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Food Science and Human Wellness 2024年第3期13卷 1543-1555页

作者： Xin Wang Weiye Xiu Ye Han Zhili Wang Yu Luo Yongqiang Ma Heilongjiang Provincial Key laboratory of Cereals and Comprehensive Processing of Cereal Resources College of Food EngineeringHarbin University of CommerceHarbin 150028China

Type 2 diabetes mellitus(T2DM)is a metabolic disease caused by a glycolipid metabolism disorder and isletβ-cell ***-80-I is a biologically active water-soluble polysaccharide isolated from sweet corncob,an agricultural *** hypoglycemic effects of SCP-80-I on T2DM mice and its mechanisms were investigated in this ***-80-I was found to significantly reduce blood glucose and lipid deposition levels in T2DM mice,as well as decrease serum leptin and increase adiponectin ***,real time-polymerase chain reaction(RT-PCR)and Western blotting results revealed that SCP-80-I could regulate the expression of several glycolipid metabolisms and insulin secretion genes and proteins,including 5'-AMP-activated protein kinase(AMPK),carnitine palmitoyltransferase I(CPTI),and acetyl coenzyme A carboxylase(ACC)in the liver and AMPK,sirtuin1(Sirtl),peroxisome proliferator-activated receptorycoactivator-1(PGC-1α),and uncoupling protein 2(UCP2)in the *** have a hypoglycemic effect,SCP-80-1 regulated glycolipid metabolism and islet cell function in the liver by regulating the AMPK/AC C/CPT1 signaling pathway and the AMPK/Sirt1/PGC-1αand AMPK/Sirtl/UCP2 signaling *** findings improve our understanding of polysaccharides derived from sweet corncob and the use of SCP-80-I in the production of hypoglycemic foods.

关键词： Sweet corn cob polysaccharide Type 2 diabetes Signal pathway 5’-AMP-activated protein kinase(AMPK)

Mast cell degranulation-triggered by SARS-CoV-2 induces tracheal-bronchial epithelial inflammation and injury

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Virologica Sinica 2024年第2期39卷 309-318页

作者： Jian-Bo Cao Shu-Tong Zhu Xiao-Shan Huang Xing-Yuan Wang Meng-Li Wu Xin Li Feng-Liang Liu Ling Chen Yong-Tang Zheng Jian-Hua Wang Guangzhou Institutes of Biomedicine and Health Chinese Academy of SciencesGuangzhou 510530China School of Life Sciences and Medicine University of Science and Technology of ChinaHefei 230026China Key laboratory of Bioactive Peptides of Yunnan Province Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of SciencesKIZCUHK Joint Laboratory of Bioresources and Molecular Research in Common DiseasesCenter for Biosafety Mega-ScienceKunming Institute of ZoologyChinese Academy of SciencesKunming 650223China University of Chinese Academy of Sciences Beijing 101408China

SARS-CoV-2 infection-induced hyper-inflammation is a key pathogenic factor of *** research,along with others',has demonstrated that mast cells(MCs)play a vital role in the initiation of hyper-inflammation caused by *** previous study,we observed that SARS-CoV-2 infection induced the accumulation of MCs in the peri-bronchus and bronchioalveolar-duct junction in humanized ***,we found that MC degranulation triggered by the spike protein resulted in inflammation in alveolar epithelial cells and capillary endothelial cells,leading to subsequent lung *** trachea and bronchus are the routes for SARS-CoV-2 transmission after virus inhalation,and inflammation in these regions could promote viral *** are widely distributed throughout the respiratory ***,in this study,we investigated the role of MCs and their degranulation in the development of inflammation in tracheal-bronchial *** analyses showed the accumulation and degranulation of MCs in the peri-trachea of humanized mice infected with *** degranulation caused lesions in trachea,and the formation of papillary hyperplasia was *** transcriptome analysis in bronchial epithelial cells,we found that MC degranulation significantly altered multiple cellular signaling,particularly,leading to upregulated immune responses and *** administration of ebastine or loratadine effectively suppressed the induction of inflammatory factors in bronchial epithelial cells and alleviated tracheal injury in *** together,our findings confirm the essential role of MC degranulation in SARS-CoV-2-induced hyper-inflammation and the subsequent tissue ***,our results support the use of ebastine or loratadine to inhibit SARS-CoV-2-triggered degranulation,thereby preventing tissue damage caused by hyper-inflammation.

关键词： SARS-CoV-2 Mast cell(MC) Bronchial epithelial cell Inflammation Tracheal injury

Bcl-xL regulates radiation-induced ferroptosis through chaperone-mediated autophagy of GPX4 in tumor cells

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Radiation Medicine and Protection 2024年第2期5卷 90-99页

作者： Jing Han Ruru Wang Bin Chen Feng Xu Liangchen Wei An Xu Lijun Wu Guoping Zhao High Magnetic Field laboratory Key Laboratory of High Magnetic Field and Ion Beam Physical BiologyChinese Academy of SciencesAnhui Province Key Laboratory of Environmental Toxicology and Pollution Control TechnologyHefei Institutes of Physical ScienceAnhui 230031China University of Science and Technology of China Hefei 230026China School of Public Health Wannan Medical CollegeWuhu 241002China

