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ATF4/TxNIP/REDD1/mTOR signaling mediates the antitumor activities of liver x receptor in pancreatic cancers

Cancer Innovation 2022年第1期1卷 55-69页

作者： Zhikang Chen xiaobo Lai Hui Ding Aijun Zhang Yufei Sun Jianhua Ling Paul J.Chiao Zihua Chen xuefeng xia The Hunan Provincial Key Lab of Precision Diagnosis and Treatment for Gastrointestinal Tumor ChangshaHunanChina Department of General Surgery Xiangya HospitalCentral South UniversityChangshaHunanChina International Joint Research Center of Minimally Invasive Endoscopic Technology Equipment&Standardization ChangshaHunanChina National Clinical Research Center for Geriatric Disorders Xiangya HospitalChangshaHunanChina Guangzhou First People's Hospital The Second Affiliated Hospital of South China University of TechnologyGuangzhouGuangdongChina Hainan Eye Hospital and Key Laboratory of Ophthalmology Zhongshan Ophthalmic CenterSun Yat-Sen UniversityHaikouHainanChina Houston Methodist Research Institute HoustonTexasUSA Department of Molecular and Cellular Oncology The University of Texas MD Anderson Cancer CenterHoustonTexasUSA GenePlus‐Beijing Institute BeijingChina

Background:Limited by difficulties in early detection and availabilities of effective treatments,pancreatic cancer is a highly malignant disease with poor prognosis.Nuclear receptors are a family of ligand‐dependent transcription factors that are highly druggable therapeutic targets playing critical roles in human physiological and pathological development,including cancer.In this study,we explored the therapeutic potential as well as the molecular mechanisms of liver x receptor(LxR)agonist GW3965 in pancreatic cancer.Methods:Soft‐agar colony formation assay,xenograft tumors,Oligonucleotide microarray,Reverse transcription real‐time polymerase chain reaction,Western immunoblotting and Immunohistochemistry were used in this study.Results:We demonstrated pleotropic in vitro activities of GW3965 in pancreatic cell lines MIA PaCa‐2 and BxPC3 including reduction of cell viability,inhibition of cell proliferation,stimulation of cell death,and suppression of colony formation,which translated to significant inhibition of xenograft tumor growth in vitro.By mapping the gene expression profiles,we identified the up‐regulations of 188 and the down‐regulations of 92 genes common to both cell lines following GW3965 treatment.Genes responsive to GW3965 represent a variety of biological pathways vital for multiple cellular functions.Specifically,we identified that the activating transcription factor 4/thioredoxin‐interacting protein/regulated in development and DNA damage responses 1/mechanistic target of rapamycin(ATF4/TxNIP/REDD1/mTOR)signaling critically controls GW3965‐mediated regulation of cell proliferation/death.The significance of the ATF4/TxNIP/REDD1/mTOR pathway was further supported by associated expressions in xenograft tumors as well as human pancreatic cancer samples.Conclusions:This study provides the pre‐clinical evidence that LxR agonist is a promising therapy for pancreatic cancer.

关键词： GW3965 liver x receptor nuclear receptors pancreatic cancer signaling pathways

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liver as a new target organ in Alzheimer's disease:insight from cholesterol metabolism and its role in amyloid-beta clearance

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Neural Regeneration Research 2025年第3期20卷 695-714页

作者： Beibei Wu Yuqing Liu Hongli Li Lemei Zhu Lingfeng Zeng Zhen Zhang Weijun Peng Department of Integrated Traditional Chinese&Western Medicine The Second Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina Academician Workstation Changsha Medical UniversityChangshaHunan ProvinceChina Yangsheng College of Traditional Chinese Medicine Guizhou University of Traditional Chinese MedicineGuiyangGuizhou ProvinceChina Qinhuangdao Shanhaiguan Pharmaceutical Co. LtdQinhuangdaoHebei ProvinceChina National Clinical Research Center for Mental Disorder The Second Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina

