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Caspase-12 is involved in stretch-induced apoptosis mediated endoplasmic reticulum stress.

Authors: Zhang, Qiang  Liu, Jianing  Chen, Shulan  Liu, Jing  Liu, Lijuan  Liu, Guirong  Wang, Fang  Jiang, Wenxin  Zhang, Caixia  Wang, Shuangyu  Yuan, Xiao 
Citation: Zhang Q, etal., Apoptosis. 2016 Apr;21(4):432-42. doi: 10.1007/s10495-016-1217-6.
Pubmed: (View Article at PubMed) PMID:26801321
DOI: Full-text: DOI:10.1007/s10495-016-1217-6

It is well recognized that mandibular growth, which is caused by a variety of functional appliances, is considered to be the result of both neuromuscular and skeletal adaptations. Accumulating evidence has demonstrated that apoptosis plays an important role in the adaptation of skeletal muscle function. However, the underlying mechanism of apoptosis that is induced by stretch continues to be incompletely understood. Endoplasmic reticulum stress (ERS), a newly defined signaling pathway, initiates apoptosis. This study seeks to determine if caspase-12 is involved in stretch-induced apoptosis mediated endoplasmic reticulum stress in myoblast and its underlying mechanism. Apoptosis was assessed by Hochest staining, DAPI staining and annexin V binding and PI staining. ER chaperones, such as GRP78, CHOP and caspase-12, were determined by reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Furthermore, caspase-12 inhibitor was used to value the mechanism of the caspase-12 pathway. Apoptosis of myoblast, which is subjected to cyclic stretch, was observed in a time-dependent manner. We found that GRP78 mRNA and protein were significantly increased and CHOP and caspase-12 were activated in myoblast that was exposed to cyclic stretch. Caspase-12 inhibition reduced stretch-induced apoptosis, and caspase-12 activated caspase-3 to induce apoptosis. We concluded that caspase-12 played an important role in stretch-induced apoptosis that is associated by endoplasmic reticulum stress by activating caspase-3.

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RGD Object Information
RGD ID: 11571826
Created: 2016-12-21
Species: All species
Last Modified: 2016-12-21
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.