The p38 MAPK inhibitor, SB203580, inhibits cell invasion by Neospora caninum

Jin, Xinqiao; Gong, Pengtao; Li, Guojiang; Zhang, Xichen; Li, Jianhua

doi:10.1007/s00436-016-5346-1

Cited by 8 publications

(8 citation statements)

References 34 publications

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“…69 However, SB203580 is mostly used in vitro or in animal experiments due to low drug selectivity and a high rate of toxic side effects. [70][71][72] Other types of inhibitors, including pyridines, pyrimidines and indoles, also have the same problem. Pamapimod (PAM), a novel p38MAPK inhibitor firstly discovered in 2008, could improve the signs and symptoms of RA and other autoimmune diseases.…”

Section: P38mapk Pathway As Therapeutic Targets In Oa Treatmentmentioning

confidence: 99%

p38MAPK Signaling Pathway in Osteoarthritis: Pathological and Therapeutic Aspects

Dai

Yang

et al. 2022

JIR

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Osteoarthritis (OA) is an aging-related joint disease, pathologically featured with degenerated articular cartilage and deformation of subchondral bone. OA has become the fourth major cause of disability in the world, imposing a huge economic burden. At present, the pathogenesis and pathophysiology of OA are still unclear. Complex regulating networks containing different biochemical signaling pathways are involved in OA pathogenesis and progression. The p38MAPK signaling pathway is a member of the MAPK signaling pathway family, which participates in the induction of cellular senescence, the differentiation of chondrocytes, the synthesis of matrix metalloproteinase (MMPs) and the production of pro-inflammatory factors. In recent years, studies on the regulating role of p38MAPK signaling pathway and the application of its inhibitors have attracted growing attention, with an increasing number of in vivo and in vitro studies. One interesting finding is that the inhibition of p38MAPK could suppress chondrocyte inflammation and ameliorate OA, indicating its therapeutic role in OA treatment. Based on this, we reviewed the mechanisms of p38MAPK signaling pathway in the pathogenesis of OA, hoping to provide new ideas for future research and OA treatment.

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Section: P38mapk Pathway As Therapeutic Targets In Oa Treatmentmentioning

confidence: 99%

p38MAPK Signaling Pathway in Osteoarthritis: Pathological and Therapeutic Aspects

Dai

Yang

et al. 2022

JIR

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“…The previous research show that the p38 MAPK signaling pathway may play an important role in regulating the odontoblastic differentiation of hDPSCs (Gong et al, ; He et al, ; Yao et al, ), but the potential mechanism still remains controversial. Interestingly, a recent study has demonstrated that miR‐143 could regulate the expression of the p38 MAPK signaling pathway (Li et al, ). Moreover, another study shows that the p38 MAPK signaling pathway inhibitor SB203580 suppresses toxoplasma gondii MAPK1 autophosphorylation and blocks intracellular toxoplasma gondii replication by directly effecting tachyzoites (Jin, Gong, Li, Zhang, & Li, ).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, a recent study has demonstrated that miR-143 could regulate the expression of the p38 MAPK signaling pathway (Li et al, 2017). Moreover, another study shows that the p38 MAPK signaling pathway inhibitor SB203580 suppresses toxoplasma gondii MAPK1 autophosphorylation and blocks intracellular toxoplasma gondii replication by directly effecting tachyzoites (Jin, Gong, Li, Zhang, & Li, 2017). In the present research, SB203580, an inhibitor of the p38 MAPK signaling pathway, was used to verify whether miR-143-5p positively regulates the p38 MAPK signaling pathway by targeting MAPK14.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA‐143‐5p is required for the promotion of odontoblasts differentiation of human dental pulp stem cells through the activation of the mitogen‐activated protein kinases 14‐dependent p38 mitogen‐activated protein kinases signaling pathway

