Activation of MAPK Is Required for ROS Generation and Exocytosis in HMC-1 Cells Induced by &lt;i&gt;Trichomonas vaginalis&lt;/i&gt;-Derived Secretory Products

Narantsogt, Giimaa; Min, Arim; Nam, Young Hee; Lee, Young Ah; Kim, Kyeong Ah; Agvaandaram, Gurbadam; Dorjsuren, Temuulen; El-Benna, Jamel; Shin, Myoung-Ho

doi:10.3347/kjp.2015.53.5.597

Cited by 6 publications

(5 citation statements)

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“…Surprising, this study showed that NF- κ B nuclear translocation occurred at 1 h transiently in T. vaginalis -treated SiHa cells and then declined at 4 h posttreatment. Narantsogt et al [ 21 ] also demonstrated that NF- κ B translocation occurs within 1 h of T. vaginalis adhesion and translocation drops dramatically by 8 h postadhesion. Considering the host-parasite relationship, early activation of NF- κ B nuclear translocation may be related to the protection from apoptotic cell death by T. vaginalis ; subsequently, T. vaginalis inhibits NF- κ B activity and leads to apoptosis in SiHa cells as a results of failure of NF- κ B p50 : p65 heterodimers to translocate to the nucleus.…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports have shown that dioscin (a natural product) and casticin (one of the main components of Fructus viticis ) induce apoptosis of HeLa and SiHa cells by promoting ROS-mediated DNA damage and the mitochondrial signaling pathway [ 19 , 20 ]. Activation of MAPK is required for ROS generation and exocytosis in HMC-1 cells by T. vaginalis -derived secretory products [ 21 ]. T. vaginalis induces IL-1 β production in human prostate epithelium through activation of ROS [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

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Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species

Quan

Kang

Yang

et al. 2017

BioMed Research International

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Trichomonas vaginalis induces apoptosis in host cells through various mechanisms; however, little is known about the relationship between apoptosis, reactive oxygen species (ROS), and NF-κB signaling pathways in the cervical mucosal epithelium. Here, we evaluated apoptotic events, ROS production, and NF-κB activity in T. vaginalis-treated cervical mucosal epithelial SiHa cells, with or without specific inhibitors, using fluorescence microscopy, DNA fragmentation assays, subcellular fractionation, western blotting, and luciferase reporter assay. SiHa cells treated with live T. vaginalis at a multiplicity of infection of 5 (MOI 5) for 4 h produced intracellular and mitochondrial ROS in a parasite-load-dependent manner. Incubation with T. vaginalis caused DNA fragmentation, cleavage of caspase 3 and PARP, and release of cytochrome c into the cytoplasm. T. vaginalis-treated SiHa cells showed transient early NF-κB p65 nuclear translocation, which dramatically dropped at 4 h after treatment. Suppression of NF-κB activity was dependent on parasite burden. However, treatment with the ROS scavenger, N-acetyl-C-cysteine (NAC), reversed the effect of T. vaginalis on apoptosis and NF-κB inactivation in SiHa cells. Taken together, T. vaginalis induces apoptosis in human cervical mucosal epithelial cells by parasite-dose-dependent ROS production through an NF-κB-regulated, mitochondria-mediated pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species

Quan

Kang

Yang

et al. 2017

BioMed Research International

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“…It also serves as the dominant system in regulating the production of MMPs, devoting to the degeneration of chondrocytes. Now it is approved that the Jun N‐terminal kinase (JNK), extracellular signal‐regulated kinase (ERK), and p38 in MAPK families are involved in the OA process . However, more research is required, as the mechanisms of MAPKs in OA are not exactly known.…”

Section: Introductionmentioning

confidence: 99%

Explore the variation of MMP3, JNK, p38 MAPKs, and autophagy at the early stage of osteoarthritis

Shi

Zhang

et al. 2016

IUBMB Life

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Osteoarthritis is a chronic disease characterized by cartilage degeneration and chondrocyte apoptosis. Mitogen-activated protein kinase (MAPK) signaling pathway plays a key role in regulating OA process. Autophagy has an important effect on the OA process, and it is believed to be regulated by MAPKs. To reveal the mechanism and the effect of JNK and p38 MAPKs on matrix metalloproteinase 3 (MMP3) and autophagy in OA, the study established OA model in rabbits, used the measurement of the Osteoarthritis Research Society International scoring system to evaluate OA model, and conducted general observation, histological observation, and Western blotting of JNK, phosphorylate-JNK (P-JNK), p38, phosphorylate-p38 (Pp38), MMP3, and light-chain 3 (LC3)-II/LC3-I to explore the variation of JNK, p38 MAPKs, and autophagy at the early stage of OA. With OA progressing at the early stage, MMP3, P-p38, and P-JNK were gradually upregulated from the baseline to the peak in study groups when compared with the control group; JNK and p38 variated of turbulence without statistical difference; and LC3-II/LC3-I had a decreasing tendency from the 0-to 15-day group. This study identifies that compromised autophagy may be related to the OA progress and that JNK and p38 MAPKs have positive regulation on MMP3 and negative regulation on autophagy. It also implicates a new therapeutic strategy for OA and other degenerate diseases based on selective MAPK inhibitors, reduction of MMP3, and autophagy. V C 2016 IUBMB Life, 68(4): [293][294][295][296][297][298][299][300][301][302] 2016

