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对凡纳滨对虾(Litopenaeus vannamei)在 WSSV 感染时乳酸脱氢酶的调控。

Regulation of lactate dehydrogenase in response to WSSV infection in the shrimp Litopenaeus vannamei.

机构信息

Centro de Investigación en Alimentación y Desarrollo (CIAD), Carretera a la Victoria KM. 0.6, Hermosillo, Sonora, C.P. 83304, Mexico.

Universidad de Sonora, Departamento de Ciencias Químico Biológicas y Agropecuarias, Universidad de Sonora Unidad Regional Sur, Lázaro Cárdenas #100, Col. Francisco Villa, Apartado Postal 85390, Navojoa, Sonora, Mexico.

出版信息

Fish Shellfish Immunol. 2018 Mar;74:401-409. doi: 10.1016/j.fsi.2018.01.011. Epub 2018 Jan 12.

DOI:10.1016/j.fsi.2018.01.011
PMID:29337249
Abstract

Lactate dehydrogenase (LDH) is key for anaerobic glycolysis. LDH is induced by the hypoxia inducible factor -1 (HIF-1). HIF-1 induces genes involved in glucose metabolism and regulates cellular oxygen homeostasis. HIF-1 is formed by a regulatory α-subunit (HIF-1α) and a constitutive β-subunit (HIF-1β). The white spot syndrome virus (WSSV) induces anaerobic glycolysis in shrimp hemocytes, associated with lactate accumulation. Although infection and lactate production are associated, the LDH role in WSSV-infected shrimp has not been examined. In this work, the effects of HIF-1 silencing on the expression of two LDH subunits (LDHvan-1 and LDHvan-2) in shrimp infected with the WSSV were studied. HIF-1α transcripts increased in gills, hepatopancreas, and muscle after WSSV infection, while HIF-1β remained constitutively expressed. The expression for both LDH subunits increased in each tissue evaluated during the WSSV infection, translating into increased enzyme activity. Glucose concentration increased in each tissue evaluated, while lactate increased in gills and hepatopancreas, but not in muscle. Silencing of HIF-1α blocked the increase of LDH expression and enzyme activity, along with glucose (all tissues) and lactate (gills and hepatopancreas) concentrations produced by WSSV infection. These results demonstrate that HIF-1 up regulates the expression of LDH subunits during WSSV infection, and that this induction contributes to substrate metabolism in energetically active tissues of infected shrimp.

摘要

乳酸脱氢酶(LDH)是无氧糖酵解的关键酶。LDH 由缺氧诱导因子-1(HIF-1)诱导。HIF-1 诱导参与葡萄糖代谢的基因,并调节细胞内氧稳态。HIF-1 由调节α亚基(HIF-1α)和组成型β亚基(HIF-1β)组成。白斑综合征病毒(WSSV)诱导虾血细胞中的无氧糖酵解,与乳酸积累有关。尽管感染和乳酸产生有关,但在 WSSV 感染的虾中 LDH 的作用尚未得到检验。在这项工作中,研究了 HIF-1 沉默对感染 WSSV 的虾中两种 LDH 亚基(LDHvan-1 和 LDHvan-2)表达的影响。WSSV 感染后,鳃、肝胰腺和肌肉中的 HIF-1α 转录本增加,而 HIF-1β 保持组成型表达。在 WSSV 感染期间,每个评估的组织中 LDH 亚基的表达均增加,导致酶活性增加。每个评估的组织中的葡萄糖浓度增加,而在鳃和肝胰腺中,但不在肌肉中,乳酸增加。HIF-1α 的沉默阻断了 WSSV 感染引起的 LDH 表达和酶活性的增加,以及葡萄糖(所有组织)和乳酸(鳃和肝胰腺)浓度的增加。这些结果表明,HIF-1 在 WSSV 感染期间上调 LDH 亚基的表达,这种诱导有助于感染虾的能量活跃组织中的底物代谢。

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