Cytokines and mesangial cells

Kidney Int Suppl. 1993 Jan;39:S26-31.


Hyperplasia of mesangial cells (MCs) precedes or accompanies progressive glomerular scarring, as is seen in chronic glomerulonephritis and diabetic glomerulosclerosis. The mechanisms causing in vivo MC proliferation and production of extracellular matrix (ECM) are incompletely understood. Cell culture studies have demonstrated that MCs produce as well as react to various polypeptide cytokines. Thus, MCs have the potential to generate soluble mediators which can, in a paracrine fashion, attract and activate inflammatory cells (platelets, monocyte-macrophages, granulocytes), for example by IL-6, IL-8, MCP-1 and GM-CSF, and exert autocrine effects on MCs themselves, such as by promoting MC proliferation (by PDGF, IL-1, IL-6) or ECM production (by TGF-beta, IL-1). Recent in vitro results have revealed that specific non-soluble ECM components (collagen III, IV; laminin) also affect MC behavior with regard to adhesion, cell replication, ECM production as well as their response to cytokines. The latter effect appears to be mediated by alterations of cytokine receptor expression on MCs in the presence of the ECM components. "Cross-talk" between MCs, cytokines, ECM and inflammatory cells is likely to be of great importance in the regulation of the MC phenotype and may play a prominent role in the initiation and progression of glomerular inflammation. First in vivo findings in rats with experimental glomerular disease and in kidney biopsies from patients with glomerulonephritis have supported this concept by demonstrating abnormal MC expression of cytokines, their receptors and ECM proteins. These MC products may promote the recruitment and activation of inflammatory cells and perpetuate MC proliferation as well as ECM build-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Publication types

  • Review

MeSH terms

  • Animals
  • Cytokines / physiology*
  • Extracellular Matrix / physiology
  • Glomerular Mesangium / cytology*
  • Glomerular Mesangium / physiology
  • Humans
  • Interleukins / physiology
  • Kidney Diseases / etiology
  • Platelet-Derived Growth Factor / physiology
  • Receptors, Platelet-Derived Growth Factor / physiology
  • Transforming Growth Factor beta / physiology


  • Cytokines
  • Interleukins
  • Platelet-Derived Growth Factor
  • Transforming Growth Factor beta
  • Receptors, Platelet-Derived Growth Factor