Crosstalk between pleural mesothelial cell and lung fibroblast contributes to pulmonary fibrosis

Liu, Fei; Fan, Yu; Lu, Yang; Cheng, Peipei; Lin, Limei; Wang, Meng; Chen, Shuai-Jun; Huang, Yi Hsiang; Song, Linjie; He, Xiaowen; Xiong, Liang; Xin, Jian-Bao; Ma, Wanli; Yue, Hong

doi:10.1016/j.bbamcr.2020.118806

Cited by 13 publications

(7 citation statements)

References 43 publications

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“…These challenged PMCs underwent a MMT and produced more collagen‐I, which directly contributed to ECM deposition (Chen et al, 2015). At the same time, these challenged PMCs could make crosstalk with lung fibroblasts, and induced cell proliferation and collagen‐I synthesis in lung fibroblasts which played a role in pulmonary fibrosis (Liu et al, 2020). As is well known, the process of pulmonary fibrosis was generally divided into the early, middle, and late stages.…”

Section: Discussionmentioning

confidence: 99%

Pleural mesothelial cell migration into lung parenchyma by calpain contributes to idiopathic pulmonary fibrosis

Zhou

Cheng

et al. 2021

Journal Cellular Physiology

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Idiopathic pulmonary fibrosis (IPF) is defined as a specific form of chronic, progressive fibrosing interstitial pneumonia. It is unknown why fibrosis in IPF distributes in the peripheral or named sub-pleural area. Migration of pleural mesothelial cells (PMC) should contribute to sub-pleural fibrosis. Calpain is known to be involved in cell migration, but the role of calpain in PMC migration has not been investigated. In this study, we found that PMCs migrated into lung parenchyma in patients with IPF. Then using Wt1 tm1(EGFP/ Cre)Wtp /J knock-in mice, we observed PMC migration into lung parenchyma in bleomycininduced pleural fibrosis models, and calpain inhibitor attenuated pulmonary fibrosis with prevention of PMC migration. In vitro studies revealed that bleomycin and transforming growth factor-β1 increased calpain activity in PMCs, and activated calpain-mediated focal adhesion (FA) turnover as well as cell migration, cell proliferation, and collagen-I synthesis. Furthermore, we determined that calpain cleaved FA kinase in both C-terminal and N-terminal regions, which mediated FA turnover. Lastly, the data revealed that activated calpain was also involved in phosphorylation of cofilin-1, and p-cofilin-1 induced PMC migration. Taken together, this study provides evidence that calpain mediates PMC migration into lung parenchyma to promote sub-pleural fibrosis in IPF.

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Section: Discussionmentioning

confidence: 99%

Pleural mesothelial cell migration into lung parenchyma by calpain contributes to idiopathic pulmonary fibrosis

Zhou

Cheng

et al. 2021

Journal Cellular Physiology

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“…Furthermore, these findings rule out any classical functional connection between CD147 and caveolin-1 in the AECs [304]. Moreover, it has been demonstrated that inhibition of CD147 can reduce collagen-I synthesis in lung fibroblasts incubated with cultured pleural mesothelial cells (PMCs) and prevent bleomycin-induced PF in an MMPs-dependent process [305]. Consequently, CD147 causes ECM degradation via regulating MMP synthesis, or it causes ECM deposition by inducing myofibroblast differentiation.…”

Section: Role Of Cd147 In Pulmonary Fibrosismentioning

confidence: 76%

Matrix Metalloproteinases and Their Inhibitors in Pulmonary Fibrosis: EMMPRIN/CD147 Comes into Play

