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Endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury:PERK as a potential target for intervention

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Neural Regeneration Research 2025年第5期20卷 1455-1466页

作者： Ju Zheng Yixin Li Ting Zhang Yanlin Fu Peiyan Long Xiao Gao Zhengwei Wang Zhizhong Guan Xiaolan Qi Wei Hong Yan Xiao key laboratory of Endemic and Ethnic Diseases Ministry of Education&Key Laboratory of Medical Molecular Biology of Guizhou ProvinceGuizhou Medical UniversityGuiyangGuizhou ProvinceChina Guizhou Center for Disease Control and Prevention GuiyangGuizhou ProvinceChina department of Histology and Embryology Guizhou Medical UniversityGuiyangGuizhou ProvinceChina Collaborative Innovation Center for Prevention and Control of Endemic and Ethnic Regional Diseases Co-constructed by the Province and ministry GuiyangGuizhou ProvinceChina

Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion *** occurs within hours after cerebral ischemia,but the relationship between ER stress and autophagy remains *** this study,we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion *** found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2 subunit alpha(e IF2α)-activating transcription factor 4(ATF4)-C/EBP homologous protein(CHOP),increased neuronal apoptosis,and induced ***,inhibition of ER stress using inhibitors or by si RNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis,indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating *** autophagy with chloroquine exacerbated ER stress-induced apoptosis,indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion *** from this study indicate that cerebral ischemia/reperfusion injury can trigger neuronal ER stress and promote autophagy,and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury.

关键词： apoptosis ATF4 autophagy C/EBP homologous protein cerebral ischemia/reperfusion injury eIF2α endoplasmic reticulum stress PERK

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Regulation and function of histone acetyltransferase MOF

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Frontiers of Medicine 2014年第1期8卷 79-83页

作者： Yang Yang Xiaofei Han Jingyun Guan Xiangzhi Li key laboratory of experimental teratology Ministry of Education Department of Cell Biology Shandong University School of MedicineJinan 250012 China

The mammalian MOF （male absent on the first）, a member of the MYST （MOZ, YBF2, SAS2, and Tip60） family of histone acetyltransferases （HATs）, is the major enzyme that catalyzes the acetylation of histone H4 on lysine 16. Acetylation of K16 is a prevalent mark associated with chromatin decondensation. MOF has recently been shown to play an essential role in maintaining normal cell functions. In this study, we discuss the important roles of MOF in DNA damage repair, apoptosis, and tumorigenesis. We also analyze the role of MOF as a key regulator of the core transcriptional network of embryonic stem cells.

关键词： MOF histone acetyltransferase DNA damage repair tumorigenesis embryonic stem cells

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CUL4B negatively regulates Toll-like receptor-triggered proinflammatory responses by repressing Pten transcription

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Cellular & Molecular immunology 2021年第2期18卷 339-349页

作者： Yu Song Peishan Li Liping Qin Zhiliang Xu Baichun Jiang Chunhong Ma Changshun Shao Yaoqin Gong key laboratory of experimental teratology Ministry of EducationInstitute of Molecular Medicine and GeneticsSchool of Basic Medical SciencesShandong UniversityJinanShandongChina key laboratory of experimental teratology Ministry of EducationDepartment of ImmunologySchool of Basic Medical ScienceShandong UniversityJinanShandongChina State key laboratory of Radiation Medicine and Protection Institutes for Translational MedicineSoochow UniversitySuzhouJiangsuChina

Toll-like receptors (TLRs) play critical roles in innate immunity and inflammation. The molecular mechanisms by which TLR signaling is fine-tuned remain to be completely elucidated. Cullin 4B (CUL4B), which assembles the CUL4B-RING E3 ligase complex (CRL4B), has been shown to regulate diverse developmental and physiological processes by catalyzing monoubiquitination for histone modification or polyubiquitination for proteasomal degradation. Here, we identified the role of CUL4B as an intrinsic negative regulator of the TLR-triggered inflammatory response. Deletion of CUL4B in macrophages increased the production of proinflammatory cytokines and decreased anti-inflammatory cytokine IL-10 production in response to pathogens that activate TLR3, TLR4, or TLR2. Myeloid cell-specific Cul4b knockout mice were more susceptible to septic shock when challenged with lipopolysaccharide, polyinosinic-polycytidylic acid or Salmonella typhimurium infection. We further demonstrated that enhanced TLR-induced inflammatory responses in the absence of CUL4B were mediated by increased GSK3β activity. Suppression of GSK3β activity efficiently blocked the TLR-triggered increase in proinflammatory cytokine production and attenuated TLR-triggered death in Cul4b mutant mice. Mechanistically, CUL4B was found to negatively regulate TLR-triggered signaling by epigenetically repressing the transcription of Pten, thus maintaining the anti-inflammatory PI3K-AKT-GSK3β pathway. The upregulation of PTEN caused by CUL4B deletion led to uncontrolled GSK3β activity and excessive inflammatory immune responses. Thus, our findings indicate that CUL4B functions to restrict TLR-triggered inflammatory responses through regulating the AKT-GSK3β pathway.

