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肥大软骨细胞中溶酶体胞吐作用及聚集蛋白聚糖降解水解酶释放的证据,在体外用和体内。

Evidence for lysosomal exocytosis and release of aggrecan-degrading hydrolases from hypertrophic chondrocytes, in vitro and in vivo.

机构信息

University of Melbourne Department of Paediatrics and Murdoch Childrens Research Institute, Royal Children's Hospital , Flemington Road, Parkville, VIC 3052 , Australia.

出版信息

Biol Open. 2012 Apr 15;1(4):318-28. doi: 10.1242/bio.2012547. Epub 2012 Feb 10.

Abstract

The abundant proteoglycan, aggrecan, is resorbed from growth plate cartilage during endochondral bone ossification, yet mice with genetically-ablated aggrecan-degrading activity have no defects in bone formation. To account for this apparent anomaly, we propose that lysosomal hydrolases degrade extracellular, hyaluronan-bound aggrecan aggregates in growth plate cartilage, and that lysosomal hydrolases are released from hypertrophic chondrocytes into growth plate cartilage via Ca(2+)-dependent lysosomal exocytosis. In this study we confirm that hypertrophic chondrocytes release hydrolases via lysosomal exocytosis in vitro and we show in vivo evidence for lysosomal exocytosis in hypertrophic chondrocytes during skeletal development. We show that lysosome-associated membrane protein 1 (LAMP1) is detected at the cell surface following in vitro treatment of epiphyseal chondrocytes with the calcium ionophore, ionomycin. Furthermore, we show that in addition to the lysosomal exocytosis markers, cathepsin D and β-hexosaminidase, ionomycin induces release of aggrecan- and hyaluronan-degrading activity from cultured epiphyseal chondrocytes. We identify VAMP-8 and VAMP7 as v-SNARE proteins with potential roles in lysosomal exocytosis in hypertrophic chondrocytes, based on their colocalisation with LAMP1 at the cell surface in secondary ossification centers in mouse tibiae. We propose that resorbing growth plate cartilage involves release of destructive hydrolases from hypertrophic chondrocytes, via lysosomal exocytosis.

摘要

富含蛋白聚糖的聚集蛋白聚糖在软骨内骨化过程中从生长板软骨中被吸收,但基因敲除聚集蛋白聚糖降解活性的小鼠在骨形成中没有缺陷。为了解释这一明显的异常现象,我们提出溶酶体水解酶降解生长板软骨中细胞外、透明质酸结合的聚集蛋白聚糖聚集体,并且溶酶体水解酶通过 Ca(2+) 依赖性溶酶体胞吐作用从肥大软骨细胞释放到生长板软骨中。在这项研究中,我们证实肥大软骨细胞通过溶酶体胞吐作用在体外释放水解酶,并在体内显示了在骨骼发育过程中肥大软骨细胞中的溶酶体胞吐作用的证据。我们发现,在体外用钙离子载体离子霉素处理骺板软骨细胞后,溶酶体相关膜蛋白 1(LAMP1)在细胞表面被检测到。此外,我们发现除了溶酶体胞吐作用标志物组织蛋白酶 D 和 β-己糖胺酶外,离子霉素还诱导培养的骺板软骨细胞释放聚集蛋白聚糖和透明质酸降解活性。我们基于 VAMP-8 和 VAMP7 在次级骨化中心的小鼠胫骨中与 LAMP1 在细胞表面的共定位,将其鉴定为参与肥大软骨细胞溶酶体胞吐作用的 v-SNARE 蛋白,具有潜在作用。我们提出,吸收生长板软骨涉及通过溶酶体胞吐作用从肥大软骨细胞释放破坏性水解酶。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02c6/3509456/8c6b4623d35e/bio-01-04-318-f01.jpg

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