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转化生长因子β1对不同关节组织焦磷酸盐生成影响的比较。

A comparison of the effect of transforming growth factor beta 1 on pyrophosphate elaboration from various articular tissues.

作者信息

Rosenthal A K, McCarty B A, Cheung H S, Ryan L M

机构信息

Department of Medicine, Medical College of Wisconsin, Milwaukee.

出版信息

Arthritis Rheum. 1993 Apr;36(4):539-42. doi: 10.1002/art.1780360415.

Abstract

OBJECTIVE

The purpose of this study was to determine the effect of transforming growth factor beta 1 (TGF beta 1) on inorganic pyrophosphate (PPi) elaboration from articular tissues to better understand the pathophysiology of calcium pyrophosphate dihydrate (CPPD) crystal deposition in the joint.

METHODS

PPi was measured in the media of adult porcine articular tissue in organ culture and monolayer cultures.

RESULTS

TGF beta 1 strongly stimulated PPi elaboration by porcine fibrocartilage and hyaline cartilage. It modestly increased PPi elaboration by ligament, and had no effect on PPi elaborated by synovium. Of all cell types tested in cell culture, only chondrocytes responded to TGF beta 1 by significantly increasing PPi elaboration.

CONCLUSION

TGF beta 1 stimulates PPi elaboration from hyaline cartilage, fibrocartilage, and ligament, indicating that there is in situ CPPD crystal formation in these tissues. The ability of tissues to respond to TGF beta 1 by increasing PPi elaboration correlates with the prevalence of CPPD crystal deposition found clinically. The unique response of chondrocyte monolayers to TGF beta 1 reinforces the key role of the chondrocyte in PPi elaboration in the joint. These findings support an etiologic role for responsiveness to TGF beta 1 in CPPD disease.

摘要

目的

本研究旨在确定转化生长因子β1(TGFβ1)对关节组织无机焦磷酸盐(PPi)生成的影响,以更好地理解二水焦磷酸钙(CPPD)晶体在关节中沉积的病理生理学。

方法

在器官培养和单层培养的成年猪关节组织培养基中测量PPi。

结果

TGFβ1强烈刺激猪纤维软骨和透明软骨生成PPi。它适度增加韧带生成PPi,对滑膜生成PPi没有影响。在细胞培养中测试的所有细胞类型中,只有软骨细胞对TGFβ1有反应,显著增加PPi生成。

结论

TGFβ1刺激透明软骨、纤维软骨和韧带生成PPi,表明这些组织中存在原位CPPD晶体形成。组织通过增加PPi生成对TGFβ1作出反应的能力与临床上发现的CPPD晶体沉积患病率相关。软骨细胞单层对TGFβ1的独特反应强化了软骨细胞在关节PPi生成中的关键作用。这些发现支持了对TGFβ1的反应性在CPPD疾病中的病因学作用。

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