Yunhan Liu

Nanjing University of Finance and Economics

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Tao Zan

Shanghai Jiao Tong University

Yimin Khoong

Shanghai Ninth People's Hospital

Shuchen Gu

Shanghai Ninth People's Hospital

Xin Huang

Shanghai Ninth People's Hospital

Shenying Luo

Shanghai Jiao Tong University

Zewei Zhang

China Academy of Building Research

Yixuan Zhao

Second Affiliated Hospital of Jilin University

Huinan Zhang

Air Force Medical University

Hsin Liang

Shanghai Ninth People's Hospital

Xue Ma

Sichuan University

Cooperative Institutions

Shanghai Jiao Tong University

Shanghai Ninth People's Hospital

Air Force Medical University

Nanjing University of Finance and Economics

Chinese Academy of Sciences

National Natural Science Foundation of China

Tongji University

Nanjing University of Chinese Medicine

Huazhong University of Science and Technology

The First People's Hospital of Changde

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An Orally Active Allosteric GLP-1 Receptor Agonist Is Neuroprotective in Cellular and Rodent Models of Stroke

PLoS ONE (2016)

Huinan Zhang Yunhan Liu Shaoyu Guan Di Qu Ling Wang

Diabetes is a major risk factor for the development of stroke. Glucagon-like peptide-1 receptor (GLP-1R) agonists have been in clinical use for the treatment of diabetes and also been reported to be neuroprotective in ischemic stroke. The quinoxaline 6,7-dichloro-2-methylsulfonyl-3-N-tert- butylaminoquinoxaline (DMB) is an agonist and allosteric modulator of the GLP-1R with the potential to increase the affinity of GLP-1 for its receptor. The aim of this study was to evaluate the neuroprotective effects of DMB on transient focal cerebral ischemia. In cultured cortical neurons, DMB activated the GLP-1R, leading to increased intracellular cAMP levels with an EC50 value about 100 fold that of exendin-4. Pretreatment of neurons with DMB protected against necrotic and apoptotic cell death was induced by oxygen-glucose deprivation (OGD). The neuroprotective effects of DMB were blocked by GLP-1R knockdown with shRNA but not by GLP-1R antagonism. In C57BL/6 mice, DMB was orally administered 30 min prior to middle cerebral artery occlusion (MCAO) surgery. DMB markedly reduced the cerebral infarct size and neurological deficits caused by MCAO and reperfusion. The neuroprotective effects were mediated by activation of the GLP-1R through the cAMP-PKA-CREB signaling pathway. DMB exhibited anti-apoptotic effects by modulating Bcl-2 family members. These results provide evidence that DMB, a small molecular GLP-1R agonist, attenuates transient focal cerebral ischemia injury and inhibits neuronal apoptosis induced by MCAO. Taken together, these data suggest that DMB is a potential neuroprotective agent against cerebral ischemia.

10.1371/journal.pone.0148827

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Citations (43)

Research Progress in Mixed Reality and Simultaneous Motion Simulation

Lecture notes in electrical engineering (2024)

Zengming Li Wei Ji Lixing Feng Huashan Lu Kaibo Zhang

10.1007/978-981-97-7139-4_119

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The application of augmented reality in plastic surgery training and education: A narrative review

Journal of Plastic Reconstructive & Aesthetic Surgery (2023)

Yi Min Khoong Shenying Luo Xin Huang Minxiong Li Shuchen Gu

Bridge (graph theory)

Narrative review

10.1016/j.bjps.2023.04.033

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An effective neighbor information mining and fusion method for recommender systems based on generative adversarial network

Expert Systems with Applications (2024)

Tiansheng Zheng Shuqing Li Yunhan Liu Zhiwang Zhang Mingfeng Jiang

Interaction information

Discriminator

10.1016/j.eswa.2024.123396

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Targeting the nuclear long noncoding transcript LSP1P5 abrogates extracellular matrix deposition by trans-upregulating CEBPA in keloids

Molecular Therapy (2024)

