热应激(HS)几乎损害了畜牧业的各个方面,包括繁殖。在猪中,这种传染性被称为季节性不孕症(SI),包括卵巢功能障碍的表型。在多个物种中,已经描述了HS诱导的高催乳素血症;因此,我们的研究目的是表征和比较HS对青春期后后备母猪发情周期卵泡期(FOL)或黄体期循环催乳素(PRL)和卵巢Janus激酶/信号转导子和转录激活因子(JAK-STAT)信号传导的影响.小母猪使用altrenogest同步发情,并且在altrenogest戒断后立即开始环境处理。对于FOL研究:青春期后后备母猪被分配到恒定的热中性(TN;n=6;20±1.2°C)或周期性HS(n=6;25至32±1.2°C)条件下5天。通过颈静脉穿刺收集血液用于在第5天在FOL中以及在第0天和第12天在LUT小母猪中进行PRL定量。分别在第5天和第12天从安乐死的FOL和LUT后备母猪获得卵巢和黄体(CL)。进行蛋白质印迹以定量催乳素受体(PRLR)和JAK/STAT途径蛋白丰度。在FOL阶段,热组之间的循环PRL无差异(P=0.20).HS对PRLR无影响(P≥0.34),信号转导和转录激活因子3(STAT3),信号转导和转录激活因子5α(STAT5α),和磷酸化信号转导和转录激活因子α/β酪氨酸694/699(pSTAT5α/βTyr694/699)丰度和Janus激酶2(JAK2),磷酸化janus激酶2酪氨酸1007/1008(pJAK2Tyr1007/1008),STAT1,磷酸化信号转导和转录激活因子1酪氨酸701(pSTAT1Tyr701),磷酸化信号转导和转录激活因子1丝氨酸727(pSTAT1Ser727),在FOL小卵巢中检测不到磷酸化的信号转导和转录激活剂3酪氨酸705(pSTAT3Tyr705)。通过HS,FOL后备母猪的卵巢pSTAT5α/βTyr694/699丰度趋于适度增加(4%;P=0.07)。在LUT阶段,循环PRL从2dpe逐渐增加到12dpe,但没有观察到热处理引起的差异(P=0.37)。HS对PRLR的CL丰度没有影响(P≥0.16),pJAK2Tyr1007/1008,JAK2,STAT1,pSTAT1Tyr701,pSTAT1Ser727,pSTAT3Tyr705,STAT5α,或pSTAT5α/βTyr694/699。在LUT阶段,HS增加了CLSTAT3丰度(11%;P<0.03)。HS(P≥0.76)对LUT后备母猪中pJAK2Tyr1007/1008和pSTAT5α/βTyr694/699的水平没有影响;然而,由于HS,CLpSTAT3Tyr705:STAT3比率趋于降低(P=0.10)。这些结果表明HS诱导的发情周期对卵巢JAK/STAT途径的依赖作用,确立该信号通路作为SI的潜在贡献者的潜在作用。
热应激(HS)对猪的繁殖产生负面影响,尽管不了解确切的机制。这项研究确定了HS是否在发情周期的两个阶段影响卵巢中的JAK-STAT信号通路:卵泡和黄体。而循环催乳素激素水平不变,卵巢JAK-STAT信号的某些方面发生了变化,这可能与HS期间猪引起的不育症有关。
Heat stress (HS) compromises almost every aspect of animal agriculture including reproduction. In pigs, this infecundity is referred to as seasonal infertility (SI), a phenotype including ovarian dysfunction. In multiple species, HS-induced hyperprolactinemia has been described; hence, our study objectives were to characterize and compare HS effects on circulating prolactin (PRL) and ovarian Janus kinase/signal transducer and activator of transcription (JAK-STAT) signaling during the follicular (FOL) or luteal (LUT) phases of the estrous cycle in postpubertal gilts. Gilts were estrus synchronized using altrenogest and environmental treatments began immediately after altrenogest withdrawal. For the FOL study: postpubertal gilts were allocated to constant thermoneutral (TN; n = 6; 20 ± 1.2 °C) or cyclical HS (n = 6; 25 to 32 ± 1.2 °C) conditions for 5 d. In the LUT study: postpubertal gilts were assigned to either TN (n = 7; 20 ± 2.6 °C) or cyclical HS (n = 7; 32 to 35 ± 2.6 °C) conditions from 2 to 12 days postestrus (dpe). Blood was collected by jugular venipuncture for PRL quantification on day 5 in the FOL and on day 0 and day 12 in the LUT gilts. Ovaries and corpora lutea (CL) were obtained from euthanized FOL and LUT gilts on day 5 and day 12, respectively. Western blotting was performed to quantify prolactin receptor (PRLR) and JAK/STAT pathway protein abundance. In the FOL phase, no difference (P = 0.20) in circulating PRL between thermal groups was observed. There was no effect (P ≥ 0.34) of HS on PRLR, signal transducer and activator of transcription 3 (STAT3), signal transducer and activator of transcription 5α (STAT5α), and phosphorylated signal transducer and activator of transcription α/β tyrosine 694/699 (pSTAT5α/βTyr694/699) abundance and Janus kinase 2 (JAK2), phosphorylated janus kinase 2 tyrosine 1007/1008 (pJAK2Tyr1007/1008), STAT1, phosphorylated signal transducer and activator of transcription 1 tyrosine 701 (pSTAT1Tyr701), phosphorylated signal transducer and activator of transcription 1 serine 727 (pSTAT1Ser727), and phosphorylated signal transducer and activator of transcription 3 tyrosine 705 (pSTAT3Tyr705) were undetectable in FOL gilt ovaries. Ovarian pSTAT5α/βTyr694/699 abundance tended to moderately increase (4%; P = 0.07) in FOL gilts by HS. In the LUT phase, circulating PRL increased progressively from 2 to 12 dpe, but no thermal treatment-induced difference (P = 0.37) was noted. There was no effect (P ≥ 0.16) of HS on CL abundance of PRLR, pJAK2Tyr1007/1008, JAK2, STAT1, pSTAT1Tyr701, pSTAT1Ser727, pSTAT3Tyr705, STAT5α, or pSTAT5α/βTyr694/699. In LUT phase, CL STAT3 abundance was increased (11%; P < 0.03) by HS. There was no impact of HS (P ≥ 0.76) on levels of pJAK2Tyr1007/1008 and pSTAT5α/βTyr694/699 in LUT gilts; however, the CL pSTAT3Tyr705:STAT3 ratio tended to be decreased (P = 0.10) due to HS. These results indicate an HS-induced estrous cycle-stage-dependent effect on the ovarian JAK/STAT pathway, establishing a potential role for this signaling pathway as a potential contributor to SI.
Heat stress (HS) negatively affects reproduction in pigs, though the precise mechanisms are not understood. This study determined if HS impacts the JAK-STAT signaling pathway in the ovary during two stages of the estrous cycle: follicular and luteal. While circulating prolactin hormone level was unchanged, there were changes to some aspects of ovarian JAK-STAT signaling that could be involved in infertility induced in pigs during HS.