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Epithelial Cell Repopulation and Preparation of Rodent Extracellular Matrix Scaffolds for Renal Tissue Development
Published on: August 10, 2015
Extracellular matrix regulates glomerular epithelial cell survival and proliferation
Krikor Bijian1, Tomoko Takano, Joan Papillon
1Department of Medicine, McGill university Health Centre, Montreal, Quebec, Canada H3A 1A1.
American Journal of Physiology. Renal Physiology
|October 16, 2003
Summary
Glomerular epithelial cell (GEC) survival is promoted by collagen adhesion, which activates focal adhesion kinase (FAK) and the ERK pathway. These signals are also activated in puromycin aminonucleoside nephrosis (PAN), suggesting a role in kidney disease.
Area of Science:
- Cell Biology
- Nephrology
- Molecular Biology
Background:
- Glomerular epithelial cell (GEC) injury and apoptosis are implicated in glomerulonephritis and kidney sclerosis.
- Understanding GEC survival mechanisms is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate signals regulating GEC survival in vitro and in vivo.
- To elucidate the role of cell adhesion and specific signaling pathways in GEC survival.
Main Methods:
- GEC culture on plastic versus collagen substrata.
- Analysis of focal adhesion kinase (FAK), c-Src, and ERK pathway activation.
- Assessment of apoptosis-related proteins (Bax, Bcl-XL) and caspase activity.
- Stable expression of FAK and MEK mutants in GECs.
- Pharmacological inhibition of the ERK pathway.
- In vivo study using the puromycin aminonucleoside nephrosis (PAN) model in rats.
Main Results:
- Collagen adhesion, compared to plastic, increased FAK, c-Src, and ERK activation, promoting GEC survival and preventing apoptosis.
- GECs on plastic showed increased proapoptotic markers (caspase-8, -9, Bax) and decreased antiapoptotic markers (Bcl-XL).
- Constitutively active FAK or MEK mutants rescued GEC survival independently of collagen.
- Ras activation of phosphatidylinositol 3-kinase (PI3K) without ERK activation, or ERK inhibition, reduced GEC survival on collagen.
- PAN model glomeruli exhibited increased beta1-integrin, FAK, c-Src, and ERK activation.
Conclusions:
- Collagen-mediated GEC survival is dependent on focal adhesion kinase (FAK) and the Ras-ERK signaling pathway.
- These survival pathways are activated in the puromycin aminonucleoside nephrosis (PAN) model, indicating their relevance in kidney injury.
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