The TGF‑&amp;beta;1/COX‑2‑dependant pathway serves a key role in the generation of OKC‑induced M2‑polarized macrophage‑like cells and angiogenesis

Cheng, Gang; Gao, Jinnan; Wang, Lianfei; Ding, Yude; Wu, Qian; Wang, Quanbing; Xiao, Jialing; Wang, Shibing

doi:10.3892/ol.2020.11900

Cited by 5 publications

(5 citation statements)

References 37 publications

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“…In several previous studies, it has been clearly demonstrated that TGF-β1 inhibits the transformation of macrophages into a pro-in ammatory phenotype (47)(48)(49). In the present study, it was thus hypothesized that Lrg1 may in uence the activation of macrophages via TGF-β1 signaling.…”

Section: Discussionmentioning

confidence: 63%

Lrg1 inhibits the activation of hepatic macrophages to alleviate NAFLD by enhancing TGF-β1 signaling

Han

YANG

et al. 2022

Preprint

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Background: Non-alcoholic fatty liver disease (NAFLD) is caused by excessive hepatic lipid deposition, and is characterized by hepatocyte steatosis, the accumulation of immune cells and the increased expression of inflammatory factors. Hepatic macrophages are the main hepatic immune cells, which play a decisive role in NAFLD. The inhibition of the M1 polarization of hepatic macrophages or the depletion of hepatic macrophages can alleviate hepatic steatosis and inflammation.Methods and Results: NAFLD mouse model was established by feeding high fat diet (HFD) for 16 weeks, the expression of Lrg1 in liver tissues was detected by Real-time PCR and Western blot. Then expression of Lrg1 in steatotic hepatocytes was detected by Real-time PCR and Western blot. Finally, Western-blot analysis, Real-time PCR, HE staining and immumohistochemical staining were performed to confirm the Lrg1 inhibits the activation of hepatic macrophages to alleviate NAFLD by enhancing TGF-β1 signaling. The results of present study demonstrated that Lrg1 inhibited the polarization of M1 liver macrophages induced by steatotic hepatocyte-derived conditioned medium by enhancing TGF-β1 signaling, and Lrg1 also alleviated liver inflammation induced by a high-fat diet (HFD) via TGF-β1 signaling. In addition, the expression level of Lrg1 was significantly decreased in liver tissues from mice with HFD-induced steatosis. Conclusion: Our findings identify that HFD-induced hepatic expression of Lrg1 was significantly downregulated，Lrg1 inhibits the infiltration of hepatic macrophages to alleviates fatty liver inflammation through enhancing TGF-β1 signaling.

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Section: Discussionmentioning

confidence: 63%

Lrg1 inhibits the activation of hepatic macrophages to alleviate NAFLD by enhancing TGF-β1 signaling

Han

YANG

et al. 2022

Preprint

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“…COX2, an NF-kB target gene, is a crucial player in inflammation and an M2 macrophage polarization modulator. [44][45][46] Our results showed that acacetin could inhibit the expression of COX2 and the ratio of p-NF-κB to NF-κB. These results suggested that acacetin protected against sepsis-induced ALI by facilitating M2 macrophage polarization via TRAF6/NF-κB/COX2 axis.…”

Section: Discussionmentioning

confidence: 71%

Acacetin protects against sepsis-induced acute lung injury by facilitating M2 macrophage polarization via TRAF6/NF-κB/COX2 axis

