Ureaplasma spp. lipid-associated membrane proteins induce human monocyte U937 cell cycle arrest through p53-independent p21 pathway

Huang, Xucheng; Qiao, Yingli; Zhou, Yixuan; Ruan, Zhi; Kong, Yingying; Li, Guoli; Xie, Xinyou; Zhang, Jun

doi:10.1016/j.ijmm.2018.07.005

Cited by 11 publications

(5 citation statements)

References 31 publications

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“…The expression of pro-inflammatory genes ( IL-1β , TNF-α , TLR2 , and TLR4 ) in bovine PBMCs increased after incubating with 0.5, 1.0, 2.0, and 4.0 µg/mL rGUDIV-103 for 2 h. However, only TNF-α and TLR4 were significantly expressed after incubating with 0.5 µg/mL rGUDIV-103 for 2 h, and TLR2 was significantly expressed after incubating with 0.5 and 1.0 µg/mL rGUDIV-103 for 6 h. In Mollicutes, cytokine production is associated with the interaction between LAMPs and TLRs [ 33 ]. TLR2 and TLR6 play important roles in signal transduction, leading to the production of pro-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

“…The roles of most of these immunogenic molecules have not yet been investigated, and identifying their functions may help elucidate the pathogenesis of Ureaplasma infections. Thirty-seven LAMPs have been described in U. diversum , and this protein group has been extensively studied in Mollicutes [ 33 , 34 , 35 ]. Heterologous expression of LAMPs derived from Mycoplasma hyopneumoniae [ 36 ], M. agalactiae [ 37 ], M. bovis [ 38 ], and other Mollicutes species has led to the development of vaccines and immunodiagnostic tests.…”

Section: Introductionmentioning

confidence: 99%

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Heterologous Expression, Purification, and Immunomodulatory Effects of Recombinant Lipoprotein GUDIV-103 Isolated from Ureaplasma diversum

et al. 2022

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Ureaplasma diversum is a bacterial pathogen that infects cattle and can cause severe inflammation of the genital and reproductive systems. Lipid-associated membrane proteins (LAMPs), including GUDIV-103, are the main virulence factors in this bacterium. In this study, we heterologously expressed recombinant GUDIV-103 (rGUDIV-103) in Escherichia coli, purified it, and evaluated its immunological reactivity and immunomodulatory effects in bovine peripheral blood mononuclear cells (PBMCs). Samples from rabbits inoculated with purified rGUDIV-103 were analysed using indirect enzyme-linked immunosorbent assay and dot blotting to confirm polyclonal antibody production and assess kinetics, respectively. The expression of this lipoprotein in field isolates was confirmed via Western blotting with anti-rGUDIV-103 serum and hydrophobic or hydrophilic proteins from 42 U. diversum strains. Moreover, the antibodies produced against the U. diversum ATCC 49783 strain recognised rGUDIV-103. The mitogenic potential of rGUDIV-103 was evaluated using a lymphoproliferation assay in 5(6)-carboxyfluorescein diacetate succinimidyl ester–labelled bovine PBMCs, where it induced lymphocyte proliferation. Quantitative polymerase chain reaction analysis revealed that the expression of interleukin-1β, toll-like receptor (TLR)-α, TLR2, TLR4, inducible nitric oxide synthase, and caspase-3–encoding genes increased more in rGUDIV-103–treated PBMCs than in untreated cells (p < 0.05). Treating PBMCs with rGUDIV-103 increased nitric oxide and hydrogen peroxide levels. The antigenic and immunogenic properties of rGUDIV-103 suggested its suitability for immunobiological application.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Heterologous Expression, Purification, and Immunomodulatory Effects of Recombinant Lipoprotein GUDIV-103 Isolated from Ureaplasma diversum

et al. 2022

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“…Previous studies have revealed that the transcription factor cellular tumor antigen p53 regulates the expression of numerous genes involved in the cell cycle and induces cell cycle arrest (8,34). p21, a general G1 phase cell cycle inhibitor, was the first p53-effector gene to be identified (35,36). In the present study, the proliferation of ESCC cells was inhibited, accompanied a decrease in cyclin D1 expression and increase in p53 and p21 expression following treatment with Cis compared with the control group.…”

Section: Discussionmentioning

confidence: 99%

Effects of cisatracurium on epithelial‑to‑mesenchymal transition in esophageal squamous cell carcinoma

