Role of the extracellular signal-regulated kinase 1/2 signaling pathway in the process of thrombin-promoting airway remodeling in ovalbumin-allergic rats

Bi, Meirong; A, Guo; Zhao, Hongyang; Sun, Xiaoning; Chen, Qiang; Yu, Li; Shi, Wei; Wang, Yan; Shen, Guohong; Zhao, Yingchun; Zhang, Nan; Xu, Ming; Qin, Mingming; Zhu, Weiwei

doi:10.3109/08923973.2014.993083

Cited by 9 publications

(3 citation statements)

References 33 publications

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“…Also, EPCR knockdown or treatment with PAR1 antibody significantly decreased MAPK3/1 phosphorylation (Q. Wang et al, 2018). In ovalbumin‐allergic rats, thrombin promotes airway remodeling via PAR1, while MAPK3/1 signaling pathway plays an important role in this process since pMAPK3/1 inhibitors effectively inhibit the airway remodeling in these rats (Bi et al, 2015). These reports provide insight into the potential role of PAR1 activation in cell proliferation through MAPK3/1 signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Ankyrin‐repeat and SOCS box‐containing protein 9 (ASB9) regulates ovarian granulosa cells function and MAPK signaling

Nosratpour

Ndiaye

2021

Molecular Reproduction Devel

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Ankyrin‐repeat and SOCS box‐containing proteins (ASB) interact with the elongin B‐C adapter via their SOCS box domain and with the cullin and ring box proteins to form E3 ubiquitin ligase complexes within the protein ubiquitination pathway. ASB9 in particular is a differentially expressed gene in ovulatory follicles (OFs) induced by the luteinizing hormone (LH) surge or hCG injection in ovarian granulosa cells (GC) while downregulated in growing dominant follicles. Although ASB9 has been involved in biological processes such as protein modification, the signaling network associated with ASB9 in GC is yet to be fully defined. We previously identified and reported ASB9 interactions and binding partners in GC including PAR1, TAOK1, and TNFAIP6/TSG6. Here, we further investigate ASB9 effects on target binding partners regulation and signaling in GC. CRISPR/Cas9‐induced inhibition of ASB9 revealed that ASB9 regulates PAR1, TAOK1, TNFAIP6 as well as genes associated with proliferation and cell cycle progression such as PCNA, CCND2, and CCNE2 while CCNA2 was not affected. Inhibition of ASB9 was also associated with increased GC number and decreased caspase3/7 activity, CASP3 expression, and BAX/BCL2 ratio. Furthermore, ASB9 induction in OF in vivo 24 h post‐hCG is concomitant with a significant decrease in phosphorylation levels of MAPK3/1 while pMAPK3/1 levels increased following ASB9 inhibition in GC in vitro. Together, these results provide strong evidence for ASB9 as a regulator of GC activity and function by modulating MAPK signaling likely through specific binding partners such as PAR1, therefore controlling GC proliferation and contributing to GC differentiation into luteal cells.

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Section: Discussionmentioning

confidence: 99%

Ankyrin‐repeat and SOCS box‐containing protein 9 (ASB9) regulates ovarian granulosa cells function and MAPK signaling

Nosratpour

Ndiaye

2021

Molecular Reproduction Devel

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“…Various small-molecular inhibitors of MAPK tested in animal models of asthma hold potential for treatment of severe corticosteroid resistant asthma and warrant further clinical investigation. The ERK1/2 signaling pathway reportedly played a more important role in the process of airway remodeling rather than acute allergic airway in ammation, and p-ERK1/2 inhibitor effectively inhibited airway remodeling in chronic asthma [41]. Kim et al reported that inhibition of p38 MAPK might attenuate allergen-induced airway in ammation and vascular leakage through modulation of VEGF expression in mice [42].…”

Section: Discussionmentioning

confidence: 99%

Mas Receptor Activation Attenuates Allergic Airway Inflammation via Inhibiting JNK/CCL2-induced Macrophage Recruitment