Alzheimer's disease,the primary cause of dementia,is characterized by neuropathologies,such as amyloid plaques,synaptic and neuronal degeneration,and neurofibrillary tangles.Although amyloid plaques are the primary characteristic of Alzheimer's disease in the central nervous system and peripheral organs,targeting amyloid-beta clearance in the central nervous system has shown limited clinical efficacy in Alzheimer's disease treatment.Metabolic abnormalities are commonly observed in patients with Alzheimer's disease.The liver is the primary peripheral organ involved in amyloid-beta metabolism,playing a crucial role in the pathophysiology of Alzheimer's disease.Notably,impaired cholesterol metabolism in the liver may exacerbate the development of Alzheimer's disease.In this review,we explore the underlying causes of Alzheimer's disease and elucidate the role of the liver in amyloid-beta clearance and cholesterol metabolism.Furthermore,we propose that restoring normal cholesterol metabolism in the liver could represent a promising therapeutic strategy for addressing Alzheimer's disease.

关键词： ABCA1 Alzheimer's disease amyloid-beta apolipoprotein E cholesterol metabolism liver liver x receptor low-density lipoprotein receptor-related protein 1 peripheral clearance tauroursodeoxycholic acid

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Comparison of Tolerogenic Dendritic Cells Induced by liver x receptor Agonist from Bone Marrow-derived Cells and Natural Tolerogenic Dendritic Cells

Comparison of Tolerogenic Dendritic Cells Induced by Liver X...

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第十届全国免疫学学术大会

作者： Haiyan xu xuyi Ma Dan Song Dong xue xiaozhou He xueguang Zhang Third Affiliated Hospital of Soochow University Biotechnological Institute of Soochow University

Background:Mouse dendritic cells(DCs)possessed the tolerogenic potentiality after induced by liver x receptor(LxR)agonist.While the characteristics and mechanisms of the induced DCs were still known little.Methods:Mouse bone marrow cells were pulsed with interleukin(IL)-4 and granulocyte-macrophage colony-stimulating factor(GM-CSF)with or without LxR agonist-T0901317 for 7 days,or induced with lipopolysaccharide for 3 days.Cellular biomarkers,inducing ability of T cell proliferation and regulatory T cells(Treg)formation,and cytokines in culture supernatants were tested,respectively.OVA-specific CD4+T cells purified from BALB/c DO11.10 RAG-/-mice were purified in Treg induction assay.NF-κB inhibitors and PI3K inhibitors were applied during cell culture.Natural t DCs(Nt DCs)isolated from mouse spleens were used as controls.Results:Compared with the N-t DCs,the morphology of T-t DCs(induced by T0901317 for 7 days)was similar to that of normal DCs but had slightly lower or moderate expression levels of CD80,CD86 and MHCⅡ.The N-t DCs couldsignificantly inhibit T cell proliferation;while T-t DCs lost their stimulatory effect on T cell viability.The co-treatment of T0901317 with NF-κB inhibitors or PI3K inhibitors propagated the inhibitory effect and resulted in significantly reduced T cell viability.The N-t DCs could induce the formation of Tregs,which was enhanced in the presence of TGF-β;However,T-t DCs did not have this capability.T-t DCs secreted much higher levels of IL-10 than did the N-t DCs.Neither the T-t DCs nor the N-t DCs produced indoleamine 2,3-dioxygenase.Conclusions:Compared with N-t DCs,T-t DCs have inhibitory effects.But they should function via different modes,involving the NF-κB and PI3K signal pathways.

关键词： Tolerant Dendritic cells liver x receptor Regulator T cells IL-10

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Activation of liver x receptor protects the Bergmann glia and Purkinje neurons in ethanol-induced developmental delay in mouse cerebellum

Activation of liver x receptor protects the Bergmann glia an...