关键词： CUL4B TLR signaling Transcriptional repression

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Regulation of cellular senescence by innate immunity

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Biophysics Reports 2023年第6期9卷 338-351页

作者： Jinxiu Hou Yi Zheng Chengjiang Gao key laboratory of Infection and Immunity Shandong Province & Key Laboratory for Experimental TeratologyMinistry of Education Shandong University department of immunology the School of Basic Medical Sciences Shandong University

During the COVID-19 pandemic, the interplay between the processes of immunity and senescence is drawing more and more intensive attention. SARS-Co V-2 infection induces senescence in lung cells,failure to clear infected cells and increased presence of inflammatory factors could lead to a cytokine storm and acute respiratory disease syndrome(ARDS), which together with aging and age-associated disease lead to 70% of COVID-19-related deaths. Studies on how senescence initiates upon viral infection and how to restrict excessive accumulation of senescent cells to avoid harmful inflammation are crucially important. Senescence can induce innate immune signaling, and innate immunity can engage cell senescence. Here, we mainly review the innate immune pathways, such as c GAS-STING, TLRs, NF-κB, and NLRP3 inflammasome, participating in the senescence process. In these pathways, IFN-I and inflammatory factors play key roles. At the end of the review, we propose the strategies by which we can improve the immune function and reduce inflammation based on these findings.

关键词： NF-κB NLRP3 inflammasome cGAS-STING IFN-I TLRs Cell senescence

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USP3 deubiquitinates and stabilizes the adapter protein ASC to regulate inflammasome activation

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Cellular & Molecular immunology 2022年第10期19卷 1141-1152页

作者： Wanxin Zhuang Lei Zhang Yi Zheng Bingyu Liu Chunhong Ma Wei Zhao Suxia Liu Feng Liu Chengjiang Gao key laboratory of Infection and Immunity of Shandong Province&key laboratory for experimental teratology of ministry of education Shandong UniversityJinanShandong250012PR China department of immunology School of Biomedical SciencesShandong UniversityJinanShandong250012PR China

Inflammasomes are essential components of the innate immune system and its defense against infections,whereas the dysregulation of inflammasome activation has a detrimental effect on human *** activation of inflammasomes is subjected to tight regulation to maintain immune homeostasis,yet the underlying mechanism remains ***,we identify USP3 as a direct deubiquitinating enzyme(DUB)for ASC,the central adapter mediating the assembly and activation of most ***3 removes the K48-linked ubiquitination on ASC and strengthens its stability by blocking proteasomal ***,USP3 promotes inflammasome activation,and this function was confirmed in mouse models of aluminum(Alum)-induced peritonitis,*** infection and flagellin-induced pneumonia in *** work unveils that USP3 functions as a key regulator of ASC ubiquitination and maintains the physiological role of ASC in mediating inflammasome activation,and we propose a new mechanism by which the ubiquitination of ASC regulates inflammasome activation.

关键词： ASC inflammasome K48-linked ubiquitination proteasomal degradation USP3

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Mechanisms and immunotherapies of HBV- and NAFLD-related hepatocellular carcinoma

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Hepatoma Research 2020年第5期6卷 82-96页

作者： Xiao-Jia Song Chun-Hong Ma key laboratory for experimental teratology of ministry of education and department of immunology School of Basic Medical ScienceShandong UniversityJinan 250012ShandongChina

Hepatitis B virus(HBV)infection remains the most important risk factor for hepatocellular carcinoma(HCC)worldwide and nonalcoholic fatty liver disease(NAFLD)has developed as major etiology of chronic liver diseases,cirrhosis and eventually HCC in the last *** nucleos(t)ide analogs are recommended as the first-line drug for patients with chronic hepatitis B,incomplete eradication of HBV serves as an obstacle for effective cure of chronic hepatitis B and even *** refers to a spectrum of hepatic metabolic disorders,compromised with multi-system *** the specificity of hepatocytes and enrichment of immune cells in liver,this review aims to summarize the mechanisms of direct pro-tumorigenesis to hepatocytes induced by HBV infection and abnormal lipid metabolism,and indirect oncogenic processes mediated by immune *** also discuss similarities and differences of immune cells between HBV-and NAFLD-HCC and finally focus on the novel immunotherapies concerning preclinical and clinical studies for liver cancer.

关键词： Hepatitis B virus nonalcoholic fatty liver disease hepatocellular carcinoma immune cells immunotherapy

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Expression of thymosin-β4, RACK1 and HMGB in adult amphioxus: implication for the evolutionary conservation of organ related functional molecules

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Progress in Natural Science:Materials International 2007年第1期17卷 49-53页

作者： ZHANG Wei, LI Baojun, LI Xinyi, WANG Lifeng, HUANG Xiangwei, HUANG Shuhong, YANG Ling and ZHANG Hongwei (Institute of Developmental Biology, College of Life Science, Shandong University, Jinan 250100, China The key laboratory of experimental teratology, ministry of education, Jinan 250100, China) [a]Institute of Developmental Biology College of Life Science Shandong University Jinan China [b]The key laboratory of experimental teratology Ministry of Education Jinan China

Vertebrate thymosin-β4, RACK1 and HMGB are important molecules functioning in embryonic development and adult life. Here we report the expression patterns of amphioxus thymosin-β4, RACK1 and HMGB genes in tissues of adult amphioxus as revealed by RT-PCR and in situ hybridization. These three genes are all strongly expressed in the central nervous system and ovary, but differently expressed in other tissues including gut, testis, wheel organ, gill and endostyle.