Hong

Chen

Shi

et al. 2020

Preprint

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Background: Defective absorption of acute allergic airway inflammation is involved in the initiation and development of chronic asthma. After allergen exposure, there is a rapid recruitment of macrophages around the airways, which promote acute inflammatory responses. The Ang-(1-7)/Mas receptor axis reportedly plays protective roles in various tissue inflammation and remodeling processes in vivo. However, the exact role of Mas receptor and their underlying mechanisms during the pathology of acute allergic airway inflammation remains unclear. Methods: Mas receptor expression was assessed in ovalbumin-induced acute asthmatic murine model. Then we estimated the anti-inflammatory role of Mas receptor in vivo and explored expressions of several known inflammatory cytokines as well as phosphorylation levels of MAPK pathways. Mas receptor functions and underlying mechanisms were studied further in the human bronchial epithelial cell line (16HBE).Results: Mas receptor expression decreased in acute allergic airway inflammation. Multiplex immunofluorescence co-localized Mas receptor and EpCAM, indicated that Mas receptor may function in the bronchial epithelium. Activating Mas receptor through AVE0991 significantly alleviated macrophage infiltration in airway inflammation, accompanied with down-regulation of CCL2 and phosphorylation levels of MAPK pathways. Further studies in 16HBE showed that AVE0991 pre-treatment inhibited LPS-induced or anisomycin-induced CCL2 increase and THP-1 macrophages migration via JNK pathways.Conclusion: Our findings suggested that Mas receptor activation significantly attenuated CCL2 dependent macrophage recruitments in acute allergic airway inflammation through JNK pathways, which indicated that Mas receptor, CCL2 and phospho-JNK could be potential targets against allergic airway inflammation.

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“…Platelets activated by the up-regulation of cluster of differentiation 154 may release the platelet δ, α and λ granules, induce pulmonary inflammation and enhance the T helper cell 2 immune response, thus aggravating asthma severity (7). The extracellular signal-regulated kinase 1/2 signaling pathway serves an important role in the process of thrombus-promoting airway remodeling in ovalbumin allergic rats (8). This suggests that coagulation is closely associated with inflammation in asthma.…”

Section: Introductionmentioning

confidence: 99%

TIPE2 is negatively correlated with tissue factor and thrombospondin-1 expression in patients with bronchial asthma

et al. 2018

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Abstract. The interaction between inflammatory processes and a hypercoagulant state may aggravate the severity of asthma and stimulate the airway remodeling of asthma. The aim of the current study was to evaluate the association between the negative inflammatory regulator tumor necrosis factor α induced protein-8 like-2 (TIPE2) and the coagulating substances tissue factor (TF) and thrombospondin-1 (TSP-1) in patients with bronchial asthma. Compared with healthy controls, TIPE2 expression was significantly downregulated, whereas TF expression was upregulated in the peripheral blood mononuclear cells (PBMCs) of patients with bronchial asthma. In addition, levels of TF and TSP-1 in the sera were up-regulated in patients with asthma compared with healthy controls. TIPE2 expression was negatively correlated with TF in the PBMCs and sera and was negatively correlated with TSP-1 levels in the sera of patients with bronchial asthma. The results of the current study indicated that anti-inflammatory TIPE2 levels are associated with levels of the coagulation substances TF and TSP-1. However, further studies are required to determine whether TIPE2 participates in the pathogenesis of asthma by interacting with the coagulation substances TF and TSP-1.

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Role of the extracellular signal-regulated kinase 1/2 signaling pathway in the process of thrombin-promoting airway remodeling in ovalbumin-allergic rats

Abstract: These results suggest that ERK1/2 signaling pathway may play an important role in the process of thrombin-promoting airway remodeling in OVA-allergic rats, and pERK1/2 inhibitor effectively inhibits the process.

Cited by 9 publications

References 33 publications

Ankyrin‐repeat and SOCS box‐containing protein 9 (ASB9) regulates ovarian granulosa cells function and MAPK signaling

Ankyrin‐repeat and SOCS box‐containing protein 9 (ASB9) regulates ovarian granulosa cells function and MAPK signaling

Mas Receptor Activation Attenuates Allergic Airway Inflammation via Inhibiting JNK/CCL2-induced Macrophage Recruitment

TIPE2 is negatively correlated with tissue factor and thrombospondin-1 expression in patients with bronchial asthma

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