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中国神经科学学会第十届全国学术会议

作者： Yang YANG Yongping TANG Yan xING Haiwei xU xiaotang FAN Department of Histology and Embryology Third Military Medical University Southwest Eye Hospital Southwest HospitalThird Military Medical University Key Lab of Visual Damage and Regeneration & Restoration of Chongqing Institute of Immunology PLAThird Military Medical University

Objective The development of cerebellar Purkinje cells and granule cells is coordinated by Bergmann glia and is particularly sensitive to ethanol exposure.liver x receptors play important roles in the development of Bergmann glia,while it has not been clarified whether the activation of liver x receptors protected the Bergmann glia and thus rescued ethanol exposure induced defects in Purkinje cell dendritogenesis.Methods In this study,the cytoarchitecture changes in Bergmann glia and their relationship with granule cells and Purkinje cells were evaluated using Golgi staining and immunohistochemistry staining for the cell marker NeuN,Calbindin and BLBP.Results It demonstrated that a brief neonatal exposure to ethanol significantly decreased the average body weight of mouse pups at postnatal days 6.Although there was no difference in the general cerebellar morphology or the number of NeuN-positive granule cells in the inner granule cell layer after ethanol exposure,the number of migrating granule cells in the molecular layer was significantly decreased,and this effect seems to be attenuated by pretreating mice with T0901317（T0）.Brief ethanol exposure also resulted in significant reduction in the number of Calbindin-positive cells and their maximum dendrite length,as well as impaired Purkinje cell dendritogenesis and delayed Bergmann glial cell development;these effects were blocked by pretreatment of TO.The treatment of TO blocked the increasing of p-catenin and LEF1expression in the cerebellum of ethanol exposured mice.Conclusion It suggests that activating liver x receptors in mice exposed to ethanol postnatally produced protection on the Bergmann glia,which plays a critical role in preventing ethanol-induced defects during cerebellar development.

关键词： cerebellum development alcohol mouse liver x receptor

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Influence of liver x receptor activation on the microenvironment of retinal degeneration mice model and its protective effect on grafted neural stem cells

Influence of liver x receptor activation on the microenviron...

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中国神经科学学会第十二届全国学术会议

作者： xiao He Dayu Sun Luodan A Siyu Chen Haiwei xu Southwest Hospital/Southwest Eye Hospital Third Military Medical University Key Lab of Visual Damage and Regeneration & Restoration of Chongqing

Objective Retinal degeneration（RD） including retinitis pigmentosa（RP） is a kind of hereditary eye disease characterized by progressive photoreceptor loss, there is no effective treatment. Stem cell transplantation is the most promising strategy of treating RD. It is well known that the fate of transplanted cells is affected by its microenvironment. However, it has not been clarified whether activation of liver x receptor can improve the protective effect on grafted neural stem cells in the degenerative retina. Methods Immunohistochemistry and Western blotting were performed to compare the effects of LxRs activation on photoreceptor apoptosis, Müller cell and microglia activation in mouse retina. The retinal function was observed by retinal electroretinogram（ERG） test. Gene expression patterns were detected by microarray technique. Neural stem cells（NSCs） C17.2 were transplanted into subretinal space of Rd1 mice at P14. Results LxRs activation significantly inhibited the expression of GFAP in Müller cells,reduced the number of activated microglia and apoptotic photoreceptor cells in Rd1 mice. ERG results showed a significant increase in b-wave amplitude of T0-treated Rd1 mice. Microarray and RT-q PCR results showed that T0 regulated the microenvironment of degenerative retina and delayed the process of retinal degeneration through the JAK3-STAT pathway. LxRs activation can increase the proliferation of L2.3 and the survival rate of neural stem cells C17.2 transplanted into vitreous cavity of Rd1 mice treated with T0 was markedly increased. Conclusion Activation of liver x receptor improves the microenvironment of retinal degeneration mice model and promotes the survival of grafted neural stem cells.

关键词： Retinal degeneration liver x receptor JAK-STAT signaling pathway Müller cells Microglia Neural stem cells

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Local Microenvironment Determines the Immunosuppressive Effect of Tolerogenic Bone Marrow-derived Dendritic Cells Pulsed by liver x receptor Agonist

Local Microenvironment Determines the Immunosuppressive Effe...

