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

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.

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

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 Butyrate ameliorate skeletal muscle atrophy in Diabetic Nephropathy via enhancing gut barrier function and GPR43 mediated PI3K/AKT/mTOR signals

2020 ◽  
Author(s):  
Gang Tang ◽  
Yi Du ◽  
Haochen Guan ◽  
Jieshuang Jia ◽  
Nan Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Diabetic Nephropathy ◽  
Muscle Atrophy ◽  
Barrier Function ◽  
Muscle Protein ◽  
C2c12 Cells ◽  
Skeletal Muscle Atrophy ◽  
Intestinal Barrier Function ◽  
Gut Barrier Function

Muscle protein catabolism in patients with diabetic nephropathy (DN) results in striking losses of muscle proteins, which increases morbidity and mortality risks. Emerging evidence shows that short-chain fatty acids (SCFAs) play an important role in the maintenance of health and disease development. Recently, the connection between butyrate (a SCFA) and DN has been revealed, although the relationship between butyrate and muscle atrophy is still not clear. In our study, we found a significant decrease in butyrate in DN using metabolomics analyses. The addition of butyrate remarkably intestinal barrier function. Concurrently, butyrate could alleviate muscle atrophy and promote PI3K/AKT/mTOR signals, and suppress oxidative stress and autophagy in the skeletal muscle of db/db mice as well as high glucose/lipopolysaccharide (HG/LPS)-induced C2C12 cells. To further explore the mechanism, we found that GPR43, the key SCFAs signaling molecule, was significantly decreased in the skeletal muscle of db/db mice and HG/LPS-induced C2C12 cells. Overexpression of GPR43 could activate PI3K/AKT/mTOR signals and inhibit oxidative stress and autophagy in HG/LPS-induced C2C12 cells. Silencing of GPR43 blocked PI3K/AKT/mTOR signals improved by butyrate, as well as suppression of oxidative stress and reduction of autophagy. Ultimately, butyrate alleviated muscle atrophy in DN via GPR43-mediated PI3K/AKT/mTOR pathway

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