Clevudine attenuates bleomycin-induced early pulmonary fibrosis via regulating M2 macrophage polarization

Li, Shuangling; Gao, Shaoyan; Jiang, Qiuyan; Liang, Qing; Luan, Jiaoyan; Zhang, Ruiqin; Zhang, Fangxia; Ruan, Hao; Li, Xiaohe; Li, Xiaoping; Yang, Cheng

doi:10.1016/j.intimp.2021.108271

Cited by 15 publications

(11 citation statements)

References 25 publications

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“…Therefore, the downregulation of collagen Iα1 expression suggests that the inhibitory effect of M2CM during fibrosis further facilitates IVD regeneration. This result was in accordance with that from previous studies; M2 macrophages attenuate fibrosis progression by secreting multiple cytokines in wound healing process 48 . Taken together, these results indicate that coculture with M2CM promotes ECM synthesis in TNF‐α‐treated NPCs.…”

Section: Discussionsupporting

confidence: 93%

“…This result was in accordance with that from previous studies; M2 macrophages attenuate fibrosis progression by secreting multiple cytokines in wound healing process. 48 Taken together, these results indicate that coculture with M2CM promotes ECM synthesis in TNF-α-treated NPCs. M2 macrophages contribute to tissue repair by producing antiinflammatory cytokines such as TGF-β, IL-10, and angiogenic vascular endothelial growth factor.…”

Section: M2cm Decreased Ivd Degeneration In Tnf-α-treated Ivd Organ C...mentioning

confidence: 57%

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M2 macrophage‐conditioned medium inhibits intervertebral disc degeneration in a tumor necrosis factor‐α‐rich environment

Luo

et al. 2022

Journal Orthopaedic Research

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BackgroundIn ammation is the primary pathological phenomenon associated with disc degeneration; accordingly, the in ammatory cytokine tumor necrosis factor (TNF-α) plays a crucial role in disc degeneration. M1 macrophages produce proin ammatory cytokines that facilitate the progression of intervertebral disc degeneration (IDD).However, the anti-in ammatory and regenerative effects of M2 macrophages on nucleus pulposus cells (NPCs) in IDD progression remain unknown. Here, we aimed to determine the role of M2 macrophages in IDD progression. MethodsM2 conditioned medium (M2CM) was harvested and puri ed from THP-1 cells; it was then used for culturing human NPCs and a mouse intervertebral disc (IVD) organ culture model. NPCs and IVD organ models were divided into the following three groups: group 1 was treated with 10% fetal bovine serum to actas the control, group 2 was treated with 10 ng/ml TNF-α, and group 3 was treated with 10 ng/ml TNFα and M2CMto act as the co-culture group. After 3 to 14 days, cell proliferation (CCK-8 assay and western blotting for proliferation markers), extracellular matrix synthesis (quantitative polymerase chain reaction, western blotting, and immuno uorescence), apoptosis (TUNEL staining and western blotting), and NPC senescence (senescence-associated beta-galactosidase staining and western blotting) were assessed. ResultsCD206 and interleukin (IL)-10 levels were increased after 48 h of induction for M2 macrophages (both p<0.01). Cell proliferation was decreased in TNF-α-treated NPCs and was inhibited by M2CM co-culture.Moreover, TNF-α treatment enhanced the apoptosis, senescence, and expression of in ammatory factorrelated genes, including IL-6, MMP-13, ADAMTS-4, and ADAMTS-5, whereas M2CM co-culture signi cantly reversed these effects. M2CM promoted aggrecan and collagen II synthesis but reduced collagen Iα1 levels in TNF-α treatment groups. Using our established three-dimensional murine IVD organ culture model, M2CM suppressed the inhibitory effect of TNF-α of the TNF-α-rich environment. ConclusionsCollectively, these results indicate that M2CM promotes cell proliferation and extracellular matrix synthesis and inhibits in ammation, apoptosis, and NPC senescence. This study therefore highlights the therapeutic potential of M2CM for IDD.

