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Research Article Free access | 10.1172/JCI119592

Extraglomerular origin of the mesangial cell after injury. A new role of the juxtaglomerular apparatus.

C Hugo, S J Shankland, D F Bowen-Pope, W G Couser, and R J Johnson

Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.

Find articles by Hugo, C. in: PubMed | Google Scholar

Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.

Find articles by Shankland, S. in: PubMed | Google Scholar

Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.

Find articles by Bowen-Pope, D. in: PubMed | Google Scholar

Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.

Find articles by Couser, W. in: PubMed | Google Scholar

Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA.

Find articles by Johnson, R. in: PubMed | Google Scholar

Published August 15, 1997 - More info

Published in Volume 100, Issue 4 on August 15, 1997
J Clin Invest. 1997;100(4):786–794. https://doi.org/10.1172/JCI119592.
© 1997 The American Society for Clinical Investigation
Published August 15, 1997 - Version history
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Abstract

We investigated the origin of the glomerular mesangial cell, a smooth muscle-like cell that provides structural support in the glomerulus. Injection of anti-Thy 1 antibody that binds the Thy 1 antigen on rat mesangial cells eliminated (> 95%) the mesangial population at 20-28 h, while Thy 1-positive cells in the juxtaglomerular apparatus (JGA) were sequestered from the circulation and survived. Single pulse labeling with [3H]thymidine at 36 h labeled Thy 1-positive cells in the JGA and hilus. Serial biopsies demonstrated the progressive migration (5-15 micron/d) and proliferation of these mesangial reserve cells until the entire glomerulus was repopulated. The regenerating mesangial population expressed contractile and migratory proteins preferentially at the leading edge of the migratory front. Single as well as multiple pulse labeling with [3H]thymidine confirmed that the entire mesangial cell repopulation originated from only a few mesangial reserve cells. These reserve cells resided in the extraglomerular mesangium in the JGA and were not renin-secreting cells, macrophages, smooth muscle cells, or endothelial cells. These studies document mesangial cell migration in the anti-Thy 1 model of mesangial proliferative glomerulonephritis and provide evidence for a new role for the juxtaglomerular apparatus in the maintenance of the mesangial cell population.

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