50 research outputs found
Hypertonic stress and cell death. Focus on "Multiple cell death pathways are independently activated by lethal hypertonicity in renal epithelial cells"
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Nephrotoxicity From Chemotherapeutic Agents: Clinical Manifestations, Pathobiology, and Prevention/Therapy
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Podocyte COX-2 Exacerbates Diabetic Nephropathy by Increasing Podocyte (Pro)renin Receptor Expression
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Macrophage-specific deletion of transforming growth factor-β1 does not prevent renal fibrosis after severe ischemia-reperfusion or obstructive injury
No full textEarly evolution of embedded clusters
No full textThis research was supported by the DFG cluster of excellence ‘Origin and Structure of the Universe’ (JED, BE).We examine the combined effects of winds and photoionizing radiation from O-type stars on embedded stellar clusters formed in model turbulent molecular clouds covering a range of masses and radii. We find that feedback is able to increase the quantities of dense gas present, but decreases the rate and efficiency of the conversion of gas to stars relative to control simulations in which feedback is absent. Star formation in these calculations often proceeds at a rate substantially slower than the freefall rate in the dense gas. This decoupling is due to the weakening of, and expulsion of gas from, the deepest parts of the clouds' potential wells where most of the star formation occurs in the control simulations. This results in large fractions of the stellar populations in the feedback simulation becoming dissociated from dense gas. However, where star formation does occur in both control and feedback simulations, it does so in dense gas, so the correlation between star formation activity and dense gas is preserved. The overall dynamical effects of feedback on the clusters are minimal, with only small fraction of stars becoming unbound, despite large quantities of gas being expelled from some clouds. This owes to the settling of the stars into virialized and stellar-dominated configurations before the onset of feedback. By contrast, the effects of feedback on the observable properties of the clusters - their U-, B- and V-band magnitudes - are strong and sudden. The time-scales on which the clusters become visible and unobscured are short compared with the time-scales which the clouds are actually destroyed.Peer reviewe
Distinct Roles for Basal and Induced COX-2 in Podocyte Injury
No full textTransgenic mice that overexpress cyclooxygenase-2 (COX-2) selectively in podocytes are more susceptible to glomerular injury by adriamycin and puromycin (PAN). To investigate the potential roles of COX-2 metabolites, we studied mice with selective deletion of prostanoid receptors and generated conditionally immortalized podocyte lines from mice with either COX-2 deletion or overexpression. Podocytes that overexpressed COX-2 were virtually indistinguishable from wild-type podocytes but were significantly more sensitive to PAN-induced injury, produced more prostaglandin E(2) and thromboxane B(2), and had greater expression of prostaglandin E2 receptor subtype 4 (EP(4)) and thromboxane receptor (TP). Treatment of COX-2-overexpressing podocytes with a TP antagonist reduced apoptosis, but treatment with an EP(4) antagonist did not. In contrast, podocytes from COX-2-knockout mice exhibited increased apoptosis, markedly decreased cell adhesion, and prominent stress fibers. In vivo, selective deletion of podocyte EP(4) did not alter the increased sensitivity to adriamycin-induced injury observed in mice overexpressing podocyte COX-2. In contrast, genetic deletion of TP in these mice prevented adriamycin-induced injury, with attenuated albuminuria and foot process effacement. These results suggest that basal COX-2 may be important for podocyte survival, but overexpression of podocyte COX-2 increases susceptibility to podocyte injury, which is mediated, in part, by activation of the thromboxane receptor.Urology & NephrologySCI(E)20ARTICLE91953-19622
