08 October 2019 : Animal Research
Tumor Necrosis Factor-α-Induced Protein 8-like 2 Downregulation Reduces CD4⁺ T Lymphocyte Apoptosis in Mice with Thermal Injury
He Huang1ABEG*, Yunliang Cui1BC, Zhaotao Tian1DF, Tanshi Li2DF, Yongming Yao3CEDOI: 10.12659/MSM.917229
Med Sci Monit 2019; 25:7547-7556
Abstract
BACKGROUND: Cellular immunity plays a crucial role in sepsis, and lymphocyte apoptosis is a key factor in immune homeostasis. Tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (TIPE2) is suggested to play a critical role in maintaining immune homeostasis. This study investigated the role of TIPE2 in CD4⁺ T lymphocyte apoptosis based on a mouse model of thermal injury.
MATERIAL AND METHODS: BALB/c male mice were randomized into 6 groups: sham, burn, burn with siTIPE2, burn with siTIPE2 control, burn with TIPE2, and burn with TIPE2 control groups. Splenic CD4⁺ T lymphocytes were collected by use of a magnetic cell sorting system.
RESULTS: We found that TIPE2 downregulation reduced the CD4⁺ T lymphocytes apoptosis in the burn with siTIPE2 group, and the protein expression of P-smad2/P-Smad3 were remarkably downregulated. In the burn with siTIPE2 group, Bcl-2 expression was increased compared with that in the sham group (P<0.05), and Bim expression was reduced (P<0.05). In the burn with TIPE2 group, the mitochondrial membrane potential was markedly reduced (P<0.01), while cytochrome C expression was clearly higher than that in the other groups (P<0.01). Activities of caspase-3, -8, and -9 were notably higher in the burn with TIPE2 group relative to those for other groups (P<0.05).
CONCLUSIONS: Downregulation of TIPE2 in vivo can reduce the apoptosis of CD4⁺ T lymphocytes following thermal damage, and activate the TGFβ downstream signaling of Smad2/Smad3, upregulating Bim, and downregulating Bcl-2.
Keywords: Burns, CD4-Positive T-Lymphocytes
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