Search

Your search keyword '"Wu, Minhao"' showing total 465 results
Start Over Author "Wu, Minhao"
465 results on '"Wu, Minhao"'

16. SLAMF7 regulates the inflammatory response in macrophages during polymicrobial sepsis

Author

Wu, Yongjian, Wang, Qiaohua, Li, Miao, Lao, Juanfeng, Tang, Huishu, Ming, Siqi, Wu, Minhao, Gong, Sitang, Li, Linhai, Liu, Lei, and Huang, Xi

Subjects
Immune response -- Physiological aspects -- Health aspects, Sepsis -- Development and progression, Membrane proteins -- Physiological aspects -- Health aspects, Macrophages -- Physiological aspects -- Health aspects, Health care industry
Abstract

Uncontrolled inflammation occurred in sepsis results in multiple organ injuries and shock, which contributes to the death of patients with sepsis. However, the regulatory mechanisms that restrict excessive inflammation are still elusive. Here, we identified an Ig-like receptor called signaling lymphocyte activation molecular family 7 (SLAMF7) as a key suppressor of inflammation during sepsis. We found that the expression of SLAMF7 on monocytes/macrophages was significantly elevated in patients with sepsis and in septic mice. SLAMF7 attenuated TLR-dependent MAPK and NF-[kappa]B signaling activation in macrophages by cooperating with Src homology 2-containing inositol-5'-phosphatase 1 (SHIP1). Furthermore, SLAMF7 interacted with SHIP1 and TNF receptor-associated factor 6 (TRAF6) to inhibit K63 ubiquitination of TRAF6. In addition, we found that tyrosine phosphorylation sites within the intracellular domain of SLAMF7 and the phosphatase domain of SHIP1 were indispensable for the interaction between SLAMF7, SHIP1, and TRAF6 and SLAMF7-mediated modulation of cytokine production. Finally, we demonstrated that SLAMF7 protected against lethal sepsis and endotoxemia by downregulating macrophage proinflammatory cytokines and suppressing inflammation-induced organ damage. Taken together, our findings reveal a negative regulatory role of SLAMF7 in polymicrobial sepsis, thus providing sights into the treatment of sepsis., Introduction Sepsis is one of the leading causes of in-hospital death, but the pathological mechanisms underlying this disease have yet to be uncovered (1). Defining the clinical criteria for the [...]

Published
2023
Full Text
View/download PDF

23. Valence-Change MnO2-Coated Arsenene Nanosheets as a Pin1 Inhibitor for Hepatocellular Carcinoma Treatment

Author

Wang, Jingguo, Liang, Siping, Zhu, Dongdong, Ma, Xiaocao, Peng, Qin, Wang, Guanzhao, Wang, Yuting, Chen, Tiantian, Wu, Minhao, Hu, Tony Y., and Zhang, Yuanqing

Abstract

The heterogeneity of hepatocellular carcinoma (HCC) can prevent effective treatment, emphasizing the need for more effective therapies. Herein, we employed arsenene nanosheets coated with manganese dioxide and polyethylene glycol (AMPNs) for the degradation of Pin1, which is universally overexpressed in HCC. By employing an “AND gate”, AMPNs exhibited responsiveness toward excessive glutathione and hydrogen peroxide within the tumor microenvironment, thereby selectively releasing AsxOyto mitigate potential side effects of As2O3. Notably, AMPNs induced the suppressing Pin1 expression while simultaneously upregulation PD-L1, thereby eliciting a robust antitumor immune response and enhancing the efficacy of anti-PD-1/anti-PD-L1 therapy. The combination of AMPNs and anti-PD-1 synergistically enhanced tumor suppression and effectively induced long-lasting immune memory. This approach did not reveal As2O3-associated toxicity, indicating that arsenene-based nanotherapeutic could be employed to amplify the response rate of anti-PD-1/anti-PD-L1 therapy to improve the clinical outcomes of HCC patients and potentially other solid tumors (e.g., breast cancer) that are refractory to anti-PD-1/anti-PD-L1 therapy.

Published
2024
Full Text
View/download PDF

30. Smart‐Responsive Multifunctional Therapeutic System for Improved Regenerative Microenvironment and Accelerated Bone Regeneration via Mild Photothermal Therapy.

Author

Wu, Minhao, Liu, Huifan, Li, Dan, Zhu, Yufan, Wu, Ping, Chen, Zhe, Chen, Feixiang, Chen, Yun, Deng, Zhouming, and Cai, Lin

Subjects
*BONE regeneration, *METHACRYLATES, *REACTIVE oxygen species, *BIOACTIVE compounds, *BONE growth, *ALGINATES
Abstract

The treatment of bone defects remains a substantial clinical challenge due to the lack of spatiotemporal management of the immune microenvironment, revascularization, and osteogenic differentiation. Herein, deferoxamine (DFO)‐loaded black phosphorus nanosheets decorated by polydopamine layer are prepared (BPPD) and compounded into gelatin methacrylate/sodium alginate methacrylate (GA) hybrid hydrogel as a smart‐responsive therapeutic system (GA/BPPD) for accelerated bone regeneration. The BPPD nanocomposites served as bioactive components and near‐infrared (NIR) photothermal agents, which conferred the hydrogel with excellent NIR/pH dual‐responsive properties, realizing the stimuli‐responsive release of DFO and PO43 − during bone regeneration. Under the action of NIR‐triggered mild photothermal therapy, the GA/BPPD hydrogel exhibited a positive effect on promoting osteogenesis and angiogenesis, eliminating excessive reactive oxygen species, and inducing macrophage polarization to the M2 phenotype. More significantly, through macrophage M2 polarization‐induced osteoimmune microenvironment, this hydrogel platform could also drive functional cytokine secretion for enhanced angiogenesis and osteogenesis. In vivo experiments further demonstrated that the GA/BPPD system could facilitate bone healing by attenuating the local inflammatory response, increasing the secretion of pro‐healing factors, stimulating endogenous cell recruitment, and accelerating revascularization. Collectively, the proposed intelligent photothermal hydrogel platform provides a promising strategy to reshape the damaged tissue microenvironment for augmented bone regeneration. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

45. TREM2/β-catenin attenuates NLRP3 inflammasome-mediated macrophage pyroptosis to promote bacterial clearance of pyogenic bacteria

Author

Wang, Yi, primary, Cao, Can, additional, Zhu, Yanting, additional, Fan, Huifeng, additional, Liu, Qiaojuan, additional, Liu, Yiting, additional, Chen, Kang, additional, Wu, Yongjian, additional, Liang, Siping, additional, Li, Meiyu, additional, Li, Lexi, additional, Liu, Xi, additional, Zhang, Yuanqing, additional, Wu, Chenglin, additional, Lu, Gen, additional, and Wu, Minhao, additional

Published
2022
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results