<scp>SHP2</scp>: The protein tyrosine phosphatase involved in chronic pulmonary inflammation and fibrosis

Chang, Chung‐Cheng; Lin, Chiou–Feng; Chen, Bing-Chang; Lin, Pei-Yun; Chen, Chia-Ling

doi:10.1002/iub.2559

Cited by 9 publications

(4 citation statements)

References 75 publications

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“…Increasing evidence supports a role for SHP2 in inflammation-mediated pulmonary diseases, such as allergic asthma, pulmonary fibrosis, acute lung injury, and chronic obstructive pulmonary diseases. 51 , 52 A high activity of SHP2 in pulmonary eosinophils of asthmatic children and in mice with allergic airway inflammation was associated with the dephosphorylation of p190-A Rho GTPase-activating protein. 53 Similarly, fibroblasts from patients with severe eosinophilic asthma showed constitutive activation of SHP2, which resulted in negative regulation of IL-6-induced STAT3 phosphorylation.…”

Section: The Signaling Pathways Regulated By the Protein Phosphatases...mentioning

confidence: 99%

Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy

Pan

Zhou

Zhang

et al. 2022

Sig Transduct Target Ther

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Inflammation is the common pathological basis of autoimmune diseases, metabolic diseases, malignant tumors, and other major chronic diseases. Inflammation plays an important role in tissue homeostasis. On one hand, inflammation can sense changes in the tissue environment, induce imbalance of tissue homeostasis, and cause tissue damage. On the other hand, inflammation can also initiate tissue damage repair and maintain normal tissue function by resolving injury and restoring homeostasis. These opposing functions emphasize the significance of accurate regulation of inflammatory homeostasis to ameliorate inflammation-related diseases. Potential mechanisms involve protein phosphorylation modifications by kinases and phosphatases, which have a crucial role in inflammatory homeostasis. The mechanisms by which many kinases resolve inflammation have been well reviewed, whereas a systematic summary of the functions of protein phosphatases in regulating inflammatory homeostasis is lacking. The molecular knowledge of protein phosphatases, and especially the unique biochemical traits of each family member, will be of critical importance for developing drugs that target phosphatases. Here, we provide a comprehensive summary of the structure, the “double-edged sword” function, and the extensive signaling pathways of all protein phosphatases in inflammation-related diseases, as well as their potential inhibitors or activators that can be used in therapeutic interventions in preclinical or clinical trials. We provide an integrated perspective on the current understanding of all the protein phosphatases associated with inflammation-related diseases, with the aim of facilitating the development of drugs that target protein phosphatases for the treatment of inflammation-related diseases.

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Section: The Signaling Pathways Regulated By the Protein Phosphatases...mentioning

confidence: 99%

Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy

Pan

Zhou

Zhang

et al. 2022

Sig Transduct Target Ther

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“…These outcomes further corroborate the significant inhibitory effect of SHP2 on the myocardial pathological and ultrastructural changes induced by sepsis. SHP2 has different physiological effects on different cells [28]. It has been found that it can inhibit the activity of Src protein by inhibiting the phosphorylation of Csk protein [29].…”

Section: Discussionmentioning

confidence: 99%

The effect and mechanism of SHP2 on sepsis induced myocardial injury via modulating Src/ERK-autophagy signal

Wang,

Jia,

Zhang

et al. 2024

Aging

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Objective: To investigate the effect and mechanism of SHP2 on myocardial injury induced by sepsis. Methods: The cardiac function of mice was examined by echocardiography, the myocardial pathological changes of mice were detected by HE staining, the ultrastructural changes of mice myocardial cells were examined by transmission electron microscopy, and the expression of p-SHP2, p-Src, p-ERK1/2, oxidative stress related proteins and apoptosis related proteins of mice myocardial cells were detected by Western blot. Moreover, apoptosis of cardiomyocytes was detected by TUNEL staining. Results: The cardiac function of model group mice was better than that of PHPS1 group, but poorer than that of sham group. The pathological changes and ultrastructural changes of myocardium of mice in model group were better than those in PHPS1 group, and no changes was found in sham group. The expression of p-SHP2 protein in model group mice was higher than that in PHPS1 group and sham group, but the expression of p-Src, p-ERK1/2, oxidative stress related protein and apoptosis related protein were lower than that in PHPS1 group while higher than that in sham group. The addition of PHPS1 inhibited the expression of p-SHP2 and increased the expression of p-Src, oxidative stress-related proteins and apoptosis-related proteins. However, the gap in the expression levels of oxidative stress-related proteins and apoptosis-related proteins narrowed with the addition of NAC. Conclusions: SHP2 can ameliorate myocardial injury induced by sepsis by inhibiting oxidative stress-mediated cardiomyocyte apoptosis through Src/ERK pathway.

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“…With the intervention of CUR, the expression of Epithelial Growth Factor Receptor (EGFR) and Proliferative Protein (Ki 67) can be adjusted ( Zhao et al, 2008 ). Mitogen activated protein kinases (MAPK)/extracellular signal regulated kinase (ERK) is an effective target for anti-fibrosis therapy ( Chang et al, 2022 ). The CUR can regulate PF progression through this signaling pathway ( Zhang et al, 2007 ).…”

Section: Discussionmentioning

confidence: 99%

Protective effects and mechanism of curcumin in animal models of pulmonary fibrosis: a preclinical systematic review and meta-analysis

Hanyu,

Zheng,

Jiaqi

et al. 2023

Front. Pharmacol.

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Introduction: At present, there is a lack of effective treatment for pulmonary fibrosis (PF), and a number of studies have confirmed that curcumin (CUR) has a good effect on PF.Research Qusetion: Is CUR effective in preclinical trials for PF and what is its mechanism of action?Methods: Animal reports of PF treated with CUR were searched from Pubmed, Embase, Web of Science and Cochrane Library from 1 January 2000 to 19 April 2023 to compare CUR treatment of PF with a no-intervention model group. A previous registration (nsply registration number: INPLASY202360084) of this review protocol was undertaken.Results: The meta-analysis included 27 publications and 29 studies involving 396 animals. CUR significantly improved the degree of fibrosis, levels of inflammation, and oxidative imbalances in lung tissue in animal models of PF. In terms fibrosis, such as HYP content (SMD = −4.96; 95% CI = −6.05 to −3.87; p = 0.000).In terms of inflammatory indicators, such as MPO activity (SMD = −2.12; 95% CI = −4.93 to 0.69; p = 0.000). In terms of oxidation index, such as MDA (SMD = −5.63; 95% CI = −9.66 to −1.6; p = 0.000).Conclusion: CUR significantly improved the degree of fibrosis, levels of inflammation, and oxidative imbalances in lung tissue in animal models of PF. Due to the quantitative and qualitative limitations of current research, more high-quality studies are needed to verify the above conclusion.

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SHP2: The protein tyrosine phosphatase involved in chronic pulmonary inflammation and fibrosis

Cited by 9 publications

References 75 publications

Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy

Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy

The effect and mechanism of SHP2 on sepsis induced myocardial injury via modulating Src/ERK-autophagy signal

Protective effects and mechanism of curcumin in animal models of pulmonary fibrosis: a preclinical systematic review and meta-analysis

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