The Experts below are selected from a list of 8142 Experts worldwide ranked by ideXlab platform
Renxian Tang - One of the best experts on this subject based on the ideXlab platform.
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hiv 1 tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via pi3k akt and erk mapk pathways
Journal of Neuroinflammation, 2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying Yang, Renxian TangAbstract:HIV-associated neurocognitive disorders (HANDs) afflict more than half of HIV-1-positive individuals. The transactivator of transcription (Tat) produced by HIV virus elicits inflammatory process and is a major neurotoxic mediator that induce neuron damage during HAND pathogenesis. Activated astrocytes are important cells involved in neuroinflammation and neuronal damage. Purinergic Receptors expressed in astrocytes participate in a positive feedback loop in virus-induced neurotoxicity. Here, we investigated that whether P2Y4R, a P2Y Receptor subtype, that expressed in astrocyte participates in Tat-induced neuronal death in vitro and in vivo. Soluble Tat protein was performed to determine the expression of P2Y4R and proinflammatory cytokines in astrocytes using siRNA technique via real-time PCR, Western blot, and immunofluorescence assays. Cytometric bead array was used to measure proinflammatory cytokine release. The TUNEL staining and MTT cell viability assay were analyzed for HT22 cell apoptosis and viability, and the ApopTag® peroxidase in situ apoptosis detection kit and cresyl violet staining for apoptosis and death of hippocampal neuron in vivo. We found that Tat challenge increased the expression of P2Y4R in astrocytes. P2Y4R signaling in astrocytes was involved in Tat-induced inflammatory cytokine production via PI3K/Akt- and ERK1/2-dependent pathways. Knockdown of P2Y4R expression significantly reduced inflammatory cytokine production and relieved Tat-mediated neuronal apoptosis in vitro. Furthermore, in vivo challenged with Tat, P2Y4R knockdown mice showed decreased inflammation and neuronal damage, especially in hippocampal CA1 region. Our data provide novel insights into astrocyte-mediated neuron damage during HIV-1 infection and suggest a potential therapeutic target for HANDs.
Feng Zhou - One of the best experts on this subject based on the ideXlab platform.
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hiv 1 tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via pi3k akt and erk mapk pathways
Journal of Neuroinflammation, 2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying Yang, Renxian TangAbstract:HIV-associated neurocognitive disorders (HANDs) afflict more than half of HIV-1-positive individuals. The transactivator of transcription (Tat) produced by HIV virus elicits inflammatory process and is a major neurotoxic mediator that induce neuron damage during HAND pathogenesis. Activated astrocytes are important cells involved in neuroinflammation and neuronal damage. Purinergic Receptors expressed in astrocytes participate in a positive feedback loop in virus-induced neurotoxicity. Here, we investigated that whether P2Y4R, a P2Y Receptor subtype, that expressed in astrocyte participates in Tat-induced neuronal death in vitro and in vivo. Soluble Tat protein was performed to determine the expression of P2Y4R and proinflammatory cytokines in astrocytes using siRNA technique via real-time PCR, Western blot, and immunofluorescence assays. Cytometric bead array was used to measure proinflammatory cytokine release. The TUNEL staining and MTT cell viability assay were analyzed for HT22 cell apoptosis and viability, and the ApopTag® peroxidase in situ apoptosis detection kit and cresyl violet staining for apoptosis and death of hippocampal neuron in vivo. We found that Tat challenge increased the expression of P2Y4R in astrocytes. P2Y4R signaling in astrocytes was involved in Tat-induced inflammatory cytokine production via PI3K/Akt- and ERK1/2-dependent pathways. Knockdown of P2Y4R expression significantly reduced inflammatory cytokine production and relieved Tat-mediated neuronal apoptosis in vitro. Furthermore, in vivo challenged with Tat, P2Y4R knockdown mice showed decreased inflammation and neuronal damage, especially in hippocampal CA1 region. Our data provide novel insights into astrocyte-mediated neuron damage during HIV-1 infection and suggest a potential therapeutic target for HANDs.
