胆固醇分子和PI3K/Akt及MAPK/ERK1/2信号通路在牛疱疹病毒1型感染MDBK细胞中的作用研究
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摘要
牛疱疹病毒1型(Bovine herpesvirus type1, BoHV-1)是牛传染性鼻气管炎病(Infectious bovine rhinotracheitis, IBR)的病原体,该病毒感染主要引起呼吸道,消化道,生殖道,眼结膜和神经等多组织、器官的炎症；由该病毒感染引起呼吸道上皮细胞的坏死和免疫抑制导致继发曼氏溶血杆菌和睡眠嗜血杆菌感染的发生而致高死亡率,以及由于生殖道感染而导致的流产对奶牛养殖业造成巨大损失潜伏感染是本病毒重要特点,感染后该病毒在神经节和扁桃体内潜伏感染使患牛终生带毒而成为重要传染源,在应激或免疫力下降时病毒被激活而发病,该病在世界各地广泛分布已经给养牛业带来巨大经济损失。
病毒感染靶细胞的过程中需要一些重要细胞分子的帮助才能完成复制周期,同时病毒与细胞相互作用的过程中可能会激活或抑制细胞的某些重要的信号传导通路,因此开展相应的基础研究寻找BoHV-1感染MDBK细胞的过程中涉及的关键分子和信号通路,对于揭示病毒与细胞相互作用的关系,从而解析该病毒的感染机理,甚至对于新药物的研发设计都具有重要意义。
Lipid rafts是大量分布于细胞膜上具有多种生物学功能的特定结构,主要由胆固醇、糖苷鞘磷脂、鞘磷脂和磷脂等成分紧密结合有序排列而构成：该结构稳定存在于脂质双层细胞膜上,主要参与跨膜运输、胞吞和胞吐过程中蛋白质的分选,细胞粘附和迁移,细胞凋亡,突触传递,细胞骨架的组织等多种生物学功能。最近研究发现Lipid rafts与多种病原微生物的感染有关,而胆固醇作为该结构的重要成分是否参与了BoHV-1感染MDBK细胞的过程值得探索并深入研究。
胆固醇分子是Lipid rafts的主要成分,通过研究胆固醇可以锚定研究Lipidrafts的功能,Methyl-β-cyclodextrin (MβCD)能够有效去除细胞胆固醇分子,可以用于Lipid rafts功能研究。本研究发现采用MβCD处理MDBK细胞可以有效的降低细胞胆固醇含量,同时能够显著抑制病毒的复制,且该抑制作用具有剂量依赖性,MβCD处理的MDBK细胞经外源水溶性胆固醇分子恢复处理后,可以部分回复病毒的复制功能,使病毒滴度增加,这表明细胞胆固醇分子的部分去除是造成该病毒滴度下降主要原因,进一步研究发现在病毒感染侵入后的阶段去除胆固醇分子对病毒的滴度影响不显著,胆固醇分子的去除并不影响病毒与MDBK细胞的结合。从病毒方面因素来考虑,采用MβCD处理病毒而降低囊膜胆固醇分子的含量也能导致病毒感染力下降,当补加外源性胆固醇分子时该抑制效应可以被部分抵消,可见胆固醇分子对于病毒的感染力具有重要作用。综上研究结果表明细胞膜胆固醇分子对于BoHV-1侵入靶细胞具有重要作用,而病毒囊膜胆固醇分子对于该病毒的感染力具有重要意义,这为深入研究该病毒致病机理打下基础。由于Lipid rafts内含有多种分子参与了细胞相关信号传导,我们推测胆固醇分子的去除,破坏了一些信号分子发挥作用的环境,导致病毒侵入的某些环节被阻断,鉴于目前BoHV-1感染的过程中激活了那些信号通路尚未见相关报道,所以该推论需要研究证实。
Phosphatidylinositol3-kinases/Akt (PI3K/Akt)信号通路是执行多种生物学功能的信号调控系统,即在PI3K的调节下Akt通过调节多种蛋白分子的活性来执行PI3K调控的多种生理学反应,如细胞存活和细胞增殖,血管生成,代谢调控和细胞迁移等。丝裂原激活的蛋白激酶(Mitogen-activated protein kinase, MAPK)超家族能够将接受的多种刺激信号跨膜传递到细胞核执行相应的生物学功能,细胞外信号调节激酶1和2(Extracellular signal-regulated kinases1and2, Erkl/2)作为MAPK超家族的成员参与调节多种细胞生物学功能如细胞增殖、细胞转化、细胞分化、细胞存活和死亡等过程。BoHV-1感染MDBK细胞的过程中是否需要该PI3K/Akt和MAPK/Erk1/2信号通路的参与尚不清楚。
