Knockdown of Heparanase Suppresses Invasion of Human Trophoblasts by Activating p38 MAPK Signaling Pathway

Che, Guanglu; Wang, Yanyun; Zhou, Bin; Gao, Linbo; Wang, Tao; Fang, Yuan; Zhang, Lin

doi:10.1155/2018/7413027

Cited by 10 publications

(9 citation statements)

References 26 publications

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“…For example, a study by Zhou et al [ 20 ] has revealed that transforming growth factor- β 1 could inhibit the apoptosis of trophoblasts induced by mercuric chlorides by suppressing the p38MAPK signaling pathway, and one other study by Ebegboni et al [ 21 ] also reported that flavonoids promoted the self-renewal and invasion of spherical stem cells of trophoblasts by inhibiting p38MAPK signaling pathway. In addition, one study by Che et al [ 22 ] also found that knockout of heparanase gene inhibits the invasion of human trophoblasts by activating the p38MAPK signaling pathway. Heparin has also been reported to inhibit excessive circulation and remodeling of porcine pulmonary artery via the p38MAPK signaling pathway, thus alleviating the pulmonary hypertension [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Quan

Zuo

2021

Computational and Mathematical Methods in Medicine

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Objective. To explore the efficacy of low molecular heparin on preeclampsia by inhibiting apoptosis of trophoblasts via the p38MAPK signaling pathway. Methods. A preeclampsia rat model was established, and the effects of low molecular heparin on preeclampsia via the p38MAPK signaling pathway were analyzed based on intervention of the rats with different combinations of low molecular heparin and p38MAPK signaling pathway activator. Furthermore, a hypoxia/reoxygenation model of trophoblasts in vitro was established to explore the effects of low molecular heparin on trophoblasts via the p38MAPK signaling pathway. Results. After treatment with low molecular heparin, pregnant rats in the heparin group showed significantly decreased blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and decreased apoptosis rate of placenta tissue cells (all P < 0.05 ) and showed more fetal rats and lowered weight of them (both P < 0.05 ) but showed no significant change in the weight of placenta (all P > 0.05 ). Pregnant rats treated with low molecular heparin and p38MAPK activator showed significantly higher blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and apoptosis rate of placenta tissue cells than those of pregnant rats in the heparin group (all P < 0.05 ) and also showed less fetal rats and lighter fetal rats than those in the heparin group (both P < 0.05 ) but showed no difference with them in the weight of placenta ( P > 0.05 ). Further analysis revealed that low molecular heparin could protect the survival and migration of trophoblasts under hypoxia/reoxygenation conditions and reduce apoptosis of them (all P < 0.05 ). Conclusion. Low molecular heparin can alleviate preeclampsia by inhibiting the p38MAPK signaling pathway and can inhibit apoptosis of trophoblasts and promote proliferation and migration of them.

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Section: Discussionmentioning

confidence: 99%

Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Quan

Zuo

2021

Computational and Mathematical Methods in Medicine

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“…MAPK, including JNK, ERK, and p38 kinase, plays pivotal roles in proliferation, invasion, and migration of cancer cells[ 33 - 36 ]. There are many studies[ 37 - 39 ] that have shown that H. pylori infection leads to increased p38MAPK in GC cells, and it has also been shown[ 40 ] that p38MAPK leads to HPA elevation. This study showed that HPA and MAPK expression was significantly higher in patients with GC than that in para-carcinoma and normal gastric tissues.…”

Section: Discussionmentioning

confidence: 99%

“…There are many studies[ 37 - 39 ] showing that H. pylori infection leads to increased p38MAPK in GC cells, and it has been shown that[ 40 ] p38MAPK leads to elevation of HPA. Therefore, we hypothesized that H. pylori infection causes an increase in HPA in GC via the MAPK pathway.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori promotes invasion and metastasis of gastric cancer by enhancing heparanase expression