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Additional file 1: of HIV-1 Tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via PI3K/Akt and ERK MAPK pathways
2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying YangAbstract:Figure S1. Distribution of GFP in CNS of mice infected by lentivirus. The lentivirus suspension of LV-sh-P2Y4R was injected into mice through the tail vein for 14 days, and then mice were sacrificed and frozen sections (15 μm) from brain tissues. GFP expression was detected under fluorescence microscope (n = 3, original amplification, × 40). Table S1. The list of primer sequences for qPCR assay. (ZIP 263 kb
Ying Yang - One of the best experts on this subject based on the ideXlab platform.
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hiv 1 tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via pi3k akt and erk mapk pathways
Journal of Neuroinflammation, 2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying Yang, Renxian TangAbstract:HIV-associated neurocognitive disorders (HANDs) afflict more than half of HIV-1-positive individuals. The transactivator of transcription (Tat) produced by HIV virus elicits inflammatory process and is a major neurotoxic mediator that induce neuron damage during HAND pathogenesis. Activated astrocytes are important cells involved in neuroinflammation and neuronal damage. Purinergic Receptors expressed in astrocytes participate in a positive feedback loop in virus-induced neurotoxicity. Here, we investigated that whether P2Y4R, a P2Y Receptor subtype, that expressed in astrocyte participates in Tat-induced neuronal death in vitro and in vivo. Soluble Tat protein was performed to determine the expression of P2Y4R and proinflammatory cytokines in astrocytes using siRNA technique via real-time PCR, Western blot, and immunofluorescence assays. Cytometric bead array was used to measure proinflammatory cytokine release. The TUNEL staining and MTT cell viability assay were analyzed for HT22 cell apoptosis and viability, and the ApopTag® peroxidase in situ apoptosis detection kit and cresyl violet staining for apoptosis and death of hippocampal neuron in vivo. We found that Tat challenge increased the expression of P2Y4R in astrocytes. P2Y4R signaling in astrocytes was involved in Tat-induced inflammatory cytokine production via PI3K/Akt- and ERK1/2-dependent pathways. Knockdown of P2Y4R expression significantly reduced inflammatory cytokine production and relieved Tat-mediated neuronal apoptosis in vitro. Furthermore, in vivo challenged with Tat, P2Y4R knockdown mice showed decreased inflammation and neuronal damage, especially in hippocampal CA1 region. Our data provide novel insights into astrocyte-mediated neuron damage during HIV-1 infection and suggest a potential therapeutic target for HANDs.
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Additional file 1: of HIV-1 Tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via PI3K/Akt and ERK MAPK pathways
2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying YangAbstract:Figure S1. Distribution of GFP in CNS of mice infected by lentivirus. The lentivirus suspension of LV-sh-P2Y4R was injected into mice through the tail vein for 14 days, and then mice were sacrificed and frozen sections (15 μm) from brain tissues. GFP expression was detected under fluorescence microscope (n = 3, original amplification, × 40). Table S1. The list of primer sequences for qPCR assay. (ZIP 263 kb
Xiaomei Liu - One of the best experts on this subject based on the ideXlab platform.
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hiv 1 tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via pi3k akt and erk mapk pathways
Journal of Neuroinflammation, 2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying Yang, Renxian TangAbstract:HIV-associated neurocognitive disorders (HANDs) afflict more than half of HIV-1-positive individuals. The transactivator of transcription (Tat) produced by HIV virus elicits inflammatory process and is a major neurotoxic mediator that induce neuron damage during HAND pathogenesis. Activated astrocytes are important cells involved in neuroinflammation and neuronal damage. Purinergic Receptors expressed in astrocytes participate in a positive feedback loop in virus-induced neurotoxicity. Here, we investigated that whether P2Y4R, a P2Y Receptor subtype, that expressed in astrocyte participates in Tat-induced neuronal death in vitro and in vivo. Soluble Tat protein was performed to determine the expression of P2Y4R and proinflammatory cytokines in astrocytes using siRNA technique via real-time PCR, Western blot, and immunofluorescence assays. Cytometric bead array was used to measure proinflammatory cytokine release. The TUNEL staining and MTT cell viability assay were analyzed for HT22 cell apoptosis and viability, and the ApopTag® peroxidase in situ apoptosis detection kit and cresyl violet staining for apoptosis and death of hippocampal neuron in vivo. We found that Tat challenge increased the expression of P2Y4R in astrocytes. P2Y4R signaling in astrocytes was involved in Tat-induced inflammatory cytokine production via PI3K/Akt- and ERK1/2-dependent pathways. Knockdown of P2Y4R expression significantly reduced inflammatory cytokine production and relieved Tat-mediated neuronal apoptosis in vitro. Furthermore, in vivo challenged with Tat, P2Y4R knockdown mice showed decreased inflammation and neuronal damage, especially in hippocampal CA1 region. Our data provide novel insights into astrocyte-mediated neuron damage during HIV-1 infection and suggest a potential therapeutic target for HANDs.
