<i>Toxoplasma gondii</i> induces autophagy and apoptosis in human umbilical cord mesenchymal stem cells via downregulation of Mcl−1

Chu, Jiaqi; Jing, Kaipeng; Gao, Xiang; P, Li; Huang, Ri-Zhen; Niu, Yanru; Yan, Shouquan; Kong, Junchao; Yu, Caiyuan; Shi, Ge; Fan, Yi‐Ming; Lee, Young-Ha; Zhou, Yu; Quan, Juan-Hua

doi:10.1080/15384101.2017.1281484

Cited by 25 publications

(14 citation statements)

References 32 publications

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“…Subsequently, we further evaluated T. gondii-induced HTR8/SVneo cell viability, and the results showed that T. gondii infection significantly reduced cell viability, with viabilities of 82.83± 4.78%, 70.37± 7.77%, and 48.50± 3.49% observed for cells infected with T. gondii for 4, 8, and 48 hr, respectively. These findings are consistent with those of our previous study showing that GFP-RH (MOI 5) T. gondii infection of human umbilical cord mesenchymal stem cells significantly reduced viability by 21 and 30% in cells infected with T. gondii for 24 and 48 hr, respectively [18].…”

Section: Discussionsupporting

confidence: 93%

Adenosine A3 Receptor Mediates ERK1/2- and JNK-Dependent TNF-α Production in Toxoplasma gondii-Infected HTR8/SVneo Human Extravillous Trophoblast Cells

Sun

et al. 2020

Korean J Parasitol

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Toxoplasma gondii is an intracellular parasite that causes severe disease when the infection occurs during pregnancy. Adenosine is a purine nucleoside involved in numerous physiological processes; however, the role of adenosine receptors in T. gondii-induced trophoblast cell function has not been investigated until now. The goal of the present study was to evaluate the intracellular signaling pathways regulated by adenosine receptors using a HTR-8/SVneo trophoblast cell model of T. gondii infection. HTR8/SVneo human extravillous trophoblast cells were infected with or without T. gondii and then evaluated for cell morphology, intracellular proliferation of the parasite, adenosine receptor expression, TNF-α production and mitogen-activated protein (MAP) kinase signaling pathways triggered by adenosine A3 receptor (A3AR). HTR8/SVneo cells infected with T. gondii exhibited an altered cytoskeletal changes, an increased infection rate and reduced viability in an infection time-dependent manner. T. gondii significantly promoted increased TNF-α production, A3AR protein levels and p38, ERK1/2 and JNK phosphorylation compared to those observed in uninfected control cells. Moreover, the inhibition of A3AR by A3AR siRNA transfection apparently suppressed the T. gondii infection-mediated upregulation of TNF-α, A3AR production and MAPK activation. In addition, T. gondii-promoted TNF-α secretion was dramatically attenuated by pretreatment with PD098059 or SP600125. These results indicate that A3AR-mediated activation of ERK1/2 and JNK positively regulates TNF-α secretion in T. gondii-infected HTR8/SVneo cells.

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Section: Discussionsupporting

confidence: 93%

Adenosine A3 Receptor Mediates ERK1/2- and JNK-Dependent TNF-α Production in Toxoplasma gondii-Infected HTR8/SVneo Human Extravillous Trophoblast Cells

Sun

et al. 2020

Korean J Parasitol

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“…tTreg-related anti/pro apoptosis genes (Bcl-2, Bcl-xL, Mcl-1, c-myc, BAX, BID, and BAD) play a key role in cell survival 26 – 29 . Of them, Mcl-1, c-myc, BAX, and BID expression were related to cell autophagy, which is essential for cell cycle and function 30 – 32 . Therefore, we qualified these genes expression by RT-PCR.…”

Section: Resultsmentioning

confidence: 99%

miR-142-3p regulates autophagy by targeting ATG16L1 in thymic-derived regulatory T cell (tTreg)

Gao

Zhang

et al. 2018

Cell Death Dis

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Thymic-derived regulatory T cell (tTreg) clinical trials show therapeutic promise in the prevention of acute graft-versus-host disease (GVHD) in allogeneic hematopoietic stem cell transplantation patients. However, strategies are needed to improve tTreg proliferative ability and survival as a means to improve tTreg therapy and reduce the requirement for producing large numbers of Treg cells for adoptive tTreg transfer. Autophagy is a self-degradative process for cytosolic components, which is involved in cells death, differentiation, lymphocyte homeostasis, and tTreg function. Studies have shown that mice with tTreg cells that have a disrupted autophagy process have defective tTreg cell generation and function, resulting in autoimmune disease and failed GVHD prevention by adoptively transferred tTreg cells. We found the attenuated autophagy status during ex vivo expansion, which leads us to determine whether tTreg cell survival could be augmented by miR-142-3p, the miRNA which is highly expressed in tTreg cells and potentially targets autophagy-related protein (ATG)-1, ATG16L1. We demonstrate that miR-142-3p downregulates ATG16L1 mRNA and production of ATG16L1, that has been linked to autoimmune diseases. Conversely, miR-142-3p knock-down improved tTreg cell expansion, survival and function in vitro and vivo. In aggregate, these studies provide a new approach that uses miR-142-3p knockdown to increase tTreg cell efficacy by increasing ATG16L1 mRNA and protein and the autophagy process.

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“…When STs are infected, the resulting syncytial damage increases parasitic infection in the villous arms, foetal structures that are in contact with maternal blood . T. gondii infection of human umbilical cord‐derived mesenchymal stem cells induces autophagic cell death (also known as type II programmed cell death) . These reports demonstrate how T. gondii can potentially destroy placental cells and successfully cross the placental barrier to infect the foetus.…”

Section: Vertical Transmission Of Toxoplasma Gondii Infection During mentioning

confidence: 87%

Cellular immunopathogenesis in primary Toxoplasma gondii infection during pregnancy

Piao

Cheng

Aosai

et al. 2018

Parasite Immunology

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Congenital toxoplasmosis is caused by the vertical transmission of infection from mother to foetus through the placenta when a pregnant woman is infected with Toxoplasma gondii (T. gondii). Congenital infection can have serious consequences, such as intrauterine abortion, foetal death and severe neurological, ocular or other organ damage in the foetus. In this review, we focus on recent publications investigating vertical transmission of T. gondii infection, cellular immunopathogenesis and protective immunity in primary toxoplasmosis during pregnancy.

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Toxoplasma gondii induces autophagy and apoptosis in human umbilical cord mesenchymal stem cells via downregulation of Mcl−1

Cited by 25 publications

References 32 publications

Adenosine A3 Receptor Mediates ERK1/2- and JNK-Dependent TNF-α Production in Toxoplasma gondii-Infected HTR8/SVneo Human Extravillous Trophoblast Cells

Adenosine A3 Receptor Mediates ERK1/2- and JNK-Dependent TNF-α Production in Toxoplasma gondii-Infected HTR8/SVneo Human Extravillous Trophoblast Cells

miR-142-3p regulates autophagy by targeting ATG16L1 in thymic-derived regulatory T cell (tTreg)

Cellular immunopathogenesis in primary Toxoplasma gondii infection during pregnancy

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