Relationships between mesangial cell proliferation and types i and iv collagen mrna levels in vitro. He, Ci-Jiang, Liliane J. Striker, Maria Tsokos, Chih-Wei Yang, and Gary E. Striker. Renal Cell Biology Section, Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Disease, Bethesda, Maryland, 20892; and Laboratory of Pathology, National Cancer Institute, Bethesda, Maryland, 20892
APStracts 2:0147C, 1995.
Changes in the composition of the mesangial extracellular matrix (ECM) and cell turnover are present in glomerular disease. To determine if ECM changes play a role in perpetuating mesangial cell dysfunction, we examined a line of mouse mesangial cells cultured on films or gels of several ECM components and also on methylcellulose, an inert substrate which prevents attachment. Cells on films of fibronectin, type IV or I collagen had persistently high growth rates and high levels of [alpha]1I and [alpha]1IV collagen mRNAs. In contrast, on gels of type IV or I collagen or matrigel, the growth rate was low. The [alpha]1IV collagen mRNA levels were low on type IV collagen gel or matrigel, whereas the [alpha]1I collagen mRNA levels remained high. In contrast, the [alpha]1I collagen mRNA levels were low on type I collagen gel, and the [alpha]1IV collagen mRNA levels were high. Cells on methylcellulose formed floating aggregates, did not proliferate, and had a 5-10 fold decrease in both [alpha]1I and [alpha]1IV collagen mRNA levels. These phenotypic changes were largely reversible. Finally, when matrigel was layered over cells on fibronectin films, [alpha]1IV collagen mRNA levels decreased, but [alpha]1I collagen mRNA levels and proliferation remained high. Thus, proliferation and [alpha]1I and [alpha]1IV collagen mRNA levels in mesangial cells, were independently regulated and depended on attachment and the nature of the adjacent matrix. 

Received 15 September 1994; accepted in final form 28 February
1995.
APS Manuscript Number C554-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 28 March 1995.