本研究发现BoHV-1感染MDBK细胞的过程中能够激活Akt和Erk1/2,包括感染的早期短暂激活和晚期持续性激活,且经紫外线灭活的病毒仍然能够在感染的早期激活Akt和Erk1/2而不能在晚期激活Akt和Erkl/2,表明病毒与细胞结合和/侵入的过程中能够激活Akt和Erk1/2,后期Akt和Erk1/2的持续性激活与病毒基因表达的过程有关；病毒诱导的Akt激活可以被PI3K抑制剂Ly294002特异性阻断,病毒诱导的Erkl/2激活可以被MAPK激酶(MAPK kinase, MEK1/2)的抑制剂U0126所抑制,这表明Akt和Erk1/2的上游激活子分别是PI3K和MEK1/2。此外用Akt的抑制剂Ly294002处理MDBK细胞导致病毒滴度下降1.5log,表明PI3K的激活对于病毒的复制具有重要意义,而MEK1/2的抑制剂处理细胞后病毒滴度无明显变化,表明抑制MAPK/Erk1/2信号通路不影响病毒的复制；进一步研究发现PI3K的激活对于该病毒的复制周期中侵入后阶段影响显著,尽管病毒与细胞结合即可激活该PI3K/Akt信号通路,但是抑制PI3K的活性并不影响病毒与细胞的结合,同样在侵入阶段抑制PI3K的活性对于该病毒的复制影响不显著；本研究首次阐明在BoHV-1感染MDBK细胞的过程中能够激活PI3K/Akt和MAPK/Erk1/2两个信号通路,特别是PI3K的激活对于病毒复制周期的侵入后阶段具有重要意义。
Lipid rafts形成一个疏水性微环境,可能是多种分子相互作用的位点和场所,我们前期的研究发现胆固醇分子参与BoHV-1感染MDBK细胞的侵入过程,而在该病毒侵入和/结合靶细胞的过程中又能激活PI3K/Akt和MAPK/Erk1/2两个信号通路,但是该信号通路的早期激活过程是否受胆固醇分子的影响并不清楚,本试验发现降低细胞表面胆固醇含量对该病毒诱导的PI3K/Akt和MAPK/Erkl/2早期激活影响不显著。
本研究首次阐明在BoHV-1感染MDBK细胞的过程中需要细胞胆固醇分子的参与才能有效的完成侵入过程,在感染的早期和晚期都能激活PI3K/Akt和MAPK/Erk14/2两个信号通路,且PI3K/Akt通路的激活对于该病毒复制具有重要意义,而细胞表面胆固醇含量的降低对该病毒诱导的PI3K/Akt和MAPK/Erk1/2早期激活影响不显著。
Bovine herpesvirus-1(BoHV-1) is an important pathogen of cattle, which mainly causes severe respiratory disease. Also it is responsible for several other infections, such us conjunctivitis, genital lesion, abortion, enteritis and encephalitis. Inflammation and cell necrosis and death of respiratory epithelia, and immunosuppression caused by the virus infection often predispose cattle to secondary or opportunistic infections in particular Mannheimia haemolytica and Haemophilus somnus, which results in enhanced morbidity and mortality. Abortions caused by the virus infection of the genital tract results in significant economic loss in the cow industry worldwide. Infection with herpesviruses is commonly characterized by the ability to establish latent infection, mainly in ganglion cells and tonsils. Once infected, the virus persists for life and may be re-activated at intervals if the host is subjected to stress or immunosuppression, for example by dexamethasone treatment. The continuous circulation of the virus among the bovine population is the cause of serious economic losses for the cattle industry worldwide.
