84 research outputs found
The regenerative potential of stem cells in acute renal failure.
Adult stem cells have been characterized in several tissues as a subpopulation of cells able to maintain, generate, and replace terminally differentiated cells in response to physiological cell turnover or tissue injury. Little is known regarding the presence of stem cells in the adult kidney but it is documented that under certain conditions, such as the recovery from acute injury, the kidney can regenerate itself by increasing the proliferation of some resident cells. The origin of these cells is largely undefined; they are often considered to derive from resident renal stem or progenitor cells. Whether these immature cells are a subpopulation preserved from the early stage of nephrogenesis is still a matter of investigation and represents an attractive possibility. Moreover, the contribution of bone marrow-derived stem cells to renal cell turnover and regeneration has been suggested. In mice and humans, there is evidence that extrarenal cells of bone marrow origin take part in tubular epithelium regeneration. Injury to a target organ can be sensed by bone marrow stem cells that migrate to the site of damage, undergo differentiation, and promote structural and functional repair. Recent studies have demonstrated that hematopoietic stem cells were mobilized following ischemia/reperfusion and engrafted the kidney to differentiate into tubular epithelium in the areas of damage. The evidence that mesenchymal stem cells, by virtue of their renoprotective property, restore renal tubular structure and also ameliorate renal function during experimental acute renal failure provides opportunities for therapeutic intervention
Turnour necrosis factor stimulates endothelin-1 gene expression in cultured bovine endothelial cells
We have studied the effect of human recombinant tumour necrosis factor-α (TNF-α) on gene expression and production of endothelin-1 in cultured bovine aortic endothelial cells. TNF-α (10 and 100 ng ml−1) increased in a time dependent manner the preproendothelin-1 mRNA levels in respect to unstimulated endothelial cells. TNF-α induced endothelin-1 gene expression was associated with a parallel increase in the release of the corresponding peptide in the culture medium. These findings suggest that the enhanced synthesis and release of endothelin-1 occurring in conditions of increased generation of TNF, may act as a modulatory factor that counteracts the hypotensive effect and the excessive platelet aggregation and adhesion induced by TNF
Protein load impairs factor H binding promoting complement-dependent dysfunction of proximal tubular cells
Intrarenal complement activation plays an important role in the progression of chronic kidney disease. A key target of the activated complement cascade is the proximal tubule, a site where abnormally filtered plasma proteins and complement factors combine to promote injury. This study determined whether protein overloading of human proximal tubular cells (HK-2) in culture enhances complement activation by impairing complement regulation. Addition of albumin or transferrin to the cells incubated with diluted human serum as a source of complement caused increased apical C3 deposition. Soluble complement receptor-1 (an inhibitor of all 3 activation pathways) blocked complement deposition while the classical and lectin pathway inhibitor, magnesium chloride–EGTA, was, ineffective. Media containing albumin as well as complement had additive proinflammatory effects as shown by increased fractalkine and transforming growth factor-β mRNA expression. This paralleled active C3 and C5b-9 generations, effects not shared by transferrin. Factor H, one of the main natural inhibitors of the alternative pathway, binds to heparan sulfate proteoglycans. Both the density of heparan sulfate and factor H binding were reduced with protein loading, thereby enhancing the albumin- and serum-dependent complement activation potential. Thus, protein overload reduces the ability of the tubule cell to bind factor H and counteract complement activation, effects instrumental to renal disease progression
Patrimônio Cultural, Memória Social e Informação: a cidade de Porto Alegre na palma da sua mão?
Aims to produce an observation on the memory traces collected by a city, Porto Alegre (Brazil), the social life of the objects inserted in this collection, in the sense not only of its patrimonialization, but also of its dynamics of memory, as well as visibility of this set of objects that are in constant movement of creation and transformation. Our analysis corpus considers two digital objects: the Porto Alegre Guide application as a support for the consolidation or creation of memories about the city of Porto Alegre and the website of the Municipality of Porto Alegre that gathers equipment and spaces valued as patrimony of the city. Attempt to understand the relation between memory, information and cultural heritage. As conclusion, observes that the multiple identities and polyphonies existing in the city of Porto Alegre and that have the potential to emerge as cultural heritage are not disclosed by the City Hall, nor by the Porto Alegre Guide application.Reflete sobre os vestÃgios memoriais colecionados por uma cidade, Porto Alegre (Brasil), a vida social dos objetos inseridos nessa coleção, no sentido não só de sua patrimonialização, mas de sua dinâmica de memoração, bem como da visibilidade desse conjunto de objetos que estão em constante movimento de criação e transformação. O corpus de análise considera dois objetos digitais: o aplicativo Porto Alegre Guide, como um suporte à consolidação ou à criação de memórias sobre a cidade de Porto Alegre e o site da Prefeitura Municipal, que reúne equipamentos e espaços valorizados como patrimônios da cidade. Objetiva, a partir dessa análise, compreender a relação entre memória, informação e patrimônio cultural. Conclui que as múltiplas identidades e polifonias existentes na cidade de Porto Alegre e que têm potencialidade para emergirem como patrimônio cultural não são divulgadas pela Prefeitura Municipal, nem pelo aplicativo Porto Alegre Guide
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