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Additional file 1: of HIV-1 Tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via PI3K/Akt and ERK MAPK pathways
2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying YangAbstract:Figure S1. Distribution of GFP in CNS of mice infected by lentivirus. The lentivirus suspension of LV-sh-P2Y4R was injected into mice through the tail vein for 14 days, and then mice were sacrificed and frozen sections (15 μm) from brain tissues. GFP expression was detected under fluorescence microscope (n = 3, original amplification, × 40). Table S1. The list of primer sequences for qPCR assay. (ZIP 263 kb
Lin Gao - One of the best experts on this subject based on the ideXlab platform.
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hiv 1 tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via pi3k akt and erk mapk pathways
Journal of Neuroinflammation, 2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying Yang, Renxian TangAbstract:HIV-associated neurocognitive disorders (HANDs) afflict more than half of HIV-1-positive individuals. The transactivator of transcription (Tat) produced by HIV virus elicits inflammatory process and is a major neurotoxic mediator that induce neuron damage during HAND pathogenesis. Activated astrocytes are important cells involved in neuroinflammation and neuronal damage. Purinergic Receptors expressed in astrocytes participate in a positive feedback loop in virus-induced neurotoxicity. Here, we investigated that whether P2Y4R, a P2Y Receptor subtype, that expressed in astrocyte participates in Tat-induced neuronal death in vitro and in vivo. Soluble Tat protein was performed to determine the expression of P2Y4R and proinflammatory cytokines in astrocytes using siRNA technique via real-time PCR, Western blot, and immunofluorescence assays. Cytometric bead array was used to measure proinflammatory cytokine release. The TUNEL staining and MTT cell viability assay were analyzed for HT22 cell apoptosis and viability, and the ApopTag® peroxidase in situ apoptosis detection kit and cresyl violet staining for apoptosis and death of hippocampal neuron in vivo. We found that Tat challenge increased the expression of P2Y4R in astrocytes. P2Y4R signaling in astrocytes was involved in Tat-induced inflammatory cytokine production via PI3K/Akt- and ERK1/2-dependent pathways. Knockdown of P2Y4R expression significantly reduced inflammatory cytokine production and relieved Tat-mediated neuronal apoptosis in vitro. Furthermore, in vivo challenged with Tat, P2Y4R knockdown mice showed decreased inflammation and neuronal damage, especially in hippocampal CA1 region. Our data provide novel insights into astrocyte-mediated neuron damage during HIV-1 infection and suggest a potential therapeutic target for HANDs.
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Additional file 1: of HIV-1 Tat enhances Purinergic P2Y4 Receptor signaling to mediate inflammatory cytokine production and neuronal damage via PI3K/Akt and ERK MAPK pathways
2019Co-Authors: Feng Zhou, Xiaomei Liu, Lin Gao, Xinxin Zhou, Qianwen Cao, Liping Niu, Jing Wang, Dongjiao Zuo, Ying YangAbstract:Figure S1. Distribution of GFP in CNS of mice infected by lentivirus. The lentivirus suspension of LV-sh-P2Y4R was injected into mice through the tail vein for 14 days, and then mice were sacrificed and frozen sections (15 μm) from brain tissues. GFP expression was detected under fluorescence microscope (n = 3, original amplification, × 40). Table S1. The list of primer sequences for qPCR assay. (ZIP 263 kb
