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基质金属蛋白酶-3中首个表皮生长因子(EGF)结构域的多种功能:分泌与内质网应激

Multiple functions of the first EGF domain in matrilin-3: Secretion and endoplasmic reticulum stress.

作者信息

Wang Yi-Chun, Liu Jing-Shi, Chen Jun-Yi, Wu Sheng-Qi, Wang Gui-Rong, Nie Jing, Zhang Shu-Kun, Guo Qu-Lian, Luo Jun-Ming

机构信息

Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

Department of Critical Care Medicine, The Affiliated Cancer Hospital of Xiangya Medical School, Central South University, Changsha, Hunan 410013, P.R. China.

出版信息

Int J Mol Med. 2015 Dec;36(6):1648-56. doi: 10.3892/ijmm.2015.2377. Epub 2015 Oct 15.

Abstract

Mutations in matrilin-3 are associated with common skeletal diseases, such as hand osteoarthritis (HOA), as well as rare chondrodysplasias, such as multiple epiphyseal dysplasia (MED) and spondyloepimetaphyseal dysplasia (SEMD). In the present study, we constructed the mutations R116W [at the von Willebrand factor, type A (vWFA) domain], T298M [at the first epidermal growth factor (EGF) domain] and C299S (at the first EGF domain), according to the mouse sequence, which are associated with human MED, HOA and SEMD, respectively, by overlap extension PCR and inserted them into an expression vector (pcDNA3.1/v5-His). We transfected these contructs into the COS-1 or MCT cells, and the results revealed that the HOA-related matrilin-3 mutation (T298M) leads to a high expression level of growth arrest DNA damage-inducible gene 153 (GADD153, also known as CHOP; an endoplasmic reticulum stress marker), as shown by western blot analysis and does not significantly affect protein secretion, as shown by immunofluorescence staining; however, osteochondroplasia, i.e., MED-related (R116W) and SEMD-related (C299S) mutations lead to both high levels of GADD153 expression and protein trafficking into the cytoplasm and form multiple vacuoles in cells, which in turn leads to insufficient protein secretion.

摘要

基质金属蛋白酶-3(matrilin-3)的突变与常见的骨骼疾病相关,如手部骨关节炎(HOA),以及罕见的软骨发育不良,如多发性骨骺发育不良(MED)和脊椎骨骺发育不良(SEMD)。在本研究中,我们根据小鼠序列构建了分别与人类MED、HOA和SEMD相关的R116W突变(位于血管性血友病因子A(vWFA)结构域)、T298M突变(位于第一个表皮生长因子(EGF)结构域)和C299S突变(位于第一个EGF结构域),通过重叠延伸PCR将它们插入表达载体(pcDNA3.1/v5-His)。我们将这些构建体转染到COS-1或MCT细胞中,结果显示,与HOA相关的基质金属蛋白酶-3突变(T298M)导致生长停滞DNA损伤诱导基因153(GADD153,也称为CHOP;一种内质网应激标志物)的高表达水平,蛋白质印迹分析表明如此,免疫荧光染色表明其对蛋白质分泌没有显著影响;然而,骨软骨发育不良,即与MED相关的(R116W)和与SEMD相关的(C299S)突变导致GADD153的高表达水平以及蛋白质转运到细胞质中并在细胞内形成多个液泡,进而导致蛋白质分泌不足。

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