Macrophages are primed to transdifferentiate into fibroblasts in malignant ascites and pleural effusions

Ito, Mamoru; Nakano, Michitaka; Ariyama, Hiroshi; Yamaguchi, Kyoko; Tanaka, Risa; Semba, Yuichiro; Sugio, Takeshi; Miyawaki, Kohta; Kikushige, Yoshikane; Mizuno, Shinichi; Isobe, Taichi; Tanoue, Kimitoshi; Taguchi, Ryosuke; Ueno, Shohei; Kawano, Takahito; Murata, Masaru; Baba, Eishi; Akashi, Koichi

doi:10.1016/j.canlet.2022.215597

Cited by 10 publications

(3 citation statements)

References 55 publications

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“…CD90 is a surface marker specific for fibroblasts. 21 , 22 Based on this, two-color immunofluorescence was used to identify the transition of cardiac fibroblasts to myofibroblasts in mouse cardiac tissue. We observed a significant increase in this transition in DM mice, which was markedly reduced after treatment with Clo ( Figure S1 B).…”

Section: Resultsmentioning

confidence: 99%

The mechanisms and therapeutic potential of clopidogrel in mitigating diabetic cardiomyopathy in db/db mice

Li,

Zhang,

Zheng

et al. 2024

iScience

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Section: Resultsmentioning

confidence: 99%

The mechanisms and therapeutic potential of clopidogrel in mitigating diabetic cardiomyopathy in db/db mice

Li,

Zhang,

Zheng

et al. 2024

iScience

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“…GATA6 is a transcription factor that macrophages rely on for their homeostasis, function, and localization ( Buechler et al, 2019 ). Moreover, there is accumulating evidence confirming that macrophages can acquire fibroblast progenitor properties in the field of fibrotic disease research ( Ito et al, 2022 ). Macrophages play a direct fibrotic role in fibrosing diseases including renal fibrosis ( Tang P. M. K. et al, 2022 ) and lung fibrosis ( Yang et al, 2021 ), via transition into myofibroblasts in a process named macrophage-to-myofibroblast transition.…”

Section: Intercellular Communicationmentioning

confidence: 99%

Intercellular communication in peritoneal dialysis

Sheng,

Shan,

Dai

et al. 2024

Front. Physiol.

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Long-term peritoneal dialysis (PD) causes structural and functional alterations of the peritoneal membrane. Peritoneal deterioration and fibrosis are multicellular and multimolecular processes. Under stimulation by deleterious factors such as non-biocompatibility of PD solution, various cells in the abdominal cavity show differing characteristics, such as the secretion of different cytokines, varying protein expression levels, and transdifferentiation into other cells. In this review, we discuss the role of various cells in the abdominal cavity and their interactions in the pathogenesis of PD. An in-depth understanding of intercellular communication and inter-organ communication in PD will lead to a better understanding of the pathogenesis of this disease, enabling the development of novel therapeutic targets.

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“…Accumulated ascites in the abdominal cavity, which are composed of cellular and acellular components, constitute a unique microenvironment for PM and the tumor cells suspended in the peritoneal fluid (11). Non-cancer cells in ascites, such as macrophages (12) and cancer-associated fibroblasts (13), interact with cancer cells and serve a pivotal role in the progression of PM. In addition, the acellular fraction of ascites, such as exosomes (14), metabolites (15), soluble growth factor (16) and chemokines (17) is involved in peritoneal dissemination, epithelial-to-mesenchymal transition (EMT), chemoresistance and cell proliferation (14,18).…”

Section: Introductionmentioning

confidence: 99%

Malignant ascites supernatant enhances the proliferation of gastric cancer cells partially via the upregulation of asparagine synthetase

Jiao,

Peng,

Wang

et al. 2023

Oncol Lett

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Malignant ascites (MA) is a common manifestation of advanced gastric cancer (GC) with peritoneal metastasis (PM), which usually indicates a poor prognosis. The present study aimed to explore the effects of MA, a unique microenvironment of PM, on the proliferation of cancer cells and investigate the underlying mechanisms. Ex vivo experiments demonstrated that GC cells treated with MA exhibited enhanced proliferation. RNA sequencing indicated that asparagine synthetase (ASNS) was one of the differentially expressed genes in GC cells following incubation with MAs. Furthermore, the present study suggested that MA induced an upregulation of ASNS expression and the stimulatory effect of MA on cancer cell proliferation was alleviated upon ASNS downregulation. Activating transcription factor 4 (ATF4), a pivotal transcription factor regulating ASNS, was upregulated when cells were treated with MA supernatant. After ATF4 knockdown, the proliferation of MA-treated GC cells and the expression of ASNS decreased. In addition, the decline in the proliferation of the ATF4-downregulated AGS GC cell line was rescued by ASNS upregulation. The findings indicated that MA could promote the proliferation of GC cells via activation of the ATF4-ASNS axis. Hence, it may be a potential target for treating GC with PM and MA.

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Macrophages are primed to transdifferentiate into fibroblasts in malignant ascites and pleural effusions

Cited by 10 publications

References 55 publications

The mechanisms and therapeutic potential of clopidogrel in mitigating diabetic cardiomyopathy in db/db mice

The mechanisms and therapeutic potential of clopidogrel in mitigating diabetic cardiomyopathy in db/db mice

Intercellular communication in peritoneal dialysis

Malignant ascites supernatant enhances the proliferation of gastric cancer cells partially via the upregulation of asparagine synthetase

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