Osteopontin expression, tubulointerstitial disease, and essential hypertension.
A role has recently been proposed for the tubulointerstitium in the pathogenesis of salt-dependent essential hypertension. In this study, biopsies from patients with essential hypertension with either minimal ("benign") or severe ("decompensated") tubulointertitial injury were analyzed for the expression of osteopontin, a protein known to modulate tubulointerstitial damage and nitric oxide production. In biopsies from patients with decompensated arteriolosclerosis, osteopontin mRNA and protein were increased in tubules in association with expression of alpha-smooth muscle actin by interstitial fibroblasts and increased type IV collagen deposition. The relevance of these findings to the pathogenesis of essential hypertension is discussed.
Department of Medicine, University of Washington, Seattle, USA.
S E
SE
Thomas
D
D
Lombardi
C
C
Giachelli
A
A
Bohle
R J
RJ
Johnson
D000199:Actins / Q000032:analysis; D000328:Adult; D003094:Collagen / Q000032:analysis; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology*; D008875:Middle Aged; D053495:Osteopontin; D012333:RNA, Messenger / Q000032:analysis; D012795:Sialoglycoproteins / Q000235:genetics*
D000199:Actins; D012333:RNA, Messenger; C506895:SPP1 protein, human; D012795:Sialoglycoproteins; D053495:Osteopontin; D003094:Collagen