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Start Over Author "Liu, Limin" Publisher elsevier b.v.
291 results on '"Liu, Limin"'

42. Bioactivated polyetheretherketone scaffold able to generate mild heat for promoting bone regeneration via activating MAPK/ERK signaling pathway.

Author

Zhu, Ce, He, Miaomiao, Wang, Juehan, Huang, Yong, Deng, Wei, Liu, Limin, Feng, Ganjun, Zhang, Li, and Song, Yueming

Subjects
BONE regeneration, PHOTOTHERMAL effect, CELLULAR signal transduction, POLYETHER ether ketone, MITOGEN-activated protein kinases, REMOTE control
Abstract

• A 3D printed PEEK-graphene composite scaffold (PG) with HA coating (PGH) for photothermally remote control of bone regeneration was well designed and prepared. • The mild heat and the boosted Ca2+/PO 4 3− release could synergistically enhance the bone regeneration ability both in vitro and in vivo. • The underlying mechanism of the bone regeneration promotion generated by PTT was confirmed to be closely related to the upregulation of HSP 70, by which the MAPK/ERK signaling pathway was activated selectively. Photothermal therapy (PTT) is a desirable way to attain on-demand hyperthermia owing to the heat generated by photothermal materials absorbing near-infrared) light. The mild heat (42 ± 0.5 °C) can not only accelerate bone tissue regeneration but also promote the release of bioactive ions from biomaterials. Based on this one-stone-two-birds strategy, a 3D printed PEEK-graphene composite scaffold (PG) with hydroxyapatite (HA) coating (PGH) for photothermally remote control of bone regeneration was well designed in this study. The results showed that the HA coating on PGH could release Ca2+ and PO 4 3– ions easily under NIR irradiation, which was ascribed to the mild heat generated from graphene in the composite scaffold. The mild heat and the boosted Ca2+/PO 4 3– release could synergistically enhance the bone regeneration ability both in vitro and in vivo. The underlying mechanism was further explored and confirmed to be closely related to the upregulation of HSP 70, by which the MAPK/ERK signaling pathway was activated selectively. The favorable results demonstrate that the 3D-printed PEEK/graphene composite scaffold is promising in the applications of bone defect repair. [Display omitted] [ABSTRACT FROM AUTHOR]

Published
2024
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45. The ERK-cPLA2-ACSL4 axis mediating M2 macrophages ferroptosis impedes mucosal healing in ulcerative colitis.

Author

Ye, Yulin, Liu, Limin, Feng, Zelin, Liu, Yifei, Miao, Junming, Wei, Xinyue, Li, Huizhen, Yang, Jie, Cao, Xiaocang, and Zhao, Jingwen

Subjects
*ULCERATIVE colitis, *MACROPHAGES, *ARACHIDONIC acid, *METABOLOMICS, *DISEASE remission, *GASTROINTESTINAL diseases
Abstract

Ulcerative colitis (UC) is a chronic gastrointestinal disease that can be managed with 5-aminosalicylic acid (5-ASA), the standard treatment for UC. However, the effectiveness of 5-ASA is not always optimal. Our study revealed that despite 5-ASA treatment, cells continued to experience excessive ferroptosis, which may hinder mucosal healing in UC and limit the success of this treatment approach in achieving disease remission. We found that combining 5-ASA with the ferroptosis inhibitor Fer-1 led to a significant inhibition of ferroptosis in macrophages present in the colon tissue, along with an increase in the proportion of M2 macrophages, suggesting that targeting ferroptosis in M2 macrophages could be a potential therapeutic strategy for alleviating UC. Our study also demonstrated that M2 macrophages are more susceptible to ferroptosis compared to M1 macrophages, and this susceptibility is associated with the activated arachidonic acid (AA) metabolism pathway mediated by ERK-cPLA2-ACSL4. Additionally, we found that the expression of cPLA2 gene pla2g4a was increased in the colon of UC patients compared to healthy controls. Furthermore, targeted metabolomics analysis revealed that the combination treatment group, as opposed to the 5-ASA treatment group, exhibited the ability to modulate AA metabolism. Overall, our findings emphasize the importance of addressing macrophage ferroptosis in order to enhance macrophage anti-inflammation, improve mucosal healing, and achieve better therapeutic outcomes for patients with UC. [Display omitted] • The ferroptosis susceptibility of M2 is greater than that of M1. • The ferroptosis susceptibility of M2 is associated with the ERK-cPLA2-ACSL4 pathway. • The dysregulation of AA contributes to the ineffectiveness of 5-ASA in rescuing ferroptosis in M2. [ABSTRACT FROM AUTHOR]

Published
2024
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