Osteopontin production by cultured kidney cells.
Osteopontin production by cultured kidney cells.
复制标题
培养的肾细胞产生骨桥蛋白。
DOI：
10.1111/j.1749-6632.1995.tb44637.x
复制
发表时间：
1995
影响因子：
5.2
通讯作者：
Beshensky,AM
中科院分区：
文献类型：
--
作者：
Worcester,EM;Kleinman,JG;Beshensky,AM
One of the roles that osteopontin is felt to play is as a regulator of crystallization. This protein has been localized to sites of both physiologic and pathologic calcifications, such as renal stones and atherosclerotic plaque,'* 2 and its structure bears similarities to proteins found in other mineralized tissue, such as mollusk Its role in modulating calcium crystal formation and growth is only partly understood. One site where this activity is of particular importance is in the kidney. Osteopontin purified both from urine'and from primary cultures of mouse kidney cells6 has been found to inhibit the growth of calcium oxalate crystals in metastably supersaturated solutions. Studies of the nature of this inhibitory activity may shed light on the ability of osteopontin to modulate calcium crystallization in general. Renal stones are a common occurrence-the lifetime prevalence of stone disease is approximately 10% in men by the seventh decade7-and 70-80% of renal stones are composed primarily of calcium salts.* Stones form because urine, and renal tubular fluid in the distal portions of the nephr~ n,**~ are often supersaturated with respect to calcium oxalate (CaOx) and calcium phosphate. This results from the necessity of excreting these rather insoluble substances in small volumes of water. Supersaturation can lead to formation of crystals of these salts, which may provide the nucleus of a renal stone. However, it has long been recognized that urine also contains substances that inhibit calcification, lO, lI which may protect against the formation of crystals and stones. The tendency to form stones may be due to abnormalities that augment the level of supersaturation (such as an increased level of calcium or oxalate excretion into the urine) or ones that diminish the amount or activity of urinary inhibitors. While the fomer situation is well documented, the latter is still primarily hypothetical, largely because the urinary inhibitors of crystallization have only begun to be identified and studied in detail in the past decade. a This work was supported by the Department of Veterans Affairs Medical Research Service and by Research Grants DK41725 and R55 DK48504 from the National Institutes of Health.
