| Literature DB >> 26499313 |
Yi-Chun Wang1, Jing-Shi Liu2, Jun-Yi Chen2, Sheng-Qi Wu3, Gui-Rong Wang4, Jing Nie2, Shu-Kun Zhang5, Qu-Lian Guo1, Jun-Ming Luo5.
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.Entities:
Mesh:
Substances:
Year: 2015 PMID: 26499313 DOI: 10.3892/ijmm.2015.2377
Source DB: PubMed Journal: Int J Mol Med ISSN: 1107-3756 Impact factor: 4.101