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Section: Discussionsupporting

confidence: 93%

Section: M2cm Decreased Ivd Degeneration In Tnf-α-treated Ivd Organ C...mentioning

confidence: 57%

M2 macrophage‐conditioned medium inhibits intervertebral disc degeneration in a tumor necrosis factor‐α‐rich environment

Luo

et al. 2022

Journal Orthopaedic Research

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“…Additionally, TBK1, as a potential therapy target for RIPF, can directly activate the AKT signaling pathway to promote EMT in alveolar epithelial cells. Moreover, the PI3K/AKT signaling pathway can be activated in bleomycin-induced pulmonary fibrosis (the expression of p-PI3K and p-AKT are increasing) [ 53 , 54 , 55 , 56 , 57 ]. In DEC-deficient mice and cells, DEC deficiency improves idiopathic pulmonary fibrosis by inhibiting the PI3K/AKT/GSK-3β/β-Catenin signaling pathway to suppress EMT in AT2 cells [ 58 ].…”

Section: Signaling Pathway Involved In Emt Of At2 Cell In Ripfmentioning

confidence: 99%

The Promising Therapeutic Approaches for Radiation-Induced Pulmonary Fibrosis: Targeting Radiation-Induced Mesenchymal Transition of Alveolar Type II Epithelial Cells

Wang¹,

Yan²,

Zhou³

et al. 2022

IJMS

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Radiation-induced pulmonary fibrosis (RIPF) is a common consequence of radiation for thoracic tumors, and is accompanied by gradual and irreversible organ failure. This severely reduces the survival rate of cancer patients, due to the serious side effects and lack of clinically effective drugs and methods. Radiation-induced pulmonary fibrosis is a dynamic process involving many complicated and varied mechanisms, of which alveolar type II epithelial (AT2) cells are one of the primary target cells, and the epithelial–mesenchymal transition (EMT) of AT2 cells is very relevant in the clinical search for effective targets. Therefore, this review summarizes several important signaling pathways that can induce EMT in AT2 cells, and searches for molecular targets with potential effects on RIPF among them, in order to provide effective therapeutic tools for the clinical prevention and treatment of RIPF.

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“…To more clearly quantify the direction of macrophage polarization, we detected the changes in the expression levels of characteristic genes and key cytokines of macrophages under the M1/M2 phenotype. 44 Compared with MHFPs alone, MHFPs combined with an AMF significantly upregulated the expression of CD 206, a marker gene of M2 phenotype macrophages, and the expression of the Arg1 cytokine, which is also directly related to M2 polarization (Fig. 6b and d).…”

Section: Resultsmentioning

confidence: 89%

Mesoporous hollow Fe₃O₄ nanoparticles regulate the behavior of neuro-associated cells through induction of macrophage polarization in an alternating magnetic field

Guo

Wei

et al. 2022

J. Mater. Chem. B

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Clevudine attenuates bleomycin-induced early pulmonary fibrosis via regulating M2 macrophage polarization

Cited by 15 publications

References 25 publications

M2 macrophage‐conditioned medium inhibits intervertebral disc degeneration in a tumor necrosis factor‐α‐rich environment

M2 macrophage‐conditioned medium inhibits intervertebral disc degeneration in a tumor necrosis factor‐α‐rich environment

The Promising Therapeutic Approaches for Radiation-Induced Pulmonary Fibrosis: Targeting Radiation-Induced Mesenchymal Transition of Alveolar Type II Epithelial Cells

Mesoporous hollow Fe₃O₄ nanoparticles regulate the behavior of neuro-associated cells through induction of macrophage polarization in an alternating magnetic field

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Clevudine attenuates bleomycin-induced early pulmonary fibrosis via regulating M2 macrophage polarization

Cited by 15 publications

References 25 publications

M2 macrophage‐conditioned medium inhibits intervertebral disc degeneration in a tumor necrosis factor‐α‐rich environment

M2 macrophage‐conditioned medium inhibits intervertebral disc degeneration in a tumor necrosis factor‐α‐rich environment

The Promising Therapeutic Approaches for Radiation-Induced Pulmonary Fibrosis: Targeting Radiation-Induced Mesenchymal Transition of Alveolar Type II Epithelial Cells

Mesoporous hollow Fe3O4 nanoparticles regulate the behavior of neuro-associated cells through induction of macrophage polarization in an alternating magnetic field

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Mesoporous hollow Fe₃O₄ nanoparticles regulate the behavior of neuro-associated cells through induction of macrophage polarization in an alternating magnetic field