Glomerular Barrier Function for Serum Proteins in Experimental Heart Failure1

2015 ◽  
pp. 144-150
Author(s):  
Wilfried Gwinner ◽  
Ulrich Frei ◽  
Cordula Matthies ◽  
Karl Martin Koch ◽  
Hilmar Stolte
Keyword(s):  
Barrier Function ◽  
Serum Proteins ◽  
Glomerular Barrier

Abstract 516: Knockdown of the Hypertension Associated Gene NOSTRIN Alters Glomerular Barrier Function in Zebrafish (Danio rerio)

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Torsten Kirsch ◽  
Jessica Kaufeld ◽  
Ron Korstanje ◽  
Dirk Hentschel ◽  
Hermann Haller ◽  
...  
Keyword(s):  
Glomerular Filtration ◽  
Barrier Function ◽  
Morphological Changes ◽  
Glomerular Filtration Barrier ◽  
Cell Dysfunction ◽  
Larval Zebrafish ◽  
Filtration Barrier ◽  
Important Regulator ◽  
Glomerular Barrier ◽  
Prime Source

The bioavailability of nitric oxide (NO) has been associated with the development and progression of vascular and renal disease. NOSTRIN (for eNOS Traffic Inducer) has primarily been recognized as one important regulator of eNOS, the prime source of NO in the cardiovascular system, with a possible role in the pathogenesis of pre-eclampsia and the development of increased intrahepatic resistance in liver disease. Here, we identified NOSTRIN in the center of a QTL-overlap region in rat and human trait loci that are associated with hypertension. Glomerular NOSTRIN expression is detectable in podocytes in human and rat glomeruli and podocytic NOSTRIN expression is diminished in hypertensive kidney disease. We show that knockdown of NOSTRIN alters the glomerular filtration barrier function in larval zebrafish, inducing proteinuria and leading to ultrastructural morphological changes on the endothelial as well as epithelial side and the GBM of the glomerular capillary loop. We also demonstrate that NOSTRIN interacts with proteins associated with the podocyte slit membrane. We conclude that NOSTRIN expression is an important factor for the integrity of the glomerular filtration barrier. Disease related alteration of NOSTRIN expression may not only affect the vascular endothelium and therefore contribute to endothelial cell dysfunction but may also contribute to the development of podocyte disease and proteinuria.

scholarly journals Shroom3, a novel GWAS renal candidate, is essential for glomerular barrier function

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Nan Cher Yeo ◽  
Caitlin O'Meara ◽  
Michael Flister ◽  
Michael Cliff ◽  
Jozef Lazar ◽  
...  
Keyword(s):  
Barrier Function ◽  
Glomerular Barrier

scholarly journals Hypertension‐Induced Renal Injury is Associated with Impaired Glomerular Barrier Function Involving Podocyte Dysfunction

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Xiaochen He ◽  
Chun Cheng Andy Chen ◽  
Sydney R. Murphy ◽  
George W. Booz ◽  
Richard J. Roman ◽  
...  
Keyword(s):  
Renal Injury ◽  
Barrier Function ◽  
Glomerular Barrier

scholarly journals Soluble FLT1 Binds Lipid Microdomains in Podocytes to Control Cell Morphology and Glomerular Barrier Function

Cell ◽  
2012 ◽  
Vol 151 (2) ◽  
pp. 384-399 ◽  
Author(s):  
Jing Jin ◽  
Karen Sison ◽  
Chengjin Li ◽  
Ruijun Tian ◽  
Monika Wnuk ◽  
...  
Keyword(s):  
Cell Morphology ◽  
Barrier Function ◽  
Control Cell ◽  
Lipid Microdomains ◽  
Glomerular Barrier

Shock-induced stress induces loss of microvascular endothelial Tie2 in the kidney which is not associated with reduced glomerular barrier function

2009 ◽  
Vol 297 (2) ◽  
pp. F272-F281 ◽  
Author(s):  
Matijs van Meurs ◽  
Neng F. Kurniati ◽  
Francis M. Wulfert ◽  
Sigridur A. Asgeirsdottir ◽  
Inge A. de Graaf ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Barrier Function ◽  
Human Kidney ◽  
Mrna Levels ◽  
Barrier Dysfunction ◽  
Molecular Control ◽  
Filtration Barrier ◽  
Glomerular Barrier

Both hemorrhagic shock and endotoxemia induce a pronounced vascular activation in the kidney which coincides with albuminuria and glomerular barrier dysfunction. We hypothesized that changes in Tie2, a vascular restricted receptor tyrosine kinase shown to control microvascular integrity and endothelial inflammation, underlie this loss of glomerular barrier function. In healthy murine and human kidney, Tie2 is heterogeneously expressed in all microvascular beds, although to different extents. In mice subjected to hemorrhagic and septic shock, Tie2 mRNA and protein were rapidly, and temporarily, lost from the renal microvasculature, and normalized within 24 h after initiation of the shock insult. The loss of Tie2 protein could not be attributed to shedding as both in mice and healthy volunteers subjected to endotoxemia, sTie2 levels in the systemic circulation did not change. In an attempt to identify the molecular control of Tie2, we activated glomerular endothelial cell cultures and human kidney slices in vitro with LPS or TNF-α, but did not observe a change in Tie2 mRNA levels. In parallel to the loss of Tie2 in vivo, an overt influx of neutrophils in the glomerular compartment, which coincided with proteinuria, was seen. As neutrophil-endothelial cell interactions may play a role in endothelial adaptation to shock, and these effects cannot be mimicked in vitro, we depleted neutrophils before shock induction. While this neutrophil depletion abolished proteinuria, Tie2 was not rescued, implying that Tie2 may not be a major factor controlling maintenance of the glomerular filtration barrier in this model.

scholarly journals Mechanisms of proteinuria in diabetic nephropathy: A study of glomerular barrier function

1982 ◽  
Vol 21 (4) ◽  
pp. 633-641 ◽  
Author(s):  
Bryan D. Myers ◽  
Jan A. Winetz ◽  
Francis Chui ◽  
Alan S. Michaels
Keyword(s):  
Diabetic Nephropathy ◽  
Barrier Function ◽  
Glomerular Barrier
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