Shuchen Gu Xin Huang Shenying Luo Yunhan Liu Yimin Khoong

Keloids are characterized by fibroblast hyperproliferation and excessive accumulation of extracellular matrix (ECM) and are a major global health care burden among cutaneous diseases. However, the function of long noncoding RNA (lncRNA)-mediated ECM remodeling during the pathogenesis of keloids is still unclear. Herein, we identified a long noncoding transcript, namely, lymphocyte-specific protein 1 pseudogene 5 (LSP1P5), that modulates ECM component deposition in keloids. First, high-throughput transcriptome analysis showed that LSP1P5 was selectively upregulated in keloids and correlated with more severe disease in a clinical keloid cohort. Therapeutically, the attenuation of LSP1P5 significantly decreased the expression of ECM markers (COL1, COL3, and FN1) both in vitro and in vivo. Intriguingly, an antifibrotic gene, CCAAT enhancer binding protein alpha (CEBPA), is a functional downstream candidate of LSP1P5. Mechanistically, LSP1P5 represses CEBPA expression by hijacking Suppressor of Zeste 12 to the promoter of CEBPA, thereby enhancing the polycomb repressive complex 2-mediated H3K27me3 and changing the chromosomal opening status of CEBPA. Taken together, these findings indicate that targeting LSP1P5 abrogates fibrosis in keloids through epigenetic regulation of CEBPA, revealing a novel antifibrotic therapeutic strategy that bridges our current understanding of lncRNA regulation, histone modification and ECM remodeling in keloids.

CEBPA

Keloid

10.1016/j.ymthe.2024.03.031

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Lean adipose tissue macrophage derived exosome confers immunoregulation to improve wound healing in diabetes

Journal of Nanobiotechnology (2023)

Wenzheng Xia Yunhan Liu X. S. Jiang Minxiong Li Shengwu Zheng

Abstract Chronic non-healing wounds, a prevalent complication of diabetes, are associated with increased mortality in diabetic patients. Excessive accumulation of M1 macrophages in diabetic wounds promotes inflammation and results in dysregulated tissue repair. Adipose tissue macrophages (ATMs) derived from healthy lean donors have the ability to improve glucose tolerance and insulin sensitivity, as well as modulate inflammation. MicroRNAs (miRs), which can be packaged into exosomes (Exos) and secreted from cells, serve as essential regulators of macrophage polarization. Here, we revealed that ATMs isolated from lean mice secrete miRs-containing Exos, which modulate macrophage polarization and promote rapid diabetic wound healing when administered to diabetes-prone db/db mice. The miRs sequence of tissue samples from wounds treated with Exos secreted by lean ATMs (Exos Lean ) revealed that miR-222-3p was up-regulated. Further analyses showed that inhibiting miR-222-3p using a miR inhibitor impaired the macrophage-reprogramming effect of Exos Lean . In the excisional skin wound mouse model, locally inhibiting miR-222-3p disrupted healing dynamics and failed to modulate macrophage polarization. Mechanistic studies revealed a connection between miR-222-3p, Bcl2l11/Bim, an inflammatory response effector, macrophage polarization, and diabetic wound healing. In summary, Exos Lean act as positive regulators of macrophage polarization by regulating miR levels in wounds and accelerating wound healing, and thus have important implications for wound management in diabetes. Graphic Abstract

Macrophage polarization

M2 Macrophage

Exosome

10.1186/s12951-023-01869-4

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Citations (26)

Improving the Effectiveness of Two Courses

Journal of Chengde Petroleum College (2003)

Yunhan Liu

This paper pres ents several vi ews on how to improve the effectiveness of Two Courses,which includes a pleasant classroom environment,impact of teacher s personality on students,mass of inform ati on and relief of self-centeredness.

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Improved negative sampling method in collaborative filtering recommendation based on Generative adversarial network

Electronic Commerce Research and Applications (2024)

Mingjie Li Yunhan Liu Weiwei Jiang Yuxuan Zhu Jiuchuan Jiang

Generative adversarial network

10.1016/j.elerap.2024.101412

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Citations (1)

Mechanism and Influencing Factors of Motion Sickness Induced by Virtual Reality Devices

Lecture notes in electrical engineering (2023)