Wang

Zhang

2019

Oncol Lett

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Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive types of cancer worldwide, with a poor prognosis. The aim of the present study was to investigate the effect of cisatracurium (Cis) on epithelial-to-mesenchymal transition (EMT) in ESCC and its potential mechanism of action. In the present study, Cis was used to treat ECA-109 cells, with cell proliferation measured by a Cell Counting Kit-8 assay and the expression of TGF-β and phospho-Smad2/3 detected by western blotting. TGF-β was then applied to induce EMT. Flow cytometry, wound healing and Transwell assays were used to evaluate cell proliferation, apoptosis, invasion and migration. In addition, cell cycle-related proteins, including cyclin D1, p53 and p21, and EMT-associated proteins, including E-cadherin (E-cad), N-cadherin (N-cad), Vimentin and Slug, were examined by western blot analysis. The results revealed that Cis inhibited the proliferation and promoted apoptosis of ESCC cells. Following treatment with Cis, the expression of TGF-β and phosphorylation of Smad2/3 were downregulated. Cis also suppressed cancer cell invasion and migration induced by TGF-β. In addition, the expression levels of cyclin D1 were decreased, accompanied by increased p53 and p21 expression. In addition, the expression level of E-cad was increased, whereas N-cad, Vimentin and Slug were significantly reduced. Taken together, the results of the present study revealed that exposure of ESCC cells to Cis inhibited EMT and reduced cell invasion and metastasis through the TGF-β/Smad signaling pathway.

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“…Taken together, these results suggested that LASS2 overexpression induced G0/G1 cell cycle arrest may via a p53-dependent pathway. However, p21 was also known to be regulated by p53-independent signaling pathway [ 35 , 36 ]. During the synthesis of phospho-sphingolipids, the generation of diacylglycerol and sphingosine-1-phosphate is necessary for the G1-S transition of cell cycle [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of LASS2 inhibits proliferation and causes G0/G1 cell cycle arrest in papillary thyroid cancer

et al. 2018

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BackgroundThe aim of this study was to investigate the role of LAG1 longevity-assurance homologue 2 (LASS2) in papillary thyroid cancer (PTC).MethodsImmunohistochemistry staining was conducted to explore the expression levels of LASS2 in PTC tissues and adjacent normal thyroid tissues and nodular goiter tissues. Western blotting and RT-qPCR were performed to explore the expression levels of LASS2 in three PTC cell lines (TPC-1, K1, BCPAP). An Adv-LASS2-GFP recombinant adenovirus vector was constructed and transduced into BCPAP cells. Then CCK-8 assay, colony formation assay, cell cycle distribution, and apoptosis were performed. Western blotting was used to examine the expression of p21, cyclin D1, cyclin-dependent kinase 4, p53 and p-p53.ResultsLASS2 was downregulated in PTC tissues compared with adjacent thyroid tissues or nodular goiter tissues. In addition, the expression of LASS2 was found to be associated with TNM stage and lymph node metastasis. BCPAP cells expressed the lowest LASS2 compared to TPC-1 cells or K1 cells. Overexpression of LASS2 significantly inhibited proliferation, promoted apoptosis and caused G0/G1 cell cycle arrest in BCPAP cells. Furthermore, overexpression of LASS2 significantly increased the expression of p21, inhibited the expression of cyclin D1 and cyclin-dependent kinase 4, and increased the expression of p-p53, but did not effect the expression of p53 in BCPAP cells.ConclusionOur findings indicate that overexpression of LASS2 inhibits PTC cell proliferation, promotes apoptosis and causes G0/G1 cell cycle arrest via a p53-dependent pathway. Thus, LASS2 may serve as a novel biomarker in PTC.

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Ureaplasma spp. lipid-associated membrane proteins induce human monocyte U937 cell cycle arrest through p53-independent p21 pathway

Cited by 11 publications

References 31 publications

Heterologous Expression, Purification, and Immunomodulatory Effects of Recombinant Lipoprotein GUDIV-103 Isolated from Ureaplasma diversum

Heterologous Expression, Purification, and Immunomodulatory Effects of Recombinant Lipoprotein GUDIV-103 Isolated from Ureaplasma diversum

Effects of cisatracurium on epithelial‑to‑mesenchymal transition in esophageal squamous cell carcinoma

Overexpression of LASS2 inhibits proliferation and causes G0/G1 cell cycle arrest in papillary thyroid cancer

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