and a marked decay was observed during Cat-/- mice aging. We propose that catalase regulates lipid metabolism in the liver by an evolutionary conserved mechanism that is determinant of lifespan without affecting general oxidative damage.


Subject(s)
Catalase/genetics , Lipid Metabolism/genetics , Longevity/genetics , PPAR gamma/genetics , Acatalasia/genetics , Acatalasia/metabolism , Aging, Premature/genetics , Aging, Premature/pathology , Animals , Diet, High-Fat/adverse effects , Fatty Liver/genetics , Fatty Liver/pathology , Humans , Hydrogen Peroxide/metabolism , Insulin Resistance/genetics , Liver/metabolism , Liver/pathology , Mice , Mice, Knockout , Obesity/genetics , Obesity/pathology , Oxidative Stress/genetics
5.
Int J Dev Biol ; 63(11-12): 605-613, 2019.
Article in English | MEDLINE | ID: mdl-32149370

ABSTRACT

Determination of cellular signaling in live embryos is key to understand the molecular processes that drive development. Here, we show that a transgenic mouse line carrying a luciferase-based gene reporter of Gli-mediated transcriptional activation (Gli-Luc) displays sonic hedgehog (Shh) signaling in discrete developmental processes during short-term cultures of whole embryos or embryo explants. The bioluminescence in E9.5 embryos was detected in regions in which Shh activity has been demonstrated. Later, in E10.5 embryos, bioluminescence intensity markedly increased, mostly corresponding to the high Shh activity of the developing midbrain and limb. Notably, the dynamic range of the Gli-Luc reporter in the developing limb revealed the progressive emergence of bioluminescence in the zone of polarizing activity, where reporter activity locally increased and spatially spread in agreement with the signaling gradient expected for Shh. In the midbrain of E9.5 mouse embryos, bioluminescence was not detected along the ventral region as expected but, instead, Shh-dependent anterior and posterior bioluminescence foci emerged by E10.5 indicating that the Gli-Luc reporter can only respond transcriptionally to relatively high levels of GliA and/or without the interaction with other transcription factors. The present work supports the use of bioluminescence to identify and study the dynamics of centers of morphogen signaling during mouse embryogenesis.


Subject(s)
Body Patterning/genetics , Embryo, Mammalian/metabolism , Gene Expression Regulation, Developmental , Hedgehog Proteins/genetics , Signal Transduction/genetics , Animals , Embryo, Mammalian/embryology , Extremities/embryology , Genes, Reporter/genetics , In Situ Hybridization/methods , Luciferases/genetics , Luciferases/metabolism , Luminescent Measurements/methods , Mesencephalon/embryology , Mesencephalon/metabolism , Mice, Transgenic , Time-Lapse Imaging/methods , Tissue Culture Techniques
6.
Free Radic Biol Med ; 49(2): 130-43, 2010 Jul 15.
Article in English | MEDLINE | ID: mdl-20353819

ABSTRACT

Reactive oxygen species (ROS), mostly derived from mitochondrial activity, can damage various macromolecules and consequently cause cell death. This ROS activity has been characterized in vitro, and correlative evidence suggests a role in various pathological conditions. In addition to this passive ROS activity, ROS also participate in cell signaling processes, though the relevance of this function in vivo is poorly understood. Throughout development, elevated cell activity is probably accompanied by highly active metabolism and, consequently, the production of large amounts of ROS. To allow proper development, cells must protect themselves from these potentially damaging ROS. However, to what degree ROS could participate as signaling molecules controlling fundamental and developmentally relevant cellular processes such as proliferation, differentiation, and death is an open question. Here we discuss why available data do not yet provide conclusive evidence on the role of ROS in development, and we review recent methods to detect ROS in vivo and genetic strategies that can be exploited specifically to resolve these uncertainties.


Subject(s)
Adult Stem Cells/physiology , Fetal Development , Mitochondria/metabolism , Molecular Probes/metabolism , Reactive Oxygen Species/metabolism , Animals , Antioxidants/metabolism , Cell Death , Cell Differentiation , Cell Proliferation , Humans , Molecular Probes/genetics , Signal Transduction
7.
Dev Biol ; 320(1): 1-11, 2008 Aug 01.
Article in English | MEDLINE | ID: mdl-18555213

ABSTRACT

Oxidative stress is considered causal of aging and pathological cell death, however, very little is known about its function in the natural processes that support the formation of an organism. It is generally thought that cells must continuously protect themselves from the possible damage caused by reactive oxygen species (ROS) (passive ROS function). However, presently, ROS are recognized as physiologically relevant molecules that mediate cell responses to a variety of stimuli, and the activities of several molecules, some developmentally relevant, are directly or indirectly regulated by oxidative stress (active ROS function). Here we review recent data that are suggestive of specific ROS functions during development of animals, particularly mammals.


