scholarly journals YKL-40 Enhanced the Permeability of HDMECs with Histamine Through Activating Akt and p38 Pathways

2021 ◽  
Author(s):  
Peimei Zhou ◽  
Lixin Fu ◽  
Tao Chen ◽  
Lin Wang ◽  
Yonghong Lu ◽  
...  
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Mrna Level ◽  
Human Mast Cell ◽  
Microvascular Endothelial Cells ◽  
Rt Pcr ◽  
Permeability Changes ◽  
Mast Cell Line ◽  
Important Marker

Abstract Background, YKL-40 is currently considered as an important marker of endothelial dysfunction. Chronic spontaneous urticaria (CSU) is a common vascular skin disease. The increased vascular permeability play an important role in the occurrence and pathogenesis of CSU.Objective, the aim of this study is to explore the role of YKL-40 on the permeability of HDMECs.Methods, in this study, the mRNA level of YKL-40 in human mast cell line (HMC-1) were detected by RT-PCR. The effects of YKL-40 on vascular permeability, VE-cadherin release, VE-cadherin disruption in human dermal microvascular endothelial cells (HDMECs) were investigated by transwell, ELISA or immunofluorescence. The phosphorylation of VE-cadherin, p38 and Akt, in histamine plus YKL-40 treated HDMECs were detected by Western Blot.Results, we found that YKL-40 significantly promoted the permeability changes and leaded to the released, disruption of VE-cadherin in HDMECs induced by histamine. Furthermore, YKL-40 also enhanced the Akt and p38 pathways. Conclusion, we suggest that YKL-40 may serve as pro-permeability cytokines, and play a role in the pathogenesis of CSU. This study will help to further elucidate the pathogenesis of CSU and provide a new target for the development of anti-histamine resistance drugs for CSU.

scholarly journals Interleukin-35 inhibited production of histamine and pro-inflammatory cytokines through suppression MAPKs pathway in HMC-1 cells

2020 ◽  
Author(s):  
Tao Chen ◽  
Lixin Fu ◽  
Qiaomei Sun ◽  
Peimei Zhou ◽  
Zai-pei Guo
Keyword(s):  
Immune Response ◽  
Inflammatory Cytokine ◽  
Human Mast Cell ◽  
Rt Pcr ◽  
Effector Cells ◽  
Response System ◽  
Mast Cell Line ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Abstract Background: IL-35 is a newly anti-inflammatory cytokine which belong to the IL-12 family. Mast cells, as one of the major effector cells in the immune response system, play important roles in the pathogenesis of chronic spontaneous urticarial (CSU). The aim of our study is to explore the inhibited role of IL-35 in HMC-1. Methods: The effects of IL-35 on cell proliferation, cytokine expression and histamine release in human mast cell line (HMC­1) were investigated by CCK8, ELISA or RT-PCR. The phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells were detected by Western Blot.Results: We found that IL-35 significantly inhibited the proliferation of HMC-1 cells stimulated by PMA and A23187. IL-35 also down-regulates the released of histamine and the mRNA expression of IL-6 and IL-17 in activated HMC-1. Furthermore, IL-35 markedly inhibited the phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells. Conclusions: This study provides first observations on the inhibitory and anti-inflammtory effect of IL-35 on activated HMC-1 cells. We suggest that IL35 may play an inhibited role in the pathogenesis of CSU.

scholarly journals Interleukin-35 inhibited the production of histamine and pro-inflammatory cytokines through suppression MAPKs pathway in HMC-1 cells

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Li-xin Fu ◽  
Tao Chen ◽  
Qiao-mei Sun ◽  
Pei-mei Zhou ◽  
Zai-pei Guo
Keyword(s):  
Human Mast Cell ◽  
Rt Pcr ◽  
Effector Cells ◽  
Response System ◽  
Anti Inflammatory ◽  
Mast Cell Line ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