关键词： amphioxus expression Thymosin-β4 RACK1 HMGB conservation.

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Monocyte-derived KCs(MoKCs)contribute to the KC pool in NASH

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Cellular & Molecular immunology 2021年第3期18卷 518-519页

作者： Yingchun Wang Lifen Gao key laboratory for experimental teratology of ministry of education Shandong Key Laboratory of Infection and Immunityand Department of ImmunologySchool of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong 250012P.R.China

Nonalcoholic fatty liver disease(NAFLD)is now recognized as the most common liver disease worldwide and has increasingly become a serious hazard to human *** consists of a spectrum of disease states ranging from simple steatosis to more severe disease termed nonalcoholic steatohepatitis(NASH),fibrosis,cirrhosis,and even hepatocellular carcinoma.

关键词： NAFLD liver NASH

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CUL4B orchestrates mesenchymal stem cell commitment by epigenetically repressing KLF4 and C/EBPδ

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Bone Research 2023年第2期11卷 427-441页

作者： Ruiqi Yu Hong Han Shuxian Chu Yijun Ding Shiqi Jin Yufeng Wang Wei Jiang Yuting Liu Yongxin Zou Molin Wang Qiao Liu Gongping Sun Baichun Jiang Yaoqin Gong The key laboratory of experimental teratology of the ministry of education and department of Genetics School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinan 250012China The key laboratory of Liquid-Solid Structural Evolution and Processing of Materials of ministry of education and Institute of Liquid Metal and Casting Technology School of Materials Science and EngineeringShandong UniversityJinan 250012China The key laboratory of experimental teratology of the ministry of education and department of Histology and Embryology School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinan 250012China

Dysregulated lineage commitment of mesenchymal stem cells(MSCs)contributes to impaired bone formation and an imbalance between adipogenesis and osteogenesis during skeletal aging and *** intrinsic cellular mechanism that regulates MSC commitment remains ***,we identified Cullin 4B(CUL4B)as a critical regulator of MSC ***4B is expressed in bone marrow MSCs(BMSCs)and downregulated with aging in mice and *** knockout of Cul4b in MSCs resulted in impaired postnatal skeletal development with low bone mass and reduced bone ***,depletion of CUL4B in MSCs aggravated bone loss and marrow adipose accumulation during natural aging or after *** addition,CUL4B deficiency in MSCs reduced bone ***,CUL4B promoted osteogenesis and inhibited adipogenesis of MSCs by repressing KLF4 and C/EBPδexpression,*** CUL4B complex directly bound to Klf4 and Cebpd and epigenetically repressed their ***,this study reveals CUL4B-mediated epigenetic regulation of the osteogenic or adipogenic commitment of MSCs,which has therapeutic implications in osteoporosis.

关键词： CUL4B impaired epigenetic

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Cullin 4B-RING E3 ligase complex in immune cell differentiation and function

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Cellular & Molecular immunology 2023年第10期20卷 1254-1256页

作者： Yu Song Shiqi Jin Gongping Sun Yaoqin Gong key laboratory of experimental teratology of the ministry of education Department of Molecular Medicine and GeneticsSchool of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong250012China key laboratory of experimental teratology of the ministry of education Department of Histology and EmbryologySchool of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong250012China

CUL4B,which encodes the scaffold protein in the CRL4B complex,is a commonly mutated gene in X-linked intellectual disability[10,11].In addition to intellectual disability,patients with CUL4B mutations present with an elevated number of monocytes in peripheral blood[10],implying a role for CUL4B in regulating monocytes/***/macrophages are critical players in innate *** et *** that depletion of CUL4B in myeloid cells aggravated lipopolysaccharide(LPS)-induced acute peritonitis[3].They further showed that after LPS stimulation,Cul4b-deficient macrophages secreted more chemokines than control macrophages,which might have accounted for the elevated infiltration of immune cells into the peritoneum[3].Our previous work demonstrated that myeloid-specific Cul4b-knockout mice exhibited reduced survival after LPS injection or Salmonella typhimurium infection compared to control mice[6].In contrast to work from Hung et al.,which showed that Cul4b-deficient macrophages secreted less TNFαand IL-6 after LPS stimulation[3],our works showed that deletion of CUL4B in macrophages increased the production of proinflammatory cytokines and decreased the expression of the anti-inflammatory cytokine IL-10 in response to the activation of Toll-like receptor(TLR).CUL4B regulation of macrophages relies on the ubiquitination activity of the CRL4B *** CRL4B complex catalyzes monoubiquitination of H2AK119 at the promoter of Pten,resulting in the repression of Pten transcription and subsequent activation of AKT and AKT-dependent inhibition of GSK3β,which suppresses TLR-triggered proinflammatory responses(Fig.1B)[6].

关键词： GSK3β elevated stimulation

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