Titre du document / Document title

Insulin-like growth factor-1 stimulates production of mesangial cell matrix components

Auteur(s) / Author(s)

SCHREIBER B. D. ; HUGHES M. L. ; GROGGEL G. C. ;

Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

Univ. Vermont coll. medicine, dep. medicine, Burlington VT, ETATS-UNIS

Résumé / Abstract

Diabetic nephropathy is characterized by mesangial cell proliferation and expansion of the mesangial matrix. Insulin-like growth factor-I (IGF-I) ) increases in the kidney early in experimental diabetes. The effect of IGF-I on mesangial cell proliferation and synthesis of extracellular matrix (ECM) proteins was examined to test the hypothesis that IGF- I stimulates mesangial cells to synthesize ECM proteins. ECM proteins were measured by immunoprecipitation after metabolic labeling of rat mesangial cells in culture. IGF-I caused a 2.4-fold increase in mesangial cell proliferation as measured by ³H-thymidine incorporation. IGF-I caused an increase in cellular laminin, fibronectin and type IV collagen, 46.8 ± 15.4%, 31.3 ± 11.4%, and 27.7 ± 12.6%. increase respectively compared to control cells. IGF-I did not effect cellular type I collagen, decrease of 8.2 ± 8.7%. There was a trend toward increased total protein synthesis by IGF-I, 36.5 ± 2.5%. In summary, IGF-I stimulates ECM component production by mesangial cells. Thus, IGF-I has the capacity to mediate the histologic changes characteristic of diabetic nephropathy.

Revue / Journal Title

Clinical nephrology   ISSN 0301-0430   CODEN CLNHBI 

Source / Source

1995, vol. 43, n^o6, pp. 368-374 (1 p.)

Langue / Language

Anglais

Editeur / Publisher

Dustri, München-Deisenhofen, ALLEMAGNE  (1973) (Revue)

Mots-clés anglais / English Keywords

Diabetes mellitus ; Etiopathogenesis ; Animal ; Cell culture ; Secretion ; Insulin ; Rat ; Growth factor ; Nephropathy ; Mesangial cell ; Urinary system disease ; Renal disease ; Endocrinopathy ; Rodentia ; Mammalia ; Vertebrata ;

Mots-clés français / French Keywords

Diabète ; Etiopathogénie ; Animal ; Culture cellulaire ; Sécrétion ; Insuline ; Rat ; Facteur croissance ; Néphropathie ; Cellule mésangiale ; Appareil urinaire pathologie ; Rein pathologie ; Endocrinopathie ; Rodentia ; Mammalia ; Vertebrata ;

Mots-clés espagnols / Spanish Keywords

Diabetes ; Etiopatogenia ; Animal ; Cultivo celular ; Secreción ; Insulina ; Rata ; Factor crecimiento ; Nefropatía ; Célula mesangial ; Aparato urinario patología ; Riñón patología ; Endocrinopatía ; Rodentia ; Mammalia ; Vertebrata ;

Localisation / Location

INIST-CNRS, Cote INIST : 16768, 35400005123550.0030