Effects of cyclic tensile stress on caspase-12 expression in chondrocytes
10.3969/j.issn.2095-4344.2016.29.011
- VernacularTitle:周期性张应力作用下软骨细胞半胱氨酸蛋白酶12的表达规律
- Author:
Zhuke CHEN
;
Xiaofei LI
;
Haining ZHANG
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2016;20(29):4334-4340
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Excessive mechanical stimulation can lead to endoplasmic reticulum stress. Endoplasmic reticulum stress plays an important role in the occurrence and development of degenerative diseases. Caspase-12 is a specific molecule of endoplasmic reticulum stress, and the intensity of endoplasmic reticulum stress can be reflected by caspase-12 expression. OBJECTIVE:To observe the expression rule of Caspase-12 in chondrocytes under the cyclic tensile stress. METHODS:Human chondrocytes were used as test subjects. After group assignment, mechanical loading system was used. The loading group and corresponding Z-ATAD-FMK inhibitor group received 2, 12, 24, 36, and 48 hours of mechanical stimulation. The blank group (0 hour) and the paired Z-ATAD-FMK inhibitor group received the same process as the loading group except the loading. After loading, cel morphology and growth were observed under the microscope. RT-PCR and western blot assay were used to detect the expression changes of caspase-12 gene and protein in each group. RESULTS AND CONCLUSION:(1) Morphological observation results demonstrated that apoptosis appeared at 2 hours after loading, peaked at 24 hours. With prolonged time, cel growth showed the trend along stress, but apoptosis weakened. It is indicated that cyclic tensile stress could make chondrocyte apoptosis. Endoplasmic reticulum stress might be activated. The model of cel s in vitro was established successful y. (2) Caspase-12 gene and protein expression showed consistent trend, and peaked at 24 hours, which showed significant differences as compared with the blank and inhibitor groups (P<0.05). (3) Cyclic tensile stress can induce chondrocyte endoplasmic reticulum stress, and affect caspase-12 expression.