For the virus successful infection of susceptible cells, series of cellular molecules must be involved for the facility of a complete life cycle. And during the cause of the virus-cell interactions, some cellular signaling pathways were involved. Thus, it is of great significance to investigate the virus infection-associated cellular molecules andsingnaling pathways, for the dissecting of virus replication mechanism. Above basic research on virus-cell interaction could also contribute to the pharmacology development, for providing some target molecule for the novel medicine design. Lipid rafts, specific membrane microdomains enriched in cholesterol,(glyco)sphingolipids and phospholipids, which tightly packaged and ordered, are known to be involved in the regulation of various biological phenomena, including membrane transport protein sorting during endocytosis and exocytosis, cell adhesion, migration, cell apoptosis, synaptic transmission and organization of the cytoskeleton et al. Accumulating evidence suggests that many pathogens require Lipid rafts at multiple stages of their life cycles. However, as an important component of Lipid raft, the role of cholesterol in the life cycle of BoHV-1infection of Madin-Darby bovine kidney (MDBK) cells remains unknown, thus it deserves extensive investigation.
Cholesterol is an important component of membrane Lipid raft, by the surveys of its role for the virus infection will contribute to understand the function of Lipid raft in the virus infection. Methyl-β-cyclodextrin (MβCD) is an effective reagent to sequester cell membrane cholesterol and was used for this research. Here, we examined the role of cholesterol for both viral envelope and target cell membrane for BoHV-1infection. Cholesterol depletion by pretreatment of MDBK cells with MβCD, inhibited the production of BoHV-1in a dose-dependent manner. This inhibitory effect was partially reversed by cholesterol replenishment, indicating that the reduction was caused by cholesterol depletion. Cholesterol depletion at the stage only had a mild effect on the virus production. However, cell membrane cholesterol depletion did not reduce the virus attachment. In addition, treatment of BoHV-1particles with MβCD also reduced the virus infectivity significantly and the effect was partially reversed by addition of exogenous cholesterol. Taken together, these data implicated that cell membrane cholesterol mainly contributed to BoHV-1entry into MDBK cells and the viral envelope cholesterol was also essential for the virus infectivity. Why Lipid raft is associated with the virus entry process is not known. We hypothesis that some molecules in the Lipid raft is associated with some cellular signal transductions as well some process of the virus entry. However, as to the information of cellular signaling pathways involved in BoHV-1infectin of into MDBK cells is not known.
Phosphatidylinositol3-kinases (PI3K) PI3K/Akt is an important signaling pathway which executes series of biological function. A number of molecules are directly or indirectly regulated by Akt, to carry out PI3K-regulated responses such as cell survival, growth, proliferation, angiogenesis, metabolism, and migration. The members of mitogen-activated protein kinase (MAPK) superfamily respond to diverse cellular stimuli through transducing signals from the cell membrane to the nucleus. Extracellular signal-regulated kinases1and2(Erkl/2) is a member of MAPK family, which regulate a wide range of cellular functions including cell proliferation, transformation, differentiation, cell survival and death. So far it is not clear whether PI3K/Akt and MAPK/Erkl/2signaling pathways are involved in the process of BoHV-linfection of MDBK cells.
This study indicated that infection of MDBK cells with BoHV-1induced an early-stage transient and a late-stage sustained activation of both PI3K/Akt and MAPK/Erkl/2signaling pathways. Analysis with the stimulation of UV-irradiated virus indicated that the virus binding and/or entry process was enough to trigger the early phase activations, while the late phase activations were viral protein expression dependent. Biphasic activation of both pathways was suppressed by the selective and potent inhibitors Ly294002for PI3K and U0126for MAPK kinase (MEK1/2), respectively. Furthermore, treatment of MDBK cells with Ly294002caused a1.5-log reduction in virus titer, while U0126had little effect on the virus production. And the inhibition effect mainly occurred at the post-entry stage of the virus replication cycle. This was the first time to reveal that BoHV-1actively induced both PI3K/Akt and MAPK/Erkl/2signaling pathways, and the activation of PI3K was important for fully efficient replication, especially for the post-entry stage.
In previous study, we reported that cholesterol-rich Lipid raft is involved in the life cycle of BoHV-1infection of MDBK cells, especially for the virus entry process. During the virus binding and/or entry process, both PI3K/Akt and MAPK/Erkl/2signaling pathways are activated. But whether Lipid raft was involved in the virus induced signaling stimulation process was not clear. The following experiments revealed that cholesterol depletion had a minor influence on the virus triggered signaling pathways.