Liu

Sheng

Shuai

et al. 2018

WJG

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AIMTo detect the mechanisms of Helicobacter pylori (H. pylori) infection in the invasion and metastasis of gastric cancer (GC).METHODSSpecimens from 99 patients with GC were collected. The correlation among H. pylori infection, heparanase (HPA) and mitogen-activated protein kinase (MAPK) expression, which was determined by immunohistochemistry, and the clinical features of GC was analysed using SPSS 22.0. Overall survival (OS) and relapse-free survival (RFS) of GC patients were estimated by the Kaplan-Meier method. Independent and multiple factors of HPA and MAPK with prognosis were determined with COX proportional hazards models. HPA and MAPK expression in MKN-45 cells infected with H. pylori was analysed using Western blot.RESULTSH. pylori infection was observed in 70 of 99 patients with GC (70.7%), which was significantly higher than that in healthy controls. H. pylori infection was related to lymph metastasis and expression of HPA and MAPK (P < 0.05); HPA expression was relevant to MAPK expression (P = 0.024). HPA and MAPK expression in MKN-45 cells was significantly upregulated following H. pylori infection and peaked at 24 h and 60 min, before decreasing (P < 0.05). SB203580, an inhibitor of MAPK, significantly decreased HPA expression. HPA was related to lymph metastasis and invasive depth. HPA positive GC cases and H. pylori positive GC cases showed poorer prognosis than HPA negative cases (P < 0.05). COX models showed that the prognosis of GC was connected with HPA expression, lymph metastasis, tissue differentiation, and invasive depth.CONCLUSIONH. pylori may promote the invasion and metastasis of GC by increasing HPA expression that may associate with MAPK activation, thus causing a poorer prognosis of GC.

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“…C-type lectin receptors are expressed mainly on myeloid cells and are involved in antifungal immunity. The MAPK signaling pathway is vital in the mediation of multiple cellular processes, which include proliferation, stress response, differentiation, motility, survival, growth, and death [29]. The PI3K-Akt signaling pathway plays a vital role in mediating survival signals in different types of neuronal cells.…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology-based Study of Simiao Yongan Decoction for Treatment of Herpes Zoster Infection

Liu¹,

Guan-yan

Wu³

et al. 2020

Preprint

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Background: Herpes zoster (HZ) is a virus that causes infectious diseases that impact the quality of life of patients. Herein, we applied network pharmacological methods to predict the target of bioactive components in Simiao Yongan Decoction (SYD) that could treat HZ. Methods: We developed a Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMP) and GenneCards databases for screening of bioactive components of SYD, their targets, and HZ related targets. A bioactive component-target network of SYD was constructed using Cytoscape. We also constructed a protein-protein interaction (PPI) network using the Search Tool for the Retrieval of Interacting Genes Database (STRING) to identify potential SYD targets for the treatment of HZ. "ClusterProfiler" in R-project was used for Gene Ontology (GO) and KEGG pathway enrichment analyses. We screened SYD hub genes based on component-target network topological parameters and confirmed the findings by molecular docking. We selected 126 bioactive components and 235 targets. Results: By assessing the topological parameters of the degree network, we identified that CDK2, CASP3, JUN, AKT1, and MAPK1 were hub genes related to SYD-based therapy against HZ. The findings showed that treatment of HZ with SYD mainly involved toll-like receptor, C-type lectin receptor, MAPK, PI3K-Akt, and other signaling pathways. The molecular docking results revealed good binding energy between the SYD bioactive compounds and hub targets. Conclusion: We showed that SYD could effectively treat HZ via multiple targets and pathways. Our results provide theoretical support for treatment of HZ with SYD and a new direction for such treatment using traditional Chinese medicine.

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Knockdown of Heparanase Suppresses Invasion of Human Trophoblasts by Activating p38 MAPK Signaling Pathway

Cited by 10 publications

References 26 publications

Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Helicobacter pylori promotes invasion and metastasis of gastric cancer by enhancing heparanase expression

Network Pharmacology-based Study of Simiao Yongan Decoction for Treatment of Herpes Zoster Infection

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