Subject(s)
Embryonic Development , Reactive Oxygen Species/metabolism , Animals , Oxidation-Reduction , Oxidative Stress , Signal Transduction
8.
Exp Cell Res ; 314(10): 2090-9, 2008 Jun 10.
Article in English | MEDLINE | ID: mdl-18452915

ABSTRACT

The formation of the proamniotic cavity is the first indication of programmed cell death associated to a morphogenetic process in mammals. Although some growth factors have been implicated in proamniotic cavitation, very little is known about the intracellular mechanisms that control the cell death process itself. Reactive oxygen species (ROS) are potent activators of cell death, thus, in the present work we evaluated the role of ROS during the cavitation of embryoid bodies (EBs), a common model to study proamniotic cavitation. During cavitation, ROS concentration increases in the inner cells of EBs, and this ROS accumulation appears to be associated with the mitochondrial respiratory activity. In agreement with a role of ROS in cavitation, EBs derived from ES cells that overproduce catalase, an enzyme that specifically degrades hydrogen peroxide, do not cavitate, and caspase activation and cell death is markedly decreased. Notably, cell death, but not the rise in ROS, during EB cavitation is caspase-dependent. The apoptosis-inducing factor (Aif) is released from the mitochondria during cavitation, but EBs derived from Aif(-/y) ES cells cavitate and ROS levels in the inner cells remain high. We conclude that hydrogen peroxide is a cell death activating signal essential for EB cavitation, suggesting that cell death during proamniotic cavitation is mediated by ROS.


Subject(s)
Cell Death/drug effects , Embryo, Mammalian , Hydrogen Peroxide/pharmacology , Oxidants/pharmacology , Reactive Oxygen Species/metabolism , Ultrasonics , Animals , Antioxidants/metabolism , Apoptosis Inducing Factor/metabolism , Caspases/metabolism , Catalase/genetics , Catalase/metabolism , Cell Death/physiology , Cell Line , Cell Survival , Embryo, Mammalian/cytology , Embryo, Mammalian/physiology , Humans , Mice , Organometallic Compounds/metabolism , Oxidative Stress , Paraquat/metabolism , Salicylates/metabolism , Vitamin K 3/metabolism
9.
Dev Biol ; 291(2): 291-9, 2006 Mar 15.
Article in English | MEDLINE | ID: mdl-16445905

ABSTRACT

Vertebrate limb development is a well-studied model of apoptosis; however, little is known about the intracellular molecules involved in activating the cell death machinery. We have shown that high levels of reactive oxygen species (ROS) are present in the interdigital 'necrotic' tissue of mouse autopod, and that antioxidants can reduce cell death. Here, we determined the expression pattern of several antioxidant enzymes in order to establish their role in defining the areas with high ROS levels. We found that the genes encoding the superoxide dismutases and catalase are expressed in autopod, but they are downregulated in the interdigital regions at the time ROS levels increased and cell death was first detected. The possible role of superoxide and/or peroxide in activating cell death is supported by the protective effect of a superoxide dismutase/catalase mimetic. Interestingly, we found that peroxidase activity and glutathione peroxidase-4 gene (Gpx4) expression were restricted to the non-apoptotic tissue (e.g., digits) of the developing autopod. Induction of cell death with retinoic acid caused an increase in ROS and decrease in peroxidase activity. Even more inhibition of glutathione peroxidase activity leads to cell death in the digits, suggesting that a decrease in antioxidant activity, likely due to Gpx4, caused an increase in ROS levels, thus triggering apoptosis.


Subject(s)
Apoptosis , Extremities/embryology , Gene Expression Regulation, Developmental , Glutathione Peroxidase/genetics , Reactive Oxygen Species/metabolism , Animals , Catalase/genetics , Glutathione Peroxidase/physiology , Mice , RNA, Messenger/analysis , Superoxide Dismutase/genetics , Tretinoin/pharmacology
SELECTION OF CITATIONS
SEARCH DETAIL
...