TSLP-induced collagen type-I synthesis through STAT3 and PRMT1 is sensitive to calcitriol in human lung fibroblasts

Jin, Ai; Tang, Xuemei; Zhai, Weiqi; Li, Yuwen; Sun, Qingzhu; Liu, Li; Yang, Xiaojun; Ren, Hui; Lu, Shemin

doi:10.1016/j.bbamcr.2021.119083

Cited by 16 publications

(20 citation statements)

References 49 publications

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“…STAT1 and CEBPB have been reported to be responsible for the regulation of PRMT1 transcription in fibroblasts 33 , 34 , 62 . However, in our work, the data showed that neither transcription factor participated in the regulation of histamine on PRMT1 expression.…”

Section: Discussionmentioning

confidence: 99%

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

Zhang

Ding

Wang

et al. 2022

Acta Pharmaceutica Sinica B

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Section: Discussionmentioning

confidence: 99%

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

Zhang

Ding

Wang

et al. 2022

Acta Pharmaceutica Sinica B

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“…Although it must be kept in mind that NF-κB and STAT3 pathways are not exclusively connected with either airway remodeling or the fibrosis process, and their actions have to be analyzed in a broader context. According to the literature, STAT3 is required for the increased COL1A2 expression observed in fibroblasts [ 54 , 55 ]. This transcription factor also operates at the post-transcriptional as well as the transcriptional level.…”

Section: Discussionmentioning

confidence: 99%

Relaxin Affects Airway Remodeling Genes Expression through Various Signal Pathways Connected with Transcription Factors

Wieczfińska

Pawliczak

2022

IJMS

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Fibrosis is one of the parameters of lung tissue remodeling in asthma. Relaxin has emerged as a natural suppressor of fibrosis, showing efficacy in the prevention of a multiple models of fibrosis. Therefore, the aim of this study was to analyze the aptitudes of relaxin, in the context of its immunomodulatory properties, in the development of airway remodeling. WI-38 and HFL1 fibroblasts, as well as epithelial cells (NHBE), were incubated with relaxin. Additionally, remodeling conditions were induced with two serotypes of rhinovirus (HRV). The expression of the genes contributing to airway remodeling were determined. Moreover, NF-κB, c-Myc, and STAT3 were knocked down to analyze the pathways involved in airway remodeling. Relaxin decreased the mRNA expression of collagen I and TGF-β and increased the expression of MMP-9 (p < 0.05). Relaxin also decreased HRV-induced expression of collagen I and α-SMA (p < 0.05). Moreover, all the analyzed transcription factors—NF-κB, c-Myc, and STAT3—have shown its influence on the pathways connected with relaxin action. Though relaxin requires further study, our results suggest that this natural compound offers great potential for inhibition of the development, or even reversing, of factors related to airway remodeling. The presented contribution of the investigated transcription factors in this process additionally increases its potential possibilities through a variety of its activity pathways.

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“…Human lung fibroblasts are also a significant source of TSLP 83,88 . Through an autocrine mechanism, TSLP can activate human lung fibroblasts 89 to release type I collagen 90 and promote the proliferation of ASM cells 91 . TSLP has also been shown to cause goblet cell hyperplasia and mucus production [92][93][94] .…”

Section: Airway Remodelingmentioning

confidence: 99%

Biologics and Airway Remodeling in Severe Asthma

Varricchi

Ferri

Pepys

et al. 2022

Preprint

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Asthma is a chronic inflammatory airway disease resulting in airflow obstruction, which in part can become irreversible to conventional therapies, defining the concept of airway remodeling. The introduction of biologics in severe asthma has led in some patients to the complete normalization of previously considered irreversible airflow obstruction. This highlights the need to distinguish a “fixed” bronchial obstruction due to structural changes unresponsive to current therapies, from a “reversible” one as demonstrated by lung function normalization during biological therapies not previously obtained even with high dose systemic glucocorticoids. The mechanisms by which exposure to environmental factors initiates the inflammatory responses that trigger airway remodeling are still incompletely understood. Alarmins represent tissue-derived cytokines that initiate immunologic events leading to inflammatory airway remodeling. Biological therapies can improve airflow obstruction by addressing these airway inflammatory changes. In addition, biologics might prevent and possibly even revert “fixed” remodeling due to structural changes. Hence, it appears clinically important to separate the therapeutic effects (early and late) of biologics as a new paradigm to evaluate the effects of these drugs and future treatments on airway remodeling in severe asthma.

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TSLP-induced collagen type-I synthesis through STAT3 and PRMT1 is sensitive to calcitriol in human lung fibroblasts

Cited by 16 publications

References 49 publications

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

Relaxin Affects Airway Remodeling Genes Expression through Various Signal Pathways Connected with Transcription Factors

Biologics and Airway Remodeling in Severe Asthma

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