Taken together, here for the first time experimental data revealed that cholesterol was required for the virus effective infection of MDBK cells at the entry stage, and it induced an early-stage transient and a late-stage sustained activation of both PI3K/Akt and MAPK/Erkl/2signaling pathway. The activation of PI3K/Akt signaling is of great significance for the virus replication especially at the post-entry stage. In addition, the depletion of cellular cholesterol had minor effect on the virus induced PI3K/Akt and MAPK/Erkl/2signaling pathways activation.
病毒感染靶细胞的过程中需要一些重要细胞分子的帮助才能完成复制周期,同时病毒与细胞相互作用的过程中可能会激活或抑制细胞的某些重要的信号传导通路,因此开展相应的基础研究寻找BoHV-1感染MDBK细胞的过程中涉及的关键分子和信号通路,对于揭示病毒与细胞相互作用的关系,从而解析该病毒的感染机理,甚至对于新药物的研发设计都具有重要意义。
Lipid rafts是大量分布于细胞膜上具有多种生物学功能的特定结构,主要由胆固醇、糖苷鞘磷脂、鞘磷脂和磷脂等成分紧密结合有序排列而构成：该结构稳定存在于脂质双层细胞膜上,主要参与跨膜运输、胞吞和胞吐过程中蛋白质的分选,细胞粘附和迁移,细胞凋亡,突触传递,细胞骨架的组织等多种生物学功能。最近研究发现Lipid rafts与多种病原微生物的感染有关,而胆固醇作为该结构的重要成分是否参与了BoHV-1感染MDBK细胞的过程值得探索并深入研究。
胆固醇分子是Lipid rafts的主要成分,通过研究胆固醇可以锚定研究Lipidrafts的功能,Methyl-β-cyclodextrin (MβCD)能够有效去除细胞胆固醇分子,可以用于Lipid rafts功能研究。本研究发现采用MβCD处理MDBK细胞可以有效的降低细胞胆固醇含量,同时能够显著抑制病毒的复制,且该抑制作用具有剂量依赖性,MβCD处理的MDBK细胞经外源水溶性胆固醇分子恢复处理后,可以部分回复病毒的复制功能,使病毒滴度增加,这表明细胞胆固醇分子的部分去除是造成该病毒滴度下降主要原因,进一步研究发现在病毒感染侵入后的阶段去除胆固醇分子对病毒的滴度影响不显著,胆固醇分子的去除并不影响病毒与MDBK细胞的结合。从病毒方面因素来考虑,采用MβCD处理病毒而降低囊膜胆固醇分子的含量也能导致病毒感染力下降,当补加外源性胆固醇分子时该抑制效应可以被部分抵消,可见胆固醇分子对于病毒的感染力具有重要作用。综上研究结果表明细胞膜胆固醇分子对于BoHV-1侵入靶细胞具有重要作用,而病毒囊膜胆固醇分子对于该病毒的感染力具有重要意义,这为深入研究该病毒致病机理打下基础。由于Lipid rafts内含有多种分子参与了细胞相关信号传导,我们推测胆固醇分子的去除,破坏了一些信号分子发挥作用的环境,导致病毒侵入的某些环节被阻断,鉴于目前BoHV-1感染的过程中激活了那些信号通路尚未见相关报道,所以该推论需要研究证实。
Phosphatidylinositol3-kinases/Akt (PI3K/Akt)信号通路是执行多种生物学功能的信号调控系统,即在PI3K的调节下Akt通过调节多种蛋白分子的活性来执行PI3K调控的多种生理学反应,如细胞存活和细胞增殖,血管生成,代谢调控和细胞迁移等。丝裂原激活的蛋白激酶(Mitogen-activated protein kinase, MAPK)超家族能够将接受的多种刺激信号跨膜传递到细胞核执行相应的生物学功能,细胞外信号调节激酶1和2(Extracellular signal-regulated kinases1and2, Erkl/2)作为MAPK超家族的成员参与调节多种细胞生物学功能如细胞增殖、细胞转化、细胞分化、细胞存活和死亡等过程。BoHV-1感染MDBK细胞的过程中是否需要该PI3K/Akt和MAPK/Erk1/2信号通路的参与尚不清楚。
本研究发现BoHV-1感染MDBK细胞的过程中能够激活Akt和Erk1/2,包括感染的早期短暂激活和晚期持续性激活,且经紫外线灭活的病毒仍然能够在感染的早期激活Akt和Erk1/2而不能在晚期激活Akt和Erkl/2,表明病毒与细胞结合和/侵入的过程中能够激活Akt和Erk1/2,后期Akt和Erk1/2的持续性激活与病毒基因表达的过程有关；病毒诱导的Akt激活可以被PI3K抑制剂Ly294002特异性阻断,病毒诱导的Erkl/2激活可以被MAPK激酶(MAPK kinase, MEK1/2)的抑制剂U0126所抑制,这表明Akt和Erk1/2的上游激活子分别是PI3K和MEK1/2。此外用Akt的抑制剂Ly294002处理MDBK细胞导致病毒滴度下降1.5log,表明PI3K的激活对于病毒的复制具有重要意义,而MEK1/2的抑制剂处理细胞后病毒滴度无明显变化,表明抑制MAPK/Erk1/2信号通路不影响病毒的复制；进一步研究发现PI3K的激活对于该病毒的复制周期中侵入后阶段影响显著,尽管病毒与细胞结合即可激活该PI3K/Akt信号通路,但是抑制PI3K的活性并不影响病毒与细胞的结合,同样在侵入阶段抑制PI3K的活性对于该病毒的复制影响不显著；本研究首次阐明在BoHV-1感染MDBK细胞的过程中能够激活PI3K/Akt和MAPK/Erk1/2两个信号通路,特别是PI3K的激活对于病毒复制周期的侵入后阶段具有重要意义。
Lipid rafts形成一个疏水性微环境,可能是多种分子相互作用的位点和场所,我们前期的研究发现胆固醇分子参与BoHV-1感染MDBK细胞的侵入过程,而在该病毒侵入和/结合靶细胞的过程中又能激活PI3K/Akt和MAPK/Erk1/2两个信号通路,但是该信号通路的早期激活过程是否受胆固醇分子的影响并不清楚,本试验发现降低细胞表面胆固醇含量对该病毒诱导的PI3K/Akt和MAPK/Erkl/2早期激活影响不显著。
