The molecular basis of age-related kidney disease.

Feng Zheng, Anna Rita Plati, Anita Banerjee, Sharon Elliot, Liliane J. Striker, Gary E. Striker

Research output: Contribution to journalArticle

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Abstract

Renal disease affects 11% of people in the United States over the age of 65, not including those with diabetes or hypertension. Although glomerular disease is the most common underlying etiology of age-related renal dysfunction, the cause of glomerular disease and whether it is the only contributor to renal failure are not known. Our studies in female mice show that renal disease in the postmenopausal period is associated with progressive glomerular enlargement and scarring, as well as abnormal renal function. To study the underlying causes of aging-related glomerular disease, we isolated and characterized glomerular smooth muscle (mesangial) cells from female mice of various ages. We found that the cells from older mice exhibit a variety of phenotypic changes, including increased concentrations of p27, a protein that serves to inhibit progression from the G1 to the S phase of the cell cycle. Because the bone marrow (BM) contains mesangial cell progenitors that can transfer the donor glomerular phenotype (normal or diseased) to recipients, we exchanged BM between postmenopausal and premenopausal mice and found that aging-related glomerular enlargement and scarring are transferred to young recipient glomeruli. In addition, BM from normal, young donors led to the regression of aging-related glomerular disease in postmenopausal recipients; namely, both glomerular enlargement and scarring were reduced. Thus, aging-related glomerular disease is an entity distinct from all other causes of renal disease, is characterized by phenotypic changes in mesangial cell progenitors, and is reversible when the phenotype of the progenitors is returned to normal.

Original languageEnglish
JournalScience of aging knowledge environment : SAGE KE
Volume2003
Issue number29
StatePublished - Jan 1 2003

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Kidney Diseases
Mesangial Cells
Kidney
Cicatrix
Bone Marrow
Postmenopause
Phenotype
S Phase
Smooth Muscle Myocytes
Renal Insufficiency
Cell Cycle
Hypertension

Cite this

Zheng, F., Plati, A. R., Banerjee, A., Elliot, S., Striker, L. J., & Striker, G. E. (2003). The molecular basis of age-related kidney disease. Science of aging knowledge environment : SAGE KE, 2003(29).

The molecular basis of age-related kidney disease. / Zheng, Feng; Plati, Anna Rita; Banerjee, Anita; Elliot, Sharon; Striker, Liliane J.; Striker, Gary E.

In: Science of aging knowledge environment : SAGE KE, Vol. 2003, No. 29, 01.01.2003.

Research output: Contribution to journalArticle

Zheng, F, Plati, AR, Banerjee, A, Elliot, S, Striker, LJ & Striker, GE 2003, 'The molecular basis of age-related kidney disease.', Science of aging knowledge environment : SAGE KE, vol. 2003, no. 29.
Zheng F, Plati AR, Banerjee A, Elliot S, Striker LJ, Striker GE. The molecular basis of age-related kidney disease. Science of aging knowledge environment : SAGE KE. 2003 Jan 1;2003(29).
Zheng, Feng ; Plati, Anna Rita ; Banerjee, Anita ; Elliot, Sharon ; Striker, Liliane J. ; Striker, Gary E. / The molecular basis of age-related kidney disease. In: Science of aging knowledge environment : SAGE KE. 2003 ; Vol. 2003, No. 29.
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