| Recently, many studies indicate that SOCS2plays an important role in body development and growth, CNS regulation, metabolic regulation, cancer, the development of skeleton and the differentiation of muscle.The imbalance of SOCS2could lead to cardiovascular disease, insulin resistance, cancer, serious infection diseases and so on. Therefore, the study of SOCS2is very necessary and important to human health and disease. Researches hasve shown the expression of mitochondrial biogenesis gene PGC-la, which is a key regulator mitochondrial biosynthesis, has increased in skeletal muscle in SOCS2knockout mice, PGC-la is a key regulator mitochondrial biosynthesis.Mitochondria regulates energy metabolism and ATP generation in many tissues such as brain, skeletal muscle, cardiac muscle, liver, adipose and nervous system, especially in the muscle and adipose tissue which need much more energy. The main function of mitochondria is to convert the products of carbohydrates, protein and fat metabolism to CO2and water. Mitochondria play an important regulatory role in many diseases, such as obesity, diabetes, cancer, neurological degenerative diseases, aging and cardiomyopathy.In order to study the function of SOCS2on mitochondria, the over-expression and interference vector of SOCS2were used to transfect C2C12and3T3-L1cells and induced cells differentiation. We analyze the effects of SOCS2on myotube formation of C2C12cells, fat deposition of3T3-L1cells, the expression of mitochondria development related genes, oxidative respiration factors. Preliminary discuss the effects of SOCS2on mitochondrial function. The main results were summarized as following:1. Over-expression of SOCS2in C2C12cells inhibited the myogenic differentiation of murine skeletal muscle C2C12cells, the expression of MyHC decreased, while interference SOCS2increased C2C12myotube formation, and the expression of MyHC increased; 2. Results of Bodipy dye indicates over-expression of SOCS2in3T3-L1cells could inhibit fat deposition, lipid droplet decreased, while interference of SOCS2increased lipid droplet;3. In C2C12cells,over-expression of SOCS2inhibited the expression of mitochondria development, oxidative respiration related genes, PGC1α, NRF-1, MDH, CPT-1, COX2, increased the expression of Cytc, while interference SOCS2increased the expression of PGC-1α, NRF-1, MDH, CPT-1, COX2(P<0.01), and decreased the expression of Cytc. However, the expression of UCP1has no change (P>0.05); While in3T3-Llcells, over-expression and interference of SOCS2, the tendency were the same as inC2C12cells except MDH gene, which increased with interference treatment and decreased after over-expression.(P<0.05);4. Western blotting indicted that over-expression SOCS2decreased the protein expression of PGC-1α, MDH, CPT-1(P<0.05), while interference SOCS2increased the expression of PGC-1α (P<0.05), MDH (P<0.01), CPT-1(P<0.01); While in3T3-Llcells,the expression of these proteins has been significantly decreased(P<0.01) and increased(P<0.01) in SOCS2over-expression and interference groups respectively;5. Over-expression of SOCS2decreased the mitochondrial membrane potential with JC-1dyeing, while interference SOCS2increased it;6. Cell immunofluorescence, Real-time PCR and Western blotting indicate that over-expression SOCS2increased the expression of Cytc (P<0.01), interference SOCS2has the opposite effect (P<0.05) in C2C12cells, while the expression of Cytc has significantly increased and decreased in3T3-L1cells after treatment with over-expression and interference of SOCS2, the expression of Cytc has significantly increased and decreasd respectively (P<0.01);Above all, the results indicate that SOCS2can regulate myotube formation,fat deposition, mitochondria development, fatty acid oxidation,oxidative respiratory. We come to the conclusion that SOCS2affect the mitochondrial function. |
