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Modulation of renal tubular cell function by RGS3
W Grüning1, T Arnould, F Jochimsen
1Renal Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston 02215, Massachusetts.
The American Journal of Physiology
|April 13, 1999
Summary
Regulators of G protein signaling 3 (RGS3) are highly expressed in kidney tubules. RGS3 inhibits kidney tubule cell migration in response to specific signaling molecules, impacting renal development and function.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- Regulators of G protein signaling (RGS) proteins terminate G protein signaling by accelerating GTPase activity.
- RGS3 exhibits high mRNA levels in the adult kidney, suggesting a significant renal role.
Purpose of the Study:
- To determine the temporal and spatial expression pattern of RGS3 in the developing and adult kidney.
- To investigate the functional role of RGS3 in modulating kidney tubular cell migration.
Main Methods:
- Generated a polyclonal antiserum against RGS3 for immunohistochemical staining of mouse renal tissue across gestational stages.
- Created inducible RGS3-expressing mouse inner medullary collecting duct (mIMCD-3) cell lines.
- Assessed cell migration in response to lysophosphatidic acid (LPA) and hepatocyte growth factor.
Main Results:
- RGS3 was highly expressed in developing and mature tubular epithelial cells of the kidney.
- Induction of RGS3 significantly reduced LPA-mediated mIMCD-3 cell migration.
- RGS3 did not affect cell migration induced by hepatocyte growth factor.
Conclusions:
- RGS3 plays a role in modulating kidney tubular cell migration, particularly in response to G protein-coupled receptor signaling like LPA.
- These findings highlight RGS3's involvement in renal development and the maintenance of adult kidney function.