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第十三届全国免疫学学术大会

作者： Haiyan xu xiaozhou He Renfang xu Third Affiliated Hospital of Soochow University

Backgrounds: In our previous study, we showed that mice bone-marrow-derived dendritic cells pulsed by liver x receptor agonist-T0901317 developed tolerogenic characteristics, and they were thereafter designated as T-tDCs.In the present study, we further investigated the suppressive effect of T-tDCs and explored its underlying mechanism.Methods: T-tDCs were generated as described in our previous study.The distribution of T-tDCs in vivo was analyzed, and the different amounts of T-tDCs cells were intravenously injected twice into the skin transplanted mice model.The status of allografts was evaluated 8, 9, 11, and 14 days after transplantation.Experimental specimens were analyzed by fluorescent multiple immunohistochemistry, real-time PCR, immunoblotting, ELISA and mixed lymphocyte reaction.Results: T-tDCs could migrate into peripheal lymphoid organs, skin, and liver.The rejection scores significantly decreased in the medium density(MD) and high density(HD) treatment groups 9 and 14 days after transplantation.The results showed that TGF-b1 levels in the skin allografts of HD groups and the IL-10 levels in the HD and low density(LD) treatment grous significantly increased, although serum TGF-b1 levels in the MD and HD groups markedly decreased.CD4FoxP3 Treg frequency in LD and HD groups significantly increased.The results of mixed lymphocyte reaction suggested the TGF-b1 and IL-10 that were secreted by T-tDCs are involved in the observed suppressive effects.LxRa is thus a candidate receptor of the LxR agonist-T0901317, and the NF-kB and PI3K signaling pathways participate in the inhibition of T-tDCs.Conclusions: The local environment of skin allografts, high levels of TGF-b1, IL-10, and Treg frequency are fundamental mechanisms utilized by T-tDCs in eliciting their suppressive effects.

关键词： Tolerogenic dendritic cells liver x receptor Transform growth factor-b1 Interleukin-10

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The LxRB-SREBP1 network regulates lipogenic homeostasis by controlling the synthesis of polyunsaturated fatty acids in goat mammary epithelial cells

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Journal of Animal Science and Biotechnology 2023年第2期14卷 614-626页

作者： Wenying Zhang Changhui Zhang Jun Luo Huifen xu Jianxin Liu Juan JLoor Hengbo Shi Institute of Dairy Science College of Animal SciencesZhejiang UniversityHangzhou 310058China College of Animal Science and Technology Northwest A&F UniversityYangling 712100China College of Animal Science and Technology Henan Agricultural UniversityZhengzhou 450046China Key Laboratory of Molecular Animal Nutrition(Zhejiang University) Ministry of EducationHangzhou310058China Mammalian Nutrition Physiology Genomics Department of Animal Sciences and Division of Nutritional SciencesUniversity of IllinoisUrbanaIL 61801USA.

Background:In rodents,research has revealed a role of liver x receptors(LxR) in controlling lipid homeostasis and regulating the synthesis of polyunsaturated fatty acids(PUFA).Recent data suggest that LxRB is the predominant LxR subtype in ruminant mammary cells,but its role in lipid metabolism is unknown.It was hypothesized that LxRB plays a role in lipid homeostasis via altering the synthesis of PUFA in the ruminant mammary gland.We used overexpression and knockdown of LxRB in goat primary mammary epithelial cells(GMEC) to evaluate abundance of lipogenic enzymes,fatty acid profiles,content of lipid stores and activity of the stearoyl-Co A desaturase(SCD1) promoter.Results:Overexpression of LxRB markedly upregulated the protein abundance of LxRB while incubation with si RNA targeting LxRB markedly decreased abundance of LxRB protein.Overexpression of LxRB plus T0901317(T09,a ligand for LxR) dramatically upregulated SCD1 and elongation of very long chain fatty acid-like fatty acid elongases 5–7(ELOVL 5–7),which are related to PUFA synthesis.Compared with the control,cells overexpressing LxRB and stimulated with T09 had greater concentrations of C16:0,16:1,18:1n7,18:1n9 and C18:2 as well as desaturation and elongation indices of C16:0.Furthermore,LxRB-overexpressing cells incubated with T09 had greater levels of triacylglycerol and cholesterol.Knockdown of LxRB in cells incubated with T09 led to downregulation of genes encoding elongases and desaturases.Knockdown of LxRB attenuated the increase in triacylglycerol and cholesterol that was induced by T09.In cells treated with dimethylsulfoxide,knockdown of LxRB increased the concentration of C16:0 at the expense of C18:0,while a significant decrease in C18:2 was observed in cells incubated with both si LxRB and T09.The abundance of sterol regulatory element binding transcription factor 1 precursor(p SREBP1) and its mature fragment(n SREBP1) was upregulated by T09,but not LxRB overexpression.In the cells cultured with T09,knockdown of LxRB downregulated the abundance

