The Experts below are selected from a list of 90 Experts worldwide ranked by ideXlab platform

Yehong Zhuo - One of the best experts on this subject based on the ideXlab platform.

  • Elevated pressure downregulates ZO-1 expression and disrupts cytoskeleton and focal adhesion in human trabecular meshwork cells.
    Molecular vision, 2011
    Co-Authors: Xuejiao Yang, Bingqian Liu, Yujing Bai, Min Chen, Mengfei Chen, Yantao Wei, Yehong Zhuo
    Abstract:

    PURPOSE To investigate the effect of elevated hydrostatic pressure on the expression and distribution of zonula occludens-1 (ZO-1), and its effect on cytoskeleton and focal adhesion in immortal human trabecular meshwork cells (iHTM) and glaucomatous human trabecular meshwork cells (GTM(3)). METHODS iHTM and GTM(3) were exposed to 60 mmHg hydrostatic pressure for 6, 12, and 24 h. As a control, the cells were incubated simultaneously in a conventional incubator. Morphology changes were observed with an inverted microscope. The expression of ZO-1was examined with western blot, and the distribution of ZO-1 was assessed by immunofluorescence. Actin cytoskeleton and focal adhesion (vinculin) were also assessed by immunofluorescence. Data were analyzed with Commercial Data Analysis software and a p

  • Mitochondria-targeted peptide MTP-131 alleviates mitochondrial dysfunction and oxidative damage in human trabecular meshwork cells.
    Investigative ophthalmology & visual science, 2011
    Co-Authors: Min Chen, Bingqian Liu, Qianying Gao, Yehong Zhuo
    Abstract:

    PURPOSE: To investigate the antioxidative ability of a novel mitochondria-targeted peptide MTP-131 in immortalized human trabecular meshwork (iHTM) and glaucomatous human trabecular meshwork (GTM(3)) cell lines. METHODS: Cultured iHTM and GTM(3) cells were pretreated with MTP-131 for 1 hour, and sustained oxidative stress was induced by subjecting TM cells to 200 μM hydrogen peroxide (H(2)O(2)) for 24 hours. Untreated cells and cells incubated with H(2)O(2) alone were used as controls. Lactate dehydrogenase (LDH) assay was used to determine cell viability. Changes of mitochondrial membrane potential (ΔΨm) and generation of intracellular reactive oxygen species (ROS) were analyzed by flow cytometry and confocal microscopy. Activation of caspase 3 was quantified by Western blotting, and apoptosis was measured by flow cytometry. Release of cytochrome c and changes in cytoskeleton were analyzed by confocal microscopy. Data were analyzed with Commercial Data Analysis software and P < 0.05 was considered to be statistically significant. RESULTS: In both iHTM and GTM(3) cells, decrease of ΔΨm and elevation of intracellular ROS were detected after sustained oxidative stress induced by H(2)O(2). When cells were pretreated with MTP-131, the H(2)O(2)-induced mitochondrial depolarization was prevented; intracellular ROS, LDH release, and apoptosis were significantly decreased; release of cytochrome c from mitochondria to cytoplasm and activation of caspase 3 were inhibited. In addition, cytoskeleton changes caused by H(2)O(2) were also alleviated by MTP-131. CONCLUSIONS: Mitochondria-targeted peptide MTP-131 could prevent both iHTM and GTM(3) cells from sustained oxidative stress induced by H(2)O(2).

Min Chen - One of the best experts on this subject based on the ideXlab platform.

  • Elevated pressure downregulates ZO-1 expression and disrupts cytoskeleton and focal adhesion in human trabecular meshwork cells.
    Molecular vision, 2011
    Co-Authors: Xuejiao Yang, Bingqian Liu, Yujing Bai, Min Chen, Mengfei Chen, Yantao Wei, Yehong Zhuo
    Abstract:

    PURPOSE To investigate the effect of elevated hydrostatic pressure on the expression and distribution of zonula occludens-1 (ZO-1), and its effect on cytoskeleton and focal adhesion in immortal human trabecular meshwork cells (iHTM) and glaucomatous human trabecular meshwork cells (GTM(3)). METHODS iHTM and GTM(3) were exposed to 60 mmHg hydrostatic pressure for 6, 12, and 24 h. As a control, the cells were incubated simultaneously in a conventional incubator. Morphology changes were observed with an inverted microscope. The expression of ZO-1was examined with western blot, and the distribution of ZO-1 was assessed by immunofluorescence. Actin cytoskeleton and focal adhesion (vinculin) were also assessed by immunofluorescence. Data were analyzed with Commercial Data Analysis software and a p

  • Mitochondria-targeted peptide MTP-131 alleviates mitochondrial dysfunction and oxidative damage in human trabecular meshwork cells.
    Investigative ophthalmology & visual science, 2011
    Co-Authors: Min Chen, Bingqian Liu, Qianying Gao, Yehong Zhuo
    Abstract:

