Pathology of the human mesangium in situ View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1992-09

AUTHORS

R. Waldherr, S. Cuzic, I. L. Noronha

ABSTRACT

Mesangial cells play an important role in the development and progression of human glomerular disease. This article summarizes some important aspects of mesangial properties and behaviour in situ. Intrinsic mesangial cells express α-smooth muscle actin and are best characterized as myofibroblasts or glomerular pericytes. The main intergin receptor in the mesangium is the α1\1 integrin. The \2 and \3 integrins have not been detected. Mesangial cells in situ fail to react with many monoclonal antibodies which stain human mesangial cells in culture, including leukocyte activation antigens. Prominent reactions in glomerular disease are mesangial expansion and progressive glomerular sclerosis, which are preceded by or associated with mesangial cell hypertrophy and/or proliferation. Mesangial enlargement is accompanied by an altered integrin expression and an abnormal composition of extracellular mesangial matrix. From the numerous autocrine and paracrine mediators identified in vitro which stimulate or inhibit mesangial cell growth and extracellular matrix synthesis, up to now only a few factors have been shown to be present in selected human glomerulopathies. These include platelet derived growth factors and platelet derived growth factor receptor β, transforming growth factors \, interleukin 1β, tumor necrosis factor α, and interleukin 6. Further identification of such mediators in situ will improve our understanding of pathological glomerular processes, particularly with respect to the multifunctional properties of the mesangial cell. More... »

PAGES

865-874

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf00180757

DOI

http://dx.doi.org/10.1007/bf00180757

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1006817369

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/1450641


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