Chang J, Frandsen S, Gadsby J E
Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606, USA.
Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606, USA.
Domest Anim Endocrinol. 2017 Jan;58:53-62. doi: 10.1016/j.domaniend.2016.07.001. Epub 2016 Jul 15.
The porcine corpus luteum (CL) displays delayed sensitivity to PGF-2α (luteolytic sensitivity, [LS]) until days 12 to 13 of cycle. The control of LS is unknown, but it is temporally associated with macrophage (which secrete tumor necrosis factor-α; TNF-α) infiltration into the CL. Other studies showed that TNF-α induces LS in vitro and that prostaglandins (PGs) may be involved in this mechanism. In experiment 1, PGF-2α and PGE secretion by luteal cells (LCs) was measured on days 4 to 14 of the estrous cycle, and the expression of PTGFS/AKR1B1 and PTGES/mPGES-1, determined by Western blot, before (day 7) vs after (day 13) the onset of LS. Results showed that the PGF-2α:PGE ratio increased significantly (P < 0.05) from day 4 to 13-14, and PTGFS/AKR1B1 and PTGES/mPGES-1 were significantly increased (P < 0.05) on day 13 (vs day 7). In experiment 2, LCs were collected from porcine CL at early (∼days 4-6) or mid (∼days 7-12) stages of the estrous cycle and cultured with 0, 0.1, 1, or 10 ng/mL TNF-α. Results showed that TNF-α significantly increased (P < 0.05) messenger RNA (mRNA) expression of cyclooxygenase (COX)-2 and mPGES-1 but not AKR1B1. TNF-α had no significant effects on AKR1B1 or mPGES protein abundance. TNF-α significantly increased (P < 0.05) PGE-2 but had no effect on PGF-2α secretion or on the PGF-2α:PGE2 ratio. In conclusion, although TNF-α increased COX2 and mPGES-1 mRNA, and PGE-2 secretion in vitro, it did not increase the PGF-2α:PGE2 ratio. Studies are currently directed toward exploring other pathways (eg, FP receptor signaling) by which TNF-α induces LS in the porcine CL.
猪黄体（CL）在发情周期的第12至13天之前对PGF-2α表现出延迟敏感性（黄体溶解敏感性，[LS]）。LS的调控机制尚不清楚，但它在时间上与巨噬细胞（分泌肿瘤坏死因子-α；TNF-α）浸润到黄体中有关。其他研究表明，TNF-α在体外可诱导LS，且前列腺素（PGs）可能参与此机制。在实验1中，在发情周期的第4至14天测量黄体细胞（LCs）分泌的PGF-2α和PGE，并通过蛋白质印迹法测定在LS开始前（第7天）与之后（第13天）PTGFS/AKR1B1和PTGES/mPGES-1的表达。结果显示，从第4天到第13 - 14天，PGF-2α:PGE比值显著增加（P < 0.05），并且在第13天（与第7天相比）PTGFS/AKR1B1和PTGES/mPGES-1显著增加（P < 0.05）。在实验2中，从发情周期早期（约第4 - 6天）或中期（约第7 - 12天）的猪黄体中收集LCs，并分别用0、0.1、1或10 ng/mL的TNF-α进行培养。结果显示，TNF-α显著增加（P < 0.05）环氧化酶（COX）-2和mPGES-1的信使核糖核酸（mRNA）表达，但对AKR1B1无影响。TNF-α对AKR1B1或mPGES蛋白丰度无显著影响。TNF-α显著增加（P < 0.05）PGE-2，但对PGF-2α分泌或PGF-2α:PGE2比值无影响。总之，尽管TNF-α在体外增加了COX2和mPGES-1的mRNA以及PGE-2的分泌，但并未增加PGF-2α:PGE2比值。目前的研究正致力于探索TNF-α在猪黄体中诱导LS的其他途径（例如，FP受体信号传导）。