Abstract Background IL-35 is a newly anti-inflammatory cytokine that belongs to the IL-12 family. Mast cells, as one of the major effector cells in the immune response system, plays an important role in the pathogenesis of chronic spontaneous urticarial (CSU). Our study aims to explore the inhibited role of IL-35 in HMC-1. Methods The effects of IL-35 on cell proliferation, cytokine expression, and histamine release in a human mast cell line (HMC­1) were investigated by CCK8, ELISA, or RT-PCR. The phosphorylation levels of ERK1/2, p38, and JNK1/2, in PMA plus A23187 induced HMC-1 cells was detected by Western Blot. Results We found that IL-35 significantly inhibited the proliferation of HMC-1 cells stimulated by PMA and A23187. IL-35 also down-regulates the release of histamine and the mRNA expression of IL-6 and IL-17 in activated HMC-1. Furthermore, IL-35 markedly inhibited the phosphorylation levels of ERK1/2, p38, and JNK1/2, in PMA plus A23187 induced HMC-1 cells. Conclusions This study provides the first observations on the inhibitory and anti-inflammatory effect of IL-35 in activated HMC-1 cells. We suggest that IL35 may play an inhibited role in the pathogenesis of CSU.

scholarly journals Interleukin-35 inhibited production of histamine and pro-inflammatory cytokines through suppression MAPKs pathway in HMC-1 cells

2020 ◽  
Author(s):  
Lixin Fu ◽  
Tao Chen ◽  
Qiaomei Sun ◽  
Peimei Zhou ◽  
Zai-pei Guo
Keyword(s):  
Immune Response ◽  
Inflammatory Cytokine ◽  
Human Mast Cell ◽  
Rt Pcr ◽  
Effector Cells ◽  
Response System ◽  
Mast Cell Line ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Abstract Background: IL-35 is a newly anti-inflammatory cytokine which belong to the IL-12 family. Mast cells, as one of the major effector cells in the immune response system, play important roles in the pathogenesis of chronic spontaneous urticarial (CSU). The aim of our study is to explore the inhibited role of IL-35 in HMC-1. Methods: The effects of IL-35 on cell proliferation, cytokine expression and histamine release in human mast cell line (HMC­1) were investigated by CCK8, ELISA or RT-PCR. The phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells were detected by Western Blot.Results: We found that IL-35 significantly inhibited the proliferation of HMC-1 cells stimulated by PMA and A23187. IL-35 also down-regulates the released of histamine and the mRNA expression of IL-6 and IL-17 in activated HMC-1. Furthermore, IL-35 markedly inhibited the phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells. Conclusions: This study provides first observations on the inhibitory and anti-inflammtory effect of IL-35 on activated HMC-1 cells. We suggest that IL35 may play an inhibited role in the pathogenesis of CSU.

scholarly journals VEGF Is Involved in the Increase of Dermal Microvascular Permeability Induced by Tryptase

2012 ◽  
Vol 2012 ◽  
pp. 1-8
Author(s):  
Qianming Bai ◽  
Xiaobo Li ◽  
Xinhong Wang ◽  
Yali Xu ◽  
Li Wang ◽  
...  
Keyword(s):  
Mast Cell ◽  
Vascular Permeability ◽  
Serine Proteases ◽  
Biological Activities ◽  
Critical Role ◽  
Rt Pcr ◽  
Protein Levels ◽  
Permeability Enhancement ◽  
Catalytic Inhibitor

Tryptases are predominantly mast cell-specific serine proteases with pleiotropic biological activities and play a critical role in skin allergic reactions, which are manifested with rapid edema and increases of vascular permeability. The exact mechanisms of mast cell tryptase promoting vascular permeability, however, are unclear and, therefore, we investigated the effect and mechanism of tryptase or human mast cells (HMC-1) supernatant on the permeability of human dermal microvascular endothelial cells (HDMECs). Both tryptase and HMC-1 supernatant increased permeability of HDMECs significantly, which was resisted by tryptase inhibitor APC366 and partially reversed by anti-VEGF antibody and SU5614 (catalytic inhibitor of VEGFR). Furthermore, addition of tryptase to HDMECs caused a significant increase of mRNA and protein levels of VEGF and its receptors (Flt-1 and Flk-1) by Real-time RT-PCR and Western blot, respectively. These results strongly suggest an important role of VEGF on the permeability enhancement induced by tryptase, which may lead to novel means of controlling allergic reaction in skin.