Wang

Nan

et al. 2018

Journal Cellular Physiology

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MicroRNAs (miRNAs) play critical roles in various biological processes including cell differentiation. Some researchers suggested that the p38 mitogen-activated protein kinases (MAPK) signaling pathway had an effect on regulating the odontoblastic differentiation of human dental pulp stem cells (hDPSCs). This study focuses on the effects of miR-143-5p on hDPSCs by regulating the p38 MAPK signaling pathway. The targeting relationship of MAPK14 and miR-143-5p targets were verified by TargetScan and dual-luciferase reporter gene assay. Through overexpression of miR-143-5p or silencing of miR-143-5p, expressions of miR-143-5p, MAPK14, Ras, MAPK kinase (MKK) 3/6, dentin sialophosphoprotein (DSPP), alkaline phosphatase (ALP), and osteocalcin (OCN) were detected by reverse transcription quantitative polymerase chain reaction. Protein expressions of MAPK14, Ras, and MKK3/6 were determined by western blot analysis. ALP and alizarin red S staining were used to detect mineralization. Initially, MAPK14 was found to be negatively regulated by miR-143-5p. Meanwhile, the upregulated miR-143-5p decreased the p38 MAPK signaling pathway related genes (MAPK14, Ras, and MKK3/6) and odontoblastic differentiation markers (ALP, DSPP, and OCN) expression. On the contrary, the downregulated miR-143-5p increased the p38 MAPK signaling pathway related genes (MAPK14, Ras, and MKK3/6) and odontoblastic differentiation markers (ALP, DSPP, and OCN) expression. Furthermore, ALP activity and mineralized nodules increased after downregulation of miR-143-5p, and after its upregulation, ALP activity and mineralized nodules decreased. Our data suggest that poor expression of miR-143-5p promotes hDPSCs odontoblastic differentiation through the activation of the p38 MAPK signaling pathway by upregulating MAPK14. K E Y W O R D S human dental pulp stem cells (hDPSCs), mitogen-activated protein kinases (MAPK) 14, microRNA-143-5p (miR-143-5p), odontoblastic differentiation, p38 MAPK signaling pathway J Cell Physiol. 2019;234:4840-4850. wileyonlinelibrary.com/journal/jcp 4840 |

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“…Serine protease inhibitors block invasion of host cells by Plasmodium falciparum ( Conseil et al, 1999 ) and Toxoplasma ( Alam, 2014 ). In Apicomplexan parasites, several kinases have been identified ( Brumlik et al, 2011 ; Wei et al, 2013 ; Brown et al, 2014 ; Jin et al, 2017 ). In addition, the existence of parasite receptor kinase protein homologs similar to mammalian host cells implies that N. caninum EGFR might participate in host immune evasion by the parasite, which needs to be further studied.…”

Section: Discussionmentioning

confidence: 99%

Activation of a Neospora caninum EGFR-Like Kinase Facilitates Intracellular Parasite Proliferation

Jin

Zhang

et al. 2017

Front. Microbiol.

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The Apicomplexan parasite Neospora caninum, an obligate intracellular protozoan, causes serious diseases in a number of mammalian species, especially in cattle. Infection with N. caninum is associated with abortions in both dairy and beef cattle worldwide which have a major economic impact on the cattle industry. However, the mechanism by which N. caninum proliferates within host cells is poorly understood. Epidermal growth factor receptor (EGFR) is a protein kinase ubiquitously expressed, present on cell surfaces in numerous species, which has been confirmed to be essential in signal transduction involved in cell growth, proliferation, survival, and many other intracellular processes. However, the presence of EGFR in N. caninum and its role in N. caninum proliferation remain unclear. In the present study, we identified a putative EGFR-like kinase in N. caninum, which could be activated in tachyzoites by infection or treatment with rNcMIC3 [containing four epidermal growth factor (EGF) domains] or human EGF. Blockade of EGFR-like in tachyzoites by AG1478 significantly reduced parasite proliferation in host cells. Our data suggested that the activation of tachyzoite EGFR-like might facilitate the intracellular proliferation of N. caninum.

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The p38 MAPK inhibitor, SB203580, inhibits cell invasion by Neospora caninum

Cited by 8 publications

References 34 publications

p38MAPK Signaling Pathway in Osteoarthritis: Pathological and Therapeutic Aspects

p38MAPK Signaling Pathway in Osteoarthritis: Pathological and Therapeutic Aspects

Downregulation of microRNA‐143‐5p is required for the promotion of odontoblasts differentiation of human dental pulp stem cells through the activation of the mitogen‐activated protein kinases 14‐dependent p38 mitogen‐activated protein kinases signaling pathway

Activation of a Neospora caninum EGFR-Like Kinase Facilitates Intracellular Parasite Proliferation

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