本研究首次阐明在BoHV-1感染MDBK细胞的过程中需要细胞胆固醇分子的参与才能有效的完成侵入过程,在感染的早期和晚期都能激活PI3K/Akt和MAPK/Erk14/2两个信号通路,且PI3K/Akt通路的激活对于该病毒复制具有重要意义,而细胞表面胆固醇含量的降低对该病毒诱导的PI3K/Akt和MAPK/Erk1/2早期激活影响不显著。
Bovine herpesvirus-1(BoHV-1) is an important pathogen of cattle, which mainly causes severe respiratory disease. Also it is responsible for several other infections, such us conjunctivitis, genital lesion, abortion, enteritis and encephalitis. Inflammation and cell necrosis and death of respiratory epithelia, and immunosuppression caused by the virus infection often predispose cattle to secondary or opportunistic infections in particular Mannheimia haemolytica and Haemophilus somnus, which results in enhanced morbidity and mortality. Abortions caused by the virus infection of the genital tract results in significant economic loss in the cow industry worldwide. Infection with herpesviruses is commonly characterized by the ability to establish latent infection, mainly in ganglion cells and tonsils. Once infected, the virus persists for life and may be re-activated at intervals if the host is subjected to stress or immunosuppression, for example by dexamethasone treatment. The continuous circulation of the virus among the bovine population is the cause of serious economic losses for the cattle industry worldwide.
For the virus successful infection of susceptible cells, series of cellular molecules must be involved for the facility of a complete life cycle. And during the cause of the virus-cell interactions, some cellular signaling pathways were involved. Thus, it is of great significance to investigate the virus infection-associated cellular molecules andsingnaling pathways, for the dissecting of virus replication mechanism. Above basic research on virus-cell interaction could also contribute to the pharmacology development, for providing some target molecule for the novel medicine design. Lipid rafts, specific membrane microdomains enriched in cholesterol,(glyco)sphingolipids and phospholipids, which tightly packaged and ordered, are known to be involved in the regulation of various biological phenomena, including membrane transport protein sorting during endocytosis and exocytosis, cell adhesion, migration, cell apoptosis, synaptic transmission and organization of the cytoskeleton et al. Accumulating evidence suggests that many pathogens require Lipid rafts at multiple stages of their life cycles. However, as an important component of Lipid raft, the role of cholesterol in the life cycle of BoHV-1infection of Madin-Darby bovine kidney (MDBK) cells remains unknown, thus it deserves extensive investigation.