scholarly journals Interleukin-35 inhibited production of histamine and pro-inflammatory cytokines through suppression MAPKs pathway in HMC-1 cells

2021 ◽  
Author(s):  
Lixin Fu ◽  
Tao Chen ◽  
Qiaomei Sun ◽  
Peimei Zhou ◽  
Zai-pei Guo
Keyword(s):  
Immune Response ◽  
Inflammatory Cytokine ◽  
Human Mast Cell ◽  
Rt Pcr ◽  
Effector Cells ◽  
Response System ◽  
Mast Cell Line ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Abstract Background: IL-35 is a newly anti-inflammatory cytokine which belong to the IL-12 family. Mast cells, as one of the major effector cells in the immune response system, play important roles in the pathogenesis of chronic spontaneous urticarial (CSU). The aim of our study is to explore the inhibited role of IL-35 in HMC-1.Methods: The effects of IL-35 on cell proliferation, cytokine expression and histamine release in human mast cell line (HMC­1) were investigated by CCK8, ELISA or RT-PCR. The phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells were detected by Western Blot.Results: We found that IL-35 significantly inhibited the proliferation of HMC-1 cells stimulated by PMA and A23187. IL-35 also down-regulates the released of histamine and the mRNA expression of IL-6 and IL-17 in activated HMC-1. Furthermore, IL-35 markedly inhibited the phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells.Conclusions: This study provides first observations on the inhibitory and anti-inflammtory effect of IL-35 on activated HMC-1 cells. We suggest that IL35 may play an inhibited role in the pathogenesis of CSU.

scholarly journals Transcriptional complexity of the HSPG2 gene in the human mast cell line, HMC-1

2014 ◽  
Vol 35 ◽  
pp. 123-131 ◽  
Author(s):  
Megan S. Lord ◽  
MoonSun Jung ◽  
Bill Cheng ◽  
John M. Whitelock
Keyword(s):  
Mast Cell ◽  
Cell Line ◽  
Human Mast Cell ◽  
Mast Cell Line

scholarly journals Cordyceps Militaris Alleviates Severity of Murine Acute Lung Injury Through miRNAs-Mediated CXCR2 Inhibition

2015 ◽  
Vol 36 (5) ◽  
pp. 2003-2011 ◽  
Author(s):  
Sheng Liu ◽  
Jian Tang ◽  
Lei Huang ◽  
Qirong Xu ◽  
Xiang Ling ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Distress Syndrome ◽  
Mrna Level ◽  
Cordyceps Militaris ◽  
Microvascular Endothelial Cells ◽  
Mouse Lung ◽  
Therapeutic Effects ◽  
Beneficial Effects

Background/Aims: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are lethal diseases in humans, and the current treatments have limited therapeutic effects. Cordyceps militaris (CM) is a caterpillar-grown traditional medicinal mushroom, and has been used as a natural invigorant for longevity, endurance, and vitality in China. Recently, purified extracts from CM have been shown to have beneficial effects on various diseases including cancer. Nevertheless, a role of CM in ALI has not been examined previously. Methods: Here, we used a bleomycin-induced ALI model to study the effects of CM on the severity of ALI in mice. The levels of CXCR2, a receptor for Interleukin 8 (IL-8) in pulmonary microvascular endothelial cells, were examined in different experimental groups. The levels of microRNA (miR)-1321 and miR-3188 were also examined in lung samples and in CM. Adeno-associated viruses carrying miR-1321 and miR-3188 were injected into bleomycin-treated mice for evaluation their effects on the severity of ALI. Results: CM treatment significantly alleviated the severity of bleomycin-induced ALI in mice. The increases in lung CXCR2 by bleomycin were significantly reduced by CM at protein level, but not at mRNA level. CM contained high levels of 2 miRNAs (miR-1321 and miR-3188) that target 3'-UTR of CXCR2 mRNA to inhibit its expression. Overexpression of miR-1321 and miR-3188 in mouse lung through AAV-mediated gene therapy mimicked the effects of CM. Conclusion: CM may alleviate severity of murine ALI through miRNAs-mediated CXCR2 inhibition.

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