TY - JOUR
T1 - Glomerular lesions in mice transgenic for growth hormone and insulinlike growth factor-I
T2 - I. Relationship between increased glomerular size and mesangial sclerosis
AU - Doi, Toshio
AU - Striker, Liliane J.
AU - Gibson, Carter C.
AU - Agodoa, Lawrence Y.C.
AU - Brinster, Ralph L.
AU - Striker, Gary E.
PY - 1990/9
Y1 - 1990/9
N2 - The glomeruli of mice transgenic for bovine growth hormone (GH mice) were disproportionately enlarged as a function of either kidney or body weight. Glomerular size correlated with mesangial sclerosis and the urine albumin/creatinine ratio. The glomerular lesions consisted of mesangial proliferation (4 to 5 weeks) followed by progressive mesangial sclerosis (19 weeks), resulting in complete glomerulosclerosis at 30 to 37 weeks. Albuminuria paralleled the glomerulosclerosis. In contrast, mice transgenic for insulinlike growth factor-I (IGF-I mice) did not develop glomerulosclerosis, even though glomerular size significantly increased. Glomerular hypertrophy, however, did not reach that in GH mice. These data suggest that high levels of circulating GH lead to a disproportionate increase in glomerular cellularity and volume, as well as glomerulosclerosis. This does not appear to be the result of high levels of circulating IGF-I stimulated by GH, as the serum IGF-I level in GH mice was lower than that in IG-FI mice.
AB - The glomeruli of mice transgenic for bovine growth hormone (GH mice) were disproportionately enlarged as a function of either kidney or body weight. Glomerular size correlated with mesangial sclerosis and the urine albumin/creatinine ratio. The glomerular lesions consisted of mesangial proliferation (4 to 5 weeks) followed by progressive mesangial sclerosis (19 weeks), resulting in complete glomerulosclerosis at 30 to 37 weeks. Albuminuria paralleled the glomerulosclerosis. In contrast, mice transgenic for insulinlike growth factor-I (IGF-I mice) did not develop glomerulosclerosis, even though glomerular size significantly increased. Glomerular hypertrophy, however, did not reach that in GH mice. These data suggest that high levels of circulating GH lead to a disproportionate increase in glomerular cellularity and volume, as well as glomerulosclerosis. This does not appear to be the result of high levels of circulating IGF-I stimulated by GH, as the serum IGF-I level in GH mice was lower than that in IG-FI mice.
UR - http://www.scopus.com/inward/record.url?scp=0025078918&partnerID=8YFLogxK
M3 - Article
C2 - 2399934
AN - SCOPUS:0025078918
SN - 0002-9440
VL - 137
SP - 541
EP - 552
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 3
ER -