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Cell biology of the glomerular podocyte.
TLDR
This review integrates recent physiological and molecular understanding of the role of podocytes during the maintenance and failure of the glomerular filtration barrier with hereditary nephrotic syndromes identified over the last 2 years. Expand
The Tie-2 ligand angiopoietin-2 is stored in and rapidly released upon stimulation from endothelial cell Weibel-Palade bodies.
TLDR
The identification of Ang-2 as a stored, rapidly available molecule in endothelial cells strongly suggests functions of the angiopoietin/Tie-2 system beyond the established roles during angiogenesis likely to be involved in rapid vascular homeostatic reactions such as inflammation and coagulation. Expand
Rearrangements of the cytoskeleton and cell contacts induce process formation during differentiation of conditionally immortalized mouse podocyte cell lines.
TLDR
The determinative steps of podocyte differentiation and process formation are studied for the first time using an inducible in vitro model and electrophysiological studies demonstrate that differentiated MPC cells respond to the vasoactive peptide bradykinin by changes in intracellular calcium concentration. Expand
Synaptopodin: An Actin-associated Protein in Telencephalic Dendrites and Renal Podocytes
TLDR
It is concluded that synaptopodin represents a novel kind of proline-rich, actin-associated protein that may play a role in modulating actin -based shape and motility of dendritic spines and podocyte foot processes. Expand
Podocin, a raft-associated component of the glomerular slit diaphragm, interacts with CD2AP and nephrin.
TLDR
It is shown, by immunoelectron microscopy, that podocin localizes to the podocyte foot process membrane, at the insertion site of the slit diaphragm, and it is postulate thatpodocin serves in the structural organization of the slat diaphagm and the regulation of its filtration function. Expand
The glomerular slit diaphragm is a modified adherens junction.
TLDR
A P-cadherin-based adherens junction is well-suited to explain the zipper-like structure of the slit diaphragm, and the present study should allow new avenues leading to the identification of additional slit diphragm-associated proteins conferring specificity to this unique cell junction. Expand
The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy.
TLDR
It is concluded that the loss of specific podocyte markers defines a novel dysregulated podocyte phenotype and suggests a common pathomechanism in collapsing FSGS, whether idiopathic or HIV-associated. Expand
Pathways to nephron loss starting from glomerular diseases-insights from animal models.
TLDR
Two mechanisms are discussed: (1) the loss of nephrons leads to compensatory mechanisms in the remaining nephons (glomerular hypertension, hyperfiltration, hypertrophy) which increase their vulnerability to any further challenge (overload hypothesis) and (2) a proteinuric glomerular disease leads to tubulointerstitial inflammation and fibrosis, accounting for the further deterioration of renal function (fibrosis hypothesis). Expand
The podocyte's response to stress: the enigma of foot process effacement.
TLDR
The hypothesis that foot process effacement represents a protective response of podocytes to escape detachment from the glomerular basement membrane is raised, raising the hypothesis that evolution has developed particular mechanisms whereby podocytes resist cell detachment. Expand
An efficient and versatile system for acute and chronic modulation of renal tubular function in transgenic mice
TLDR
A conditional knockout of the gene encoding tuberous sclerosis complex-1 was achieved, which resulted in the early outgrowth of giantpolycystic kidneys reminiscent of autosomal recessive polycystic kidney disease. Expand
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