    PURPOSE: To investigate the antioxidative ability of a novel mitochondria-targeted peptide MTP-131 in immortalized human trabecular meshwork (iHTM) and glaucomatous human trabecular meshwork (GTM(3)) cell lines. METHODS: Cultured iHTM and GTM(3) cells were pretreated with MTP-131 for 1 hour, and sustained oxidative stress was induced by subjecting TM cells to 200 μM hydrogen peroxide (H(2)O(2)) for 24 hours. Untreated cells and cells incubated with H(2)O(2) alone were used as controls. Lactate dehydrogenase (LDH) assay was used to determine cell viability. Changes of mitochondrial membrane potential (ΔΨm) and generation of intracellular reactive oxygen species (ROS) were analyzed by flow cytometry and confocal microscopy. Activation of caspase 3 was quantified by Western blotting, and apoptosis was measured by flow cytometry. Release of cytochrome c and changes in cytoskeleton were analyzed by confocal microscopy. Data were analyzed with Commercial Data Analysis software and P < 0.05 was considered to be statistically significant. RESULTS: In both iHTM and GTM(3) cells, decrease of ΔΨm and elevation of intracellular ROS were detected after sustained oxidative stress induced by H(2)O(2). When cells were pretreated with MTP-131, the H(2)O(2)-induced mitochondrial depolarization was prevented; intracellular ROS, LDH release, and apoptosis were significantly decreased; release of cytochrome c from mitochondria to cytoplasm and activation of caspase 3 were inhibited. In addition, cytoskeleton changes caused by H(2)O(2) were also alleviated by MTP-131. CONCLUSIONS: Mitochondria-targeted peptide MTP-131 could prevent both iHTM and GTM(3) cells from sustained oxidative stress induced by H(2)O(2).

Bingqian Liu - One of the best experts on this subject based on the ideXlab platform.

  • Elevated pressure downregulates ZO-1 expression and disrupts cytoskeleton and focal adhesion in human trabecular meshwork cells.
    Molecular vision, 2011
    Co-Authors: Xuejiao Yang, Bingqian Liu, Yujing Bai, Min Chen, Mengfei Chen, Yantao Wei, Yehong Zhuo
    Abstract:

    PURPOSE To investigate the effect of elevated hydrostatic pressure on the expression and distribution of zonula occludens-1 (ZO-1), and its effect on cytoskeleton and focal adhesion in immortal human trabecular meshwork cells (iHTM) and glaucomatous human trabecular meshwork cells (GTM(3)). METHODS iHTM and GTM(3) were exposed to 60 mmHg hydrostatic pressure for 6, 12, and 24 h. As a control, the cells were incubated simultaneously in a conventional incubator. Morphology changes were observed with an inverted microscope. The expression of ZO-1was examined with western blot, and the distribution of ZO-1 was assessed by immunofluorescence. Actin cytoskeleton and focal adhesion (vinculin) were also assessed by immunofluorescence. Data were analyzed with Commercial Data Analysis software and a p

  • Mitochondria-targeted peptide MTP-131 alleviates mitochondrial dysfunction and oxidative damage in human trabecular meshwork cells.
    Investigative ophthalmology & visual science, 2011
    Co-Authors: Min Chen, Bingqian Liu, Qianying Gao, Yehong Zhuo
    Abstract:

    PURPOSE: To investigate the antioxidative ability of a novel mitochondria-targeted peptide MTP-131 in immortalized human trabecular meshwork (iHTM) and glaucomatous human trabecular meshwork (GTM(3)) cell lines. METHODS: Cultured iHTM and GTM(3) cells were pretreated with MTP-131 for 1 hour, and sustained oxidative stress was induced by subjecting TM cells to 200 μM hydrogen peroxide (H(2)O(2)) for 24 hours. Untreated cells and cells incubated with H(2)O(2) alone were used as controls. Lactate dehydrogenase (LDH) assay was used to determine cell viability. Changes of mitochondrial membrane potential (ΔΨm) and generation of intracellular reactive oxygen species (ROS) were analyzed by flow cytometry and confocal microscopy. Activation of caspase 3 was quantified by Western blotting, and apoptosis was measured by flow cytometry. Release of cytochrome c and changes in cytoskeleton were analyzed by confocal microscopy. Data were analyzed with Commercial Data Analysis software and P < 0.05 was considered to be statistically significant. RESULTS: In both iHTM and GTM(3) cells, decrease of ΔΨm and elevation of intracellular ROS were detected after sustained oxidative stress induced by H(2)O(2). When cells were pretreated with MTP-131, the H(2)O(2)-induced mitochondrial depolarization was prevented; intracellular ROS, LDH release, and apoptosis were significantly decreased; release of cytochrome c from mitochondria to cytoplasm and activation of caspase 3 were inhibited. In addition, cytoskeleton changes caused by H(2)O(2) were also alleviated by MTP-131. CONCLUSIONS: Mitochondria-targeted peptide MTP-131 could prevent both iHTM and GTM(3) cells from sustained oxidative stress induced by H(2)O(2).