Chuliá-Peris

Carreres-Rey

Gabasa

et al. 2022

IJMS

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Pulmonary fibrosis (PF) is characterized by aberrant extracellular matrix (ECM) deposition, activation of fibroblasts to myofibroblasts and parenchymal disorganization, which have an impact on the biomechanical traits of the lung. In this context, the balance between matrix metalloproteinases (MMPs) and their tissue inhibitors of metalloproteinases (TIMPs) is lost. Interestingly, several MMPs are overexpressed during PF and exhibit a clear profibrotic role (MMP-2, -3, -8, -11, -12 and -28), but a few are antifibrotic (MMP-19), have both profibrotic and antifibrotic capacity (MMP7), or execute an unclear (MMP-1, -9, -10, -13, -14) or unknown function. TIMPs are also overexpressed in PF; hence, the modulation and function of MMPs and TIMP are more complex than expected. EMMPRIN/CD147 (also known as basigin) is a transmembrane glycoprotein from the immunoglobulin superfamily (IgSF) that was first described to induce MMP activity in fibroblasts. It also interacts with other molecules to execute non-related MMP actions well-described in cancer progression, migration, and invasion. Emerging evidence strongly suggests that CD147 plays a key role in PF not only by MMP induction but also by stimulating fibroblast myofibroblast transition. In this review, we study the structure and function of MMPs, TIMPs and CD147 in PF and their complex crosstalk between them.

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“…Cardiac-specific silencing of CD147 alleviated myocardial dysfunction and attenuated myocardial fibrosis in diabetic mice, whereas its overexpression aggravated myocardial dysfunction with excessive collagen accumulation in control or diabetic mice. Previous studies have also indicated the profibrotic effect of CD147 in interstitial lung diseases, liver cirrhosis, and diabetic nephropathy 19 , 27 , 28 . In vitro data consistently demonstrated that CD147 knockdown significantly inhibited the HG-indued activation of cardiac fibroblasts as seen by the downregulated expression of fibrotic markers and reduced proliferation of CFs.…”

Section: Discussionmentioning

confidence: 92%

N-glycosylation-mediated CD147 accumulation induces cardiac fibrosis in the diabetic heart through ALK5 activation

Liu¹,

Peng²,

Hu³

et al. 2023

Int. J. Biol. Sci.

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Emerging evidence has implicated the important role of fibrosis in diabetic cardiomyopathy (DCM), while the underlying mechanism remains unclear. Considering the distinct and overlapping roles of Cluster of Differentiation 147 (CD147) in the pathogenesis of fibrotic diseases, we aim to investigate the role of CD147 in the fibrosis of DCM and explore its underlying mechanism. AAV9-mediated cardiac-specific CD147 silencing attenuated cardiac fibrosis and cardiac function in diabetic mice. CD147 knockdown significantly inhibited high glucose (HG)-induced activation of CFs. Mechanistically, CD147 directly bound to type I transcription growth factor β (TGF-β) receptor I (ALK5), promoting ALK5 activation and endocytosis to induce SMAD2/3 phosphorylation and nuclear translocation. In addition, HG prevented the ubiquitin-proteasome-dependent degradation of CD147 by promoting GNT-V-mediated N-glycosylation. As a result, cardiac-specific CD147 overexpression in control mice mimicked diabetes-induced cardiac fibrosis, aggravating cardiac function. Importantly, CD147 was also upregulated in serum and myocardial specimens from patients with diabetes compared with non-diabetes, accompanied by echocardiographic indices of cardiac dysfunction and excessive collagen deposition. Our study provides the first evidence that CD147 acts as a pivotal factor to promote diabetic cardiac fibrosis, and may contribute to the development of future CD147-based therapeutic strategies for DCM.

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Crosstalk between pleural mesothelial cell and lung fibroblast contributes to pulmonary fibrosis

Cited by 13 publications

References 43 publications

Pleural mesothelial cell migration into lung parenchyma by calpain contributes to idiopathic pulmonary fibrosis

Pleural mesothelial cell migration into lung parenchyma by calpain contributes to idiopathic pulmonary fibrosis

Matrix Metalloproteinases and Their Inhibitors in Pulmonary Fibrosis: EMMPRIN/CD147 Comes into Play

N-glycosylation-mediated CD147 accumulation induces cardiac fibrosis in the diabetic heart through ALK5 activation

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