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Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Alterations in human glomerular epithelial cells interacting with nonenzymatically glycosylated matrix
U Krishnamurti1, E Rondeau, J D Sraer
1Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota 55455, USA. kris0019@maroon.tc.umn.edu
The Journal of Biological Chemistry
|November 5, 1997
Summary
Diabetic nephropathy alters kidney cell interactions with the extracellular matrix. Matrix glycation disrupts cell signaling, potentially driving kidney disease progression in diabetes.
Area of Science:
- Nephrology
- Cell Biology
- Diabetology
Background:
- Diabetic nephropathy is a long-term complication of diabetes affecting kidney permselective barriers.
- Advanced glycosylation end products (AGEs) from nonenzymatic glycosylation correlate with diabetic complications.
- Cell-matrix interactions are crucial for biological processes and are mediated by integrins.
Purpose of the Study:
- To investigate the impact of nonenzymatic matrix glycation on human glomerular epithelial cells.
- To examine how altered cell-matrix interactions affect intracellular signaling pathways.
Main Methods:
- Cultured human glomerular epithelial cells.
- Exposure to nonenzymatically glycated extracellular matrix.
- Assessed cell spreading, focal adhesion kinase (FAK) phosphorylation, and mitogen-activated protein kinase (MAPK) activity.
Main Results:
- Matrix glycation significantly altered human glomerular epithelial cell interactions.
- Observed defective cell spreading on glycated matrix.
- Demonstrated reduced FAK phosphorylation and MAPK activity.
Conclusions:
- Nonenzymatic matrix glycation interferes with normal cell-matrix interactions in the kidney.
- Disrupted intracellular signaling pathways may contribute to diabetic nephropathy.
- Altered cell-matrix communication could lead to differential gene expression implicated in kidney disease.
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