Xuejiao Yang - One of the best experts on this subject based on the ideXlab platform.

  • Pannexin 1 Channels Contribute to IL-1β Expression via NLRP3/Caspase-1 Inflammasome in Aspergillus Fumigatus Keratitis
    Current eye research, 2019
    Co-Authors: Xuejiao Yang, Guiqiu Zhao, Junwei Yan, Chengye Che, Hengrui Zheng, Guoqiang Zhu, Jie Zhang
    Abstract:

    Purpose: Pannexin 1 channels are deemed to play important roles in inflammation. However, there is limited information regarding their roles in fungal infection diseases, especially fungal keratitis. This study aimed to investigate the role of pannexin 1 channels in Aspergillus fumigatus (A. fumigatus) keratitis. Materials and Methods: Mouse models or immortalized human corneal epithelial cells (HCECs) were infected with or without A. fumigatus for given time. The expression of pannexin 1 channels was tested by qPCR, western blot and immunofluorescence staining. Mice of A. fumigatus keratitis were pretreated with carbenoxolone (CBX) or 2'(3')-O-(4-Benzoylbenzoyl) adenosine-5'-triphosphate (BzATP) to block or activate the opening of pannexin 1 channels respectively. The clinical score was recorded. Cornea tissues were examined for the downstream signals of pannexin 1 channels, including NLRP3, Caspase-1 and IL-1β, and myeloperoxidase (MPO) by PCR and ELISA. Data were analyzed with Commercial Data Analysis software and a P < 0.05 was considered to be statistically significant. Results: Upon A. fumigatus infection, pannexin 1 expression increased at both the mRNA and the protein levels in mice corneas (P< 0.05, n = 3). Immunofluorescence indicated that pannexin 1 channels were mainly located in the corneal epithelial layer, and they were upregulated after A. fumigatus infection. In vitro, the same tendency was found at the mRNA and the protein levels in HCECs (P< 0.05, n = 8). In mouse model, blockage of pannexin 1 channels by CBX caused more severely keratitis. The downstream signals of pannexin 1 channels (NLRP3/Caspase-1/IL-1β) and MPO were down-regulated. Whereas activation the opening of pannexin 1 channels by BzATP reduced corneal infection with increased expression of Caspase-1 and IL-1β. Conclusions: Pannexin 1 channels play important roles in the regulation of progression and leucocytes aggregation during corneal A. fumigatus infection via the NLRP3/Caspase-1/IL-β pathway.

  • Elevated pressure downregulates ZO-1 expression and disrupts cytoskeleton and focal adhesion in human trabecular meshwork cells.
    Molecular vision, 2011
    Co-Authors: Xuejiao Yang, Bingqian Liu, Yujing Bai, Min Chen, Mengfei Chen, Yantao Wei, Yehong Zhuo
    Abstract:

    PURPOSE To investigate the effect of elevated hydrostatic pressure on the expression and distribution of zonula occludens-1 (ZO-1), and its effect on cytoskeleton and focal adhesion in immortal human trabecular meshwork cells (iHTM) and glaucomatous human trabecular meshwork cells (GTM(3)). METHODS iHTM and GTM(3) were exposed to 60 mmHg hydrostatic pressure for 6, 12, and 24 h. As a control, the cells were incubated simultaneously in a conventional incubator. Morphology changes were observed with an inverted microscope. The expression of ZO-1was examined with western blot, and the distribution of ZO-1 was assessed by immunofluorescence. Actin cytoskeleton and focal adhesion (vinculin) were also assessed by immunofluorescence. Data were analyzed with Commercial Data Analysis software and a p

Mengfei Chen - One of the best experts on this subject based on the ideXlab platform.

  • Elevated pressure downregulates ZO-1 expression and disrupts cytoskeleton and focal adhesion in human trabecular meshwork cells.
    Molecular vision, 2011
    Co-Authors: Xuejiao Yang, Bingqian Liu, Yujing Bai, Min Chen, Mengfei Chen, Yantao Wei, Yehong Zhuo
    Abstract:

    PURPOSE To investigate the effect of elevated hydrostatic pressure on the expression and distribution of zonula occludens-1 (ZO-1), and its effect on cytoskeleton and focal adhesion in immortal human trabecular meshwork cells (iHTM) and glaucomatous human trabecular meshwork cells (GTM(3)). METHODS iHTM and GTM(3) were exposed to 60 mmHg hydrostatic pressure for 6, 12, and 24 h. As a control, the cells were incubated simultaneously in a conventional incubator. Morphology changes were observed with an inverted microscope. The expression of ZO-1was examined with western blot, and the distribution of ZO-1 was assessed by immunofluorescence. Actin cytoskeleton and focal adhesion (vinculin) were also assessed by immunofluorescence. Data were analyzed with Commercial Data Analysis software and a p