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“…TvSP induced upregulation of CD63 expression and reactive oxygen species (ROS) generation in HMC-1 cells via activation of mitogen-activated protein kinases (MAPKs) (35). T. vaginalis-derived LTB 4 can induce HMC-1 cells to release IL-8 via LTB 4 receptor (BLT)-dependent activation of NF-B and CREB (21).…”

mentioning

confidence: 99%

“…In previous studies, we found that TvSP or T. vaginalis-derived LTB 4 can induce exocytosis and interleukin-8 (IL-8) production in human granulocytes (34)(35)(36)(37). TvSP induced upregulation of CD63 expression and reactive oxygen species (ROS) generation in HMC-1 cells via activation of mitogen-activated protein kinases (MAPKs) (35).…”

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confidence: 99%

SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄

et al. 2017

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Trichomonas vaginalis is a sexually transmitted parasite that causes vaginitis in women and itself secretes lipid mediator leukotriene B 4 (LTB 4 ). Mast cells are important effector cells of tissue inflammation during infection with parasites.Membrane-bridging SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complexes are critical for fusion during exocytosis. Although T. vaginalis-derived secretory products (TvSP) have been shown to induce exocytosis in mast cells, information regarding the signaling mechanisms between mast cell activation and TvSP is limited. In this study, we found that SNAP23-dependent surface trafficking of LTB 4 receptor 1 (BLT1) is required for nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2)-mediated exocytotic degranulation of mast cells induced by TvSP. First, stimulation with TvSP induced exocytotic degranulation and reactive oxygen species (ROS) generation in HMC-1 cells. Next, TvSP-induced ROS generation and exocytosis were strongly inhibited by transfection of BLT1 small interfering RNA (siRNA). TvSP induced trafficking of BLT1 from the cytosol to the plasma membrane. We also found that knockdown of SNAP23 abrogated TvSPinduced ROS generation, exocytosis, and surface trafficking of BLT1 in HMC-1 cells. By coimmunoprecipitation, there was a physical interaction between BLT1 and SNAP23 in TvSP-stimulated HMC-1 cells. Taken together, our results suggest that SNAP23-dependent surface trafficking of BLT1 is essential for exocytosis in human mast cells induced by T. vaginalis-secreted LTB 4 . Our data collectively demonstrate a novel regulatory mechanism for SNAP23-dependent mast cell activation of T. vaginalis-secreted LTB 4 involving surface trafficking of BLT1. These results can help to explain how the cross talk mechanism between parasite and host can govern deliberately tissue inflammatory responses.KEYWORDS Trichomonas vaginalis, LTB 4 , human mast cells, SNAP23, NOX2, BLT1, surface trafficking, exocytotic degranulation T richomonas vaginalis is a lumen-dwelling protozoan parasite with flagella, which infects the genitourinary tract in humans via sexual intercourse (1, 2). Of note, in women it causes vaginitis or cervicitis leading to inflammatory and allergic symptoms, including vaginal discharge with a foul odor and an increased number of leukocytes, and vulvovaginal pruritus (3-6). During the infection, tight junctional proteins between

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Activation of MAPK Is Required for ROS Generation and Exocytosis in HMC-1 Cells Induced by <i>Trichomonas vaginalis</i>-Derived Secretory Products

Cited by 6 publications

References 32 publications

Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species

Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species

Explore the variation of MMP3, JNK, p38 MAPKs, and autophagy at the early stage of osteoarthritis

SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄

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Activation of MAPK Is Required for ROS Generation and Exocytosis in HMC-1 Cells Induced by <i>Trichomonas vaginalis</i>-Derived Secretory Products

Cited by 6 publications

References 32 publications

Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species

Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species

Explore the variation of MMP3, JNK, p38 MAPKs, and autophagy at the early stage of osteoarthritis

SNAP23-Dependent Surface Translocation of Leukotriene B 4 (LTB 4 ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB 4

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SNAP23-Dependent Surface Translocation of Leukotriene B ₄ (LTB ₄ ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB ₄