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维生素 D 缺乏性软骨中的蛋白聚糖合成:从维生素 D 缺乏状态恢复。

Proteoglycan synthesis in vitamin D-deficient cartilage: recovery from vitamin D deficiency.

作者信息

Carrino D A, Lidor C, Edelstein S, Caplan A I

机构信息

Department of Biology, Case Western Reserve University, Cleveland, Ohio 44106.

出版信息

Connect Tissue Res. 1989;19(2-4):135-47. doi: 10.3109/03008208909043894.

Abstract

Vitamin D appears to be required for mineralization of skeletal elements. There is also evidence that cartilage proteoglycans may be involved in the regulation of mineralization. Previous studies have shown an alteration in the structure of the proteoglycans of the epiphyseal growth cartilage as a result of the decrease in serum calcium related to deficiency of dietary vitamin D. Vitamin D deficiency also induces a thickening of the epiphyseal growth plate presumably because of the inhibition of maturation of the growth plate chondrocytes. In order to compare the effect on proteoglycan structure with that on growth plate morphology, the proteoglycans of healing epiphyseal cartilage were characterized. The results indicate that, consistent with previous data, in vitamin D-deficient hatching chicks, the proteoglycans of the growth cartilage, but not of the articular cartilage, are smaller in monomer size with slightly smaller chondroitin sulfate chains whose sulfation pattern is unaltered. Sternal cartilage proteoglycans are unaffected. During recovery from vitamin D deficiency, the proteoglycans isolated from the growth cartilage are still not completely normal one day after supplementation with vitamin D, but are indistinguishable from normal by four days. In addition, the results conflict with those of a previous study in which only growth cartilage of hatchling chicks, not sternal or articular cartilage, was reported to synthesize large proteoglycans. Instead, all of these cartilages in the normal chicken have been found in this study to produce large proteoglycans of a size typical for mammalian cartilage and embryonic chick cartilage.

摘要

维生素D似乎是骨骼矿化所必需的。也有证据表明软骨蛋白聚糖可能参与矿化调节。先前的研究表明,由于膳食维生素D缺乏导致血清钙降低,骺生长软骨的蛋白聚糖结构会发生改变。维生素D缺乏还会导致骺生长板增厚,这可能是因为生长板软骨细胞的成熟受到抑制。为了比较对蛋白聚糖结构和生长板形态的影响,对愈合中的骺软骨的蛋白聚糖进行了表征。结果表明,与先前的数据一致,在维生素D缺乏的刚孵出的雏鸡中,生长软骨而非关节软骨的蛋白聚糖单体尺寸较小,硫酸软骨素链略短,但其硫酸化模式未改变。胸骨软骨蛋白聚糖未受影响。在从维生素D缺乏状态恢复的过程中,补充维生素D一天后,从生长软骨中分离出的蛋白聚糖仍未完全恢复正常,但四天后与正常情况无法区分。此外,该结果与先前一项研究的结果相矛盾,在先前的研究中,据报道只有刚孵出雏鸡的生长软骨,而非胸骨或关节软骨,能合成大型蛋白聚糖。相反,在本研究中发现,正常鸡的所有这些软骨都会产生大小与哺乳动物软骨和胚胎雏鸡软骨典型大小相同的大型蛋白聚糖。

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