Cholesterol is an important component of membrane Lipid raft, by the surveys of its role for the virus infection will contribute to understand the function of Lipid raft in the virus infection. Methyl-β-cyclodextrin (MβCD) is an effective reagent to sequester cell membrane cholesterol and was used for this research. Here, we examined the role of cholesterol for both viral envelope and target cell membrane for BoHV-1infection. Cholesterol depletion by pretreatment of MDBK cells with MβCD, inhibited the production of BoHV-1in a dose-dependent manner. This inhibitory effect was partially reversed by cholesterol replenishment, indicating that the reduction was caused by cholesterol depletion. Cholesterol depletion at the stage only had a mild effect on the virus production. However, cell membrane cholesterol depletion did not reduce the virus attachment. In addition, treatment of BoHV-1particles with MβCD also reduced the virus infectivity significantly and the effect was partially reversed by addition of exogenous cholesterol. Taken together, these data implicated that cell membrane cholesterol mainly contributed to BoHV-1entry into MDBK cells and the viral envelope cholesterol was also essential for the virus infectivity. Why Lipid raft is associated with the virus entry process is not known. We hypothesis that some molecules in the Lipid raft is associated with some cellular signal transductions as well some process of the virus entry. However, as to the information of cellular signaling pathways involved in BoHV-1infectin of into MDBK cells is not known.
Phosphatidylinositol3-kinases (PI3K) PI3K/Akt is an important signaling pathway which executes series of biological function. A number of molecules are directly or indirectly regulated by Akt, to carry out PI3K-regulated responses such as cell survival, growth, proliferation, angiogenesis, metabolism, and migration. The members of mitogen-activated protein kinase (MAPK) superfamily respond to diverse cellular stimuli through transducing signals from the cell membrane to the nucleus. Extracellular signal-regulated kinases1and2(Erkl/2) is a member of MAPK family, which regulate a wide range of cellular functions including cell proliferation, transformation, differentiation, cell survival and death. So far it is not clear whether PI3K/Akt and MAPK/Erkl/2signaling pathways are involved in the process of BoHV-linfection of MDBK cells.
This study indicated that infection of MDBK cells with BoHV-1induced an early-stage transient and a late-stage sustained activation of both PI3K/Akt and MAPK/Erkl/2signaling pathways. Analysis with the stimulation of UV-irradiated virus indicated that the virus binding and/or entry process was enough to trigger the early phase activations, while the late phase activations were viral protein expression dependent. Biphasic activation of both pathways was suppressed by the selective and potent inhibitors Ly294002for PI3K and U0126for MAPK kinase (MEK1/2), respectively. Furthermore, treatment of MDBK cells with Ly294002caused a1.5-log reduction in virus titer, while U0126had little effect on the virus production. And the inhibition effect mainly occurred at the post-entry stage of the virus replication cycle. This was the first time to reveal that BoHV-1actively induced both PI3K/Akt and MAPK/Erkl/2signaling pathways, and the activation of PI3K was important for fully efficient replication, especially for the post-entry stage.
In previous study, we reported that cholesterol-rich Lipid raft is involved in the life cycle of BoHV-1infection of MDBK cells, especially for the virus entry process. During the virus binding and/or entry process, both PI3K/Akt and MAPK/Erkl/2signaling pathways are activated. But whether Lipid raft was involved in the virus induced signaling stimulation process was not clear. The following experiments revealed that cholesterol depletion had a minor influence on the virus triggered signaling pathways.
Taken together, here for the first time experimental data revealed that cholesterol was required for the virus effective infection of MDBK cells at the entry stage, and it induced an early-stage transient and a late-stage sustained activation of both PI3K/Akt and MAPK/Erkl/2signaling pathway. The activation of PI3K/Akt signaling is of great significance for the virus replication especially at the post-entry stage. In addition, the depletion of cellular cholesterol had minor effect on the virus induced PI3K/Akt and MAPK/Erkl/2signaling pathways activation.
引文
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