关键词： Elongase Lipid homeostasis liver x receptor Mammary gland Polyunsaturated fatty acids

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Remembering your A, B, C’s: Alzheimer’s disease and ABCA1

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Acta Pharmaceutica Sinica B 2022年第3期12卷 995-1018页

作者： Cutler T.Lewandowski Megan S.Laham Gregory R.J.Thatcher Department of Pharmaceutical Sciences University of Illinois College of PharmacyChicagoIL 60612USA Department of Pharmacology and Toxicology University of Arizona College of PharmacyTucsonAZ 85721USA

The function of ATP binding cassette protein A1(ABCA1)is central to cholesterol mobilization.Reduced ABCA1 expression or activity is implicated in Alzheimer’s disease(AD)and other disorders.Therapeutic approaches to boost ABCA1 activity have yet to be translated successfully to the clinic.The risk factors for AD development and progression,including comorbid disorders such as type2 diabetes and cardiovascular disease,highlight the intersection of cholesterol transport and inflammation.Upregulation of ABCA1 can positively impact APOE lipidation,insulin sensitivity,peripheral vascular and blood-brain barrier integrity,and anti-inflammatory signaling.Various strategies towards ABCA1-boosting compounds have been described,with a bias toward nuclear hormone receptor(NHR)agonists.These agonists display beneficial preclinical effects;however,important side effects have limited development.In particular,ligands that bind liver x receptor(LxR),the primary NHR that controls ABCA1 expression,have shown positive effects in AD mouse models;however,lipogenesis and unwanted increases in triglyceride production are often observed.The longstanding approach,focusing on LxRβvs.LxRa selectivity,is over-simplistic and has failed.Novel approaches such as phenotypic screening may lead to small molecule NHR modulators that elevate ABCA1 function without inducing lipogenesis and are clinically translatable.

关键词： Alzheimer’s disease Cardiovascular disease Cholesterol Drug discovery liver x receptor Nuclear hormone receptor Type 2 diabetes

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Effect of Marine Collagen Peptides on Markers of Metabolic Nuclear receptors in Type 2 Diabetic Patients with/without Hypertension

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Biomedical and Environmental Sciences 2010年第2期23卷 113-120页

作者： CuI-FENG ZHU GUAN-ZHI LI HONG-BIN PENG FAN ZHANG YUN CHEN YONG LI Department of Nutrition and Food Hygiene School of Public Health Peking University Beijing 10083 China Department of Nutrition Shenzhen Hospital of Peking University Shenzhen 518036 Guangdong China. Department of Endocrinology Shenzhen Hospital of Peking University Shenzhen 518036 Guangdong China. Department of Ultrasound Division Shenzhen Hospital of Peking University Shenzhen 518036 Guangdong China.

