SRF2015 POSTER PRESENTATIONS (1) (56 abstracts)
Expression and possible role of receptor-interacting protein kinase (RIPK) 1 and 3 in the bovine CL
Takuo Hojo 1 , Anna Szostek 1 , Agnieszka Jonczyk 1 , Karolina Łukasik 1 , Katarzyna Piotrowska-Tomala 1 , Kiyoshi Okuda 2 & Dariusz Jan Skarzynski 1
1Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland; 2Graduate School of Environment and Life Science Okayama University, Okayama, Japan.
Programmed necrosis or necroptosis is an alternative form of cell death that is regulated by a caspase-independent pathway. The aim of the study was to determine if necroptosis participate in bovine CL luteolysis. In Experiment 1. the RIPK1 and RIPK3 mRNA transcription was determined in bovine i) CLs from early, developing, mid, late and regressed-stage (n=4 for each stage), ii) CLs after colpotomy collected within 0-, 2-, 4- and 12-h (each n=4) after intramuscular prostaglandin F2α (PGF) injection on Days 10–12 of oestrous cycle, iii) luteal steroidogenic (LSC) and endothelial (LEC) cells from mid luteal phase in vitro. In Experiment 2. Mid-CL-derived LSC were cultured with PGF (1.0 μM), TNF (2.3 nM) and/or interferon γ (IFNG: 2.5 nM) for 12, 24 and 48 h. Moreover, LSC were treated by TNF?IFNG with or without inhibitor for RIPKs, necrostatin-1 (Nec-1), in dose-dependent manner for 24 h. After culture, cell viability and mRNA transcription of CASP3, CASP8 were determined. RIPK1 and RIPK3 were up-regulated: i) in late and regressed CL compared to early and developing CL (P<0.05) and ii) in CL collected within 4- and 12-h after PGF injection (P<0.05). TNF in combination with IFNG increased RIPK1, but not RIPK3, expression after 24 h in LSC (P<0.05). Although high concentration of Nec-1 prevented LSC from TNF?IFNG-induced cell death (P<0.05), it didn’t affect CASP3 and CASP8 expressions. These findings suggest that RIPKs-dependent cell death can be one of potent mechanism of bovine CL regression.
Supported by the NRC grant 2013/11/D/NZ9/02685.
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