Abstract
It is now 60 years since Zimmerman's classic paper appeared describing the concept of the mesangium as a structural entity consisting of both cells and extracellular matrix that occupies the centrilobular region of the glomerular tuft [1]. The normal mesangium is now considered to possess two principal cell populations: the mesangial cell that represents the predominant type and a resident bone marrow-derived phagocytic cell that appears capable of a variety of immunological functions. On the basis of information gleaned from the study of renal biopsies by immunohistochemistry together with information from several models of renal disease, it is likely that both these intrinsic cells play an important role in the initiation and progression of glomerular injury. These studies, however, have in the main been of a descriptive nature, documenting the changes in the number of mesangial cells, the amount of the surrounding matrix and the infiltration of leukocytes. More recently the use of tissue culture as a model system to study the mesangial cell has allowed new insights into the function of this cell, and in certain cases has permitted speculation as to possible mechanisms that contribute to the pathogenesis of renal disease. Thus in vitro several studies have provided information about the response of mesangial cells to co-culture with macrophages and exposure to soluble mediators including cytokines and growth factors, vasoactive peptides, lipids, immune complexes and glucose in an attempt to shed light on glomerular diseases such as IgA nephropathy, membranoproliferative glomerulonephritis and diabetic nephropathy in which mesangial cell proliferation and or expansion of the mesangial matrix are commonly observed.
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