Objective To explore Effects of marine collagen peptides （MCPs） on markers of metablic nuclear receptors, i.e peroxisome proliferator-activated receptor （PPARs）, liver x receptor （LxRs） and farnesoid x receptor （FxRs） in type 2 diabetic patients with/without hypertension. Method Study population consisted of 200 type 2 diabetic patients with/without hypertension and 50 healthy subjects, all of whom were randomly assigned to MCPs-treated diabetics （n=50）, placebo-treated diabetics （n=50）, MCPs-treated diabetics with hypertension （n=50）, placebo-treated diabetics with hypertension （n=50）, and healthy controls （n=50）. MCPs or placebo （water-soluble starch） were given daily before breakfast and bedtime over three months. Levels of free fatty acid, cytochrome P450, leptin, resistin, adiponectin, bradykinin, NO, and Prostacyclin were determined before intervention, and 1.5 months, and 3 months after intervention. Hypoglycemia and the endpoint events during the study were recorded and compared among the study groups. Result At the end of the study period, MCPs-treated patients showed marked improvement compared with patients receiving placebo. The protection exerted by MCPs seemed more profound in diabetics than in diabetics with hypertension. In particular, after MCPs intervention, levels of free fatty acid, hs-CRP, resistin, Prostacyclin decreased significantly in diabetics and tended to decrease in diabetic and hypertensive patients whereas levels of cytochrome P450, leptin, NO tended to decrease in diabetics with/without hypertension. Meanwhile, levels of adiponectin and bradykinin rose markedly in diabetics following MCPs administration. Conclusion MCPs could offer protection against diabetes and hypertension by affecting levels of molecules involved in diabetic and hypertensive pathogenesis. Regulation on metabolic nuclear receptors by MCPs may be the possible underlying mechanism for its observed effects in the study. Further study into its action may shed light on development of new drugs based on bioactive pept

关键词： Marine collagen peptide Peroxisome proliferator-activated receptor （PPAR） liver x receptor Famesoid x receptor Metabolic nuclear receptor

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Effect of Quercetin on Atherosclerosis Based on Expressions of ABCA1, LxR-α and PCSK9 in ApoE-/- Mice

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Chinese Journal of Integrative Medicine 2020年第2期26卷 114-121页

作者： LI Shan-shan CAO Hui SHEN Ding-zhu CHEN Chuan xING San-li DOU Fang-fang JIA Qing-ling Shanghai Geriatric Institute of Chinese Medicine Shanghai University of Traditional Chinese Medicine

Objective:To investigate the effect of quercetin on ATP binding cassette transporter A1(ABCA1),liver x receptor(LxR),and proprotein convertase subtilisin/kexin type 9(PCSK9)expressions in apoE-knockout(ApoE-/-)mice.Methods:The high-fat diet-induced atherosclerosis(AS)in ApoE-/-mice was established.Thirtysix mice were divided into 3 groups using random number table method:model group(n=12),quercetin group(n=12),and atorvastatin group(n=12),with C57BL/6J mice of the same strain and age as the control group(n=12).Quercetin group and atorvastatin group were administrated with quercetin and atorvastatin by oral gavage,with doses of 12.5 and 4 mg/(kg・d),respectively.Animals in the control and model groups were given an equal volume of distilled water by oral gavage once per day for a total of 12 weeks.Western blot and immunohistochemical methods were employed to determine the aortic ABCA1,LxR-a and PCSK9 protein expressi on.En zyme linked imm uno sorbent assay method was used to detect the expressi on of serum total cholesterol(TC),triglyceride(TG),high density lipoprotein-cholesterol(HDL-C),low density lipoproteincholesterol(LDL-C),tumor necrosis factor-a(TNF-a),interleukin-6(IL-6),and IL-10,combined with tissue pathological exami nation.Results:ApoE-/-mice fed with a high-fat diet had no table atherosclerosis lesions,with reduced ABCA1,LxR-a and IL-10 levels(all Pxpression,and increased TC and LDL-C con tents(all Pxpressions of PCSK9,TNF-a and IL-6 were significantly reduced(all Pxpressions of ABCA1 and LxR-a were increased significantly(all Pxpressions of ABCA1,LxR-a and PCSK9 in ApoE,mice.

关键词： quercetin atherosclerosis ATP binding cassette transporter A1 liver x receptor proprotein convertase subtilisin/kexin type 9

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