Chang,

Wang,

Cheng

et al. 2023

Innate Immun

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Acute lung injury (ALI) is the leading cause of death in patients with sepsis syndrome and without effective protective or therapeutic treatments. Acacetin, a natural dietary flavonoid, reportedly exerts several biological effects, such as anti-tumor, anti-inflammatory, and anti-oxidative effects. However, acacetin's effect and underlying mechanism on sepsis-induced ALI remain unclear. Here, the mouse model was established to explore the impact of acacetin on sepsis-induced ALI. Acacetin significantly increased ALI murine survival and attenuated lung injury in histological examinations. Additionally, acacetin down-regulated myeloperoxidase activity, protein concentration, and number of neutrophils and macrophages in bronchoalveolar lavage fluid. Subsequently, inflammatory cytokines, including TNF-α, IL-1β, and IL-6, were examined. Results showed that acacetin dramatically suppressed the production of TNF-α, IL-1β, and IL-6. These above results indicated that acacetin attenuated sepsis-induced ALI by inhibiting the inflammatory response. Moreover, acacetin inhibited the expression of markers for M1-type (iNOS, CD86) macrophages and promoted the expression of markers for M2-type (CD206, Arg1) macrophages by western blot. In addition, acacetin down-regulated the expression TRAF6, NF-κB, and Cyclooxygenase-2 (COX2) by western blot. The high concentration of acacetin had a better effect than the low concentration. Besides, over-expression of TRAF6 up-regulated the expression of COX2, CD86, and iNOS, and the ratio of p-NF-κB to NF-κB increased the mRNA levels of TNF-α, IL-1β, and IL-6, down-regulated the expression of CD206 and Arg1. The effects of TRAF6 were the opposite of acacetin. And TRAF6 could offset the impact of acacetin. This study demonstrated that acacetin could prevent sepsis-induced ALI by facilitating M2 macrophage polarization via TRAF6/NF-κB/COX2 axis.

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“…2 g. Additionally, APW-CP showed promising results in M1 polarization and inhibited MDA-MB-231 cell invasion. The MMP-9 and TGF-β are M2 macrophage markers and play roles in tumor progression 54 . To clarify the effect of APW-CP treatment on polarized macrophages, the gene expression of MMP9 and TGFB1 was performed by qRT-PCR.…”

Section: Discussionmentioning

confidence: 99%

M1 macrophages polarized by crude polysaccharides isolated from Auricularia polytricha exhibit anti-tumor effect on human breast cancer cells

Nilkhet,

Mongkolpobsin,

Sillapachaiyaporn

et al. 2024

Sci Rep

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Breast cancer has been reported to correlate with the infiltration of tumor-associated macrophages (TAMs) or M2-like macrophages in tumor microenvironment (TME) that could promote breast cancer progression. In contrast, M1-like macrophages displayed anti-tumor activity toward cancer. This study was focused on Auricularia polytricha (AP), a cloud ear mushroom, which has been reported for anti-tumor activity and immunomodulation. AP extracts were screened on differentiated THP-1 macrophages (M0). Results demonstrated that water extract (APW) and crude polysaccharides (APW-CP) could upregulate M1-related genes and cytokines production (IL-6, IL-1 β and TNF-α) significantly. Moreover, APW and APW-CP showed a high expression of CD86 (M1 marker) compared to M0. The NF-κB signaling pathway is crucial for pro-inflammatory gene regulation. The APW and APW-CP treatment showed the induction of the NF-κB pathway in a dose-dependent manner, which related to the β-glucan content in the extracts. Furthermore, APW-CP polarized macrophages were investigated for anti-tumor activity on human breast cancer cells (MCF-7 and MDA-MB-231). Results showed that APW-CP could inhibit the invasion of breast cancer cells and induce apoptosis. Therefore, M1 macrophages polarized by APW-CP showed anti-tumor activity against the breast cancer cells and β-glucan may be the potential M1-phenotype inducer.

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The TGF‑β1/COX‑2‑dependant pathway serves a key role in the generation of OKC‑induced M2‑polarized macrophage‑like cells and angiogenesis

Cited by 5 publications

References 37 publications

Lrg1 inhibits the activation of hepatic macrophages to alleviate NAFLD by enhancing TGF-β1 signaling

Lrg1 inhibits the activation of hepatic macrophages to alleviate NAFLD by enhancing TGF-β1 signaling

Acacetin protects against sepsis-induced acute lung injury by facilitating M2 macrophage polarization via TRAF6/NF-κB/COX2 axis

M1 macrophages polarized by crude polysaccharides isolated from Auricularia polytricha exhibit anti-tumor effect on human breast cancer cells

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