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猪子宫内膜热休克蛋白在着床期受妊娠状态、热应激和阿尔特诺雌酮补充的影响存在差异。

Porcine endometrial heat shock proteins are differentially influenced by pregnancy status, heat stress, and altrenogest supplementation during the peri-implantation period.

机构信息

Department of Animal Science, Iowa State University, Ames, IA 50011, USA.

出版信息

J Anim Sci. 2022 Jul 1;100(7). doi: 10.1093/jas/skac129.

DOI:10.1093/jas/skac129
PMID:35772767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9246672/
Abstract

Heat stress (HS) deleteriously affects multiple components of porcine reproduction and is causal to seasonal infertility. Environment-induced hyperthermia causes a HS response (HSR) typically characterized by increased abundance of intracellular heat shock proteins (HSP). Gilts exposed to HS during the peri-implantation period have compromised embryo survival, however if (or how) HS disrupts the porcine endometrium is not understood. Study objectives were to evaluate the endometrial HSP abundance in response to HS during this period and assess the effect of oral progestin (altrenogest; ALT) supplementation. Postpubertal gilts (n = 42) were artificially inseminated during behavioral estrus (n = 28) or were kept cyclic (n = 14), and randomly assigned to thermal neutral (TN; 21 ± 1 °C) or diurnal HS (35 ± 1 °C for 12 h/31.6 ± 1 °C for 12 h) conditions from day 3 to 12 postestrus (dpe). Seven of the inseminated gilts from each thermal treatment group received ALT (15 mg/d) during this period. Using quantitative PCR, transcript abundance of HSP family A (Hsp70) member 1A (HSPA1A, P = 0.001) and member 6 (HSPA6, P < 0.001), and HSP family B (small) member 8 (HSB8, P = 0.001) were increased while HSP family D (Hsp60) member 1 (HSPD1, P = 0.01) was decreased in the endometrium of pregnant gilts compared to the cyclic gilts. Protein abundance of HSPA1A decreased (P = 0.03) in pregnant gilt endometrium due to HS, while HSP family B (small) member 1 (HSPB1) increased (P = 0.01) due to HS. Oral ALT supplementation during HS reduced the transcript abundance of HSP90α family class B member 1 (HSP90AB1, P = 0.04); but HS increased HSP90AB1 (P = 0.001), HSPA1A (P = 0.02), and HSPA6 (P = 0.04) transcript abundance irrespective of ALT. ALT supplementation decreased HSP90α family class A member 1 (HSP90AA1, P = 0.001) protein abundance, irrespective of thermal environment, whereas ALT only decreased HSPA6 (P = 0.02) protein abundance in TN gilts. These results indicate a notable shift of HSP in the porcine endometrium during the peri-implantation period in response to pregnancy status and heat stress.

摘要

热应激(HS)对猪繁殖的多个环节都有不良影响,是季节性不孕的主要原因。环境引起的过热会导致 HS 反应(HSR),其特征通常是细胞内热休克蛋白(HSP)的丰度增加。在着床期暴露于 HS 的母猪胚胎存活率降低,但是 HS 如何破坏猪的子宫内膜尚不清楚。本研究的目的是评估该时期 HS 对内源性 HSP 丰度的影响,并评估口服孕激素(阿尔特诺雌酮;ALT)补充的效果。(发情)后(postpubertal)小母猪(n = 42)在行为发情时进行人工授精(n = 28)或保持周期性发情(n = 14),并随机分配到热中性(TN;21 ± 1°C)或昼夜 HS(35 ± 1°C 12 小时/31.6 ± 1°C 12 小时)条件下,从发情后 3 天到 12 天(dpe)。每个热处理组的 7 只授精小母猪在此期间接受 ALT(15mg/d)治疗。通过定量 PCR,与周期性发情的小母猪相比,妊娠小母猪的 HSP 家族 A(Hsp70)成员 1A(HSPA1A,P = 0.001)和成员 6(HSPA6,P < 0.001)和 HSP 家族 B(小)成员 8(HSB8,P = 0.001)的转录丰度增加,而 HSP 家族 D(Hsp60)成员 1(HSPD1,P = 0.01)的转录丰度降低。HS 导致妊娠小母猪的子宫内膜中 HSPA1A 蛋白丰度降低(P = 0.03),而 HSP 家族 B(小)成员 1(HSPB1)则因 HS 而增加(P = 0.01)。HS 期间口服 ALT 补充降低了 HSP90α 家族 B 类成员 1(HSP90AB1,P = 0.04)的转录丰度;但 HS 增加了 HSP90AB1(P = 0.001)、HSPA1A(P = 0.02)和 HSPA6(P = 0.04)的转录丰度,无论 ALT 补充与否。无论热环境如何,ALT 补充均降低 HSP90α 家族 A 成员 1(HSP90AA1,P = 0.001)的蛋白丰度,而 ALT 仅降低 TN 小母猪的 HSPA6(P = 0.02)蛋白丰度。这些结果表明,在着床期,猪子宫内膜中的 HSP 发生了显著变化,以应对妊娠状态和热应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/b48ab3fff871/skac129_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/722c3f5e3b26/skac129_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/1e245639ae12/skac129_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/58ab8c5b713d/skac129_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/7dea4618abc3/skac129_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/3c4a133ed635/skac129_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/b48ab3fff871/skac129_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/722c3f5e3b26/skac129_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/1e245639ae12/skac129_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/58ab8c5b713d/skac129_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/7dea4618abc3/skac129_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/3c4a133ed635/skac129_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3697/9246672/b48ab3fff871/skac129_fig6.jpg

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