Objective:To investigate the role and the molecular mechanisms of apoptotic signaling in ferroptosis to regulate tumor ***:Reactive oxygen species(ROS)and lipid peroxide levels were detected in Mouse embryonic fibroblasts(MEFs)with Bcl-xL or Mcl-1 deficiency induced by *** formation,ROS,lipid peroxidation and the transcription/translation levels of PTGS2 were measured in Bcl-xL knockdown tumor cells induced by 5 Gyγ-rays or co-treated with ferrostatin-1(Ferr-1).The protein levels of LPCAT3,ACSL4 and PEBP1 in Bcl-xL knockout MEF cells were evaluated in Bcl-xL knockout MEF cells ***,the interaction of heat shock protein 90(HSP90)with Bcl-xL,GPX4,or LAMP2A was detected by protein mass spectrometry and immunoprecipitation ***:Manipulating Bcl-xL levels facilitated radiation-induced ferroptosis by augmenting the enzymatic oxidation of polyunsaturated fatty acids(PUFAs)and enhancing chaperone-mediated autophagy(CMA)of glutathione peroxidase 4(GPX4)(MEF cell line:t=4.540,Pcell line:t=56.16,Pcell line:t=14.75,P<0.01;t=7.363,P<0.05).Downregulating Bcl-xL expression promoted the activity of acyl-CoA synthetase long-chain family member 4(ACSL4),thus increasing the enzymatic oxidation of PUFAs(t=4.258,P<0.01).Moreover,depletion of Bcl-xL expedited the CMA process targeting GPX4 by facilitating the association of GPX4 with heat shock protein 90(HSP90)and LAMP2A following radiation *** degradation of GPX4 led to the accumulation of lipid peroxides,ultimately triggering ***:Our study provides initial insights into the regulatory role of Bcl-xL in ferroptosis and underscores the potential of targeting Bcl-xL as a promising therapeutic strategy for cancer by modulating both apoptotic and ferroptotic pathways.

关键词： Bcl-xL Ferroptosis GPX4 Chaperone-mediated autophagy Lipid peroxidation

Tim4 deficiency reduces CD301b+macrophage and aggravates periodontitis bone loss

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International Journal of Oral Science 2024年第2期16卷 280-292页

作者： Ziming Wang Hao Zeng Can Wang Jiaolong Wang Jing Zhang Shuyuan Qu Yue Han Liu Yang Yueqi Ni Wenan Peng Huan Liu Hua Tang Qin Zhao Yufeng Zhang State Key laboratory of Oral&Maxillofacial Reconstruction and Regeneration Key Laboratory of Oral Biomedicine Ministry of EducationHubei Key Laboratory of StomatologySchool&Hospital of StomatologyTaikang Center for Life and Medical SciencesWuhan UniversityWuhanChina School of Stomatology Nanchang UniversityNanchangChina Institute of Infection and Immunity Science and Technology Innovation CenterShandong First Medical University&Shandong Academy of Medical SciencesJinanChina Medical Research Institute School of MedicineWuhan UniversityWuhanChina

Periodontitis is a common chronic inflammatory disease that causes the periodontal bone destruction and may ultimately result in tooth *** the progression of periodontitis,the osteoimmunology microenvironment in periodontitis is damaged and leads to the formation of pathological alveolar bone ***301b^(+)macrophages are specific to the osteoimmunology microenvironment,and are emerging as vital booster for conducting bone ***,the key upstream targets of CD301b^(+)macrophages and their potential mechanism in periodontitis remain *** this study,we concentrated on the role of Tim4,a latent upstream regulator of CD301b^(+)*** first demonstrated that the transcription level of Timd4(gene name of Tim4)in CD301b^(+)macrophages was significantly upregulated compared to CD301b−macrophages via high-throughput RNA ***,several Tim4-related functions such as apoptotic cell clearance,phagocytosis and engulfment were positively regulated by CD301b^(+)*** single-cell RNA sequencing analysis subsequently discovered that Cd301b and Timd4 were specifically co-expressed in *** following flow cytometric analysis indicated that Tim4 positive expression rates in total macrophages shared highly synchronized dynamic changes with the proportions of CD301b^(+)macrophages as periodontitis ***,the deficiency of Tim4 in mice decreased CD301b^(+)macrophages and eventually magnified alveolar bone resorption in ***,Tim4 controlled the p38 MAPK signaling pathway to ultimately mediate CD301b^(+)macrophages *** a word,Tim4 might regulate CD301b^(+)macrophages through p38 MAPK signaling pathway in periodontitis,which provided new insights into periodontitis immunoregulation as well as help to develop innovative therapeutic targets and treatment strategies for periodontitis.

关键词： period upstream eventually

Simultaneously targeting extracellular vesicle trafficking and TGF-β receptor kinase activity blocks signaling hyperactivation and metastasis

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Signal Transduction and Targeted Therapy 2024年第1期9卷 308-325页

作者： Adilson Fonseca Teixeira Yanhong Wang Josephine Iaria Peter ten Dijke Hong-Jian Zhu Department of Surgery(The Royal Melbourne Hospital) The University of MelbourneParkvilleVICAustralia Huagene Institute Kecheng Science and Technology ParkPukou DistrictNanjingJiangsuChina Department of cell and Chemical Biology Oncode InstituteLeiden University Medical CenterLeidenThe Netherlands

Metastasis is the leading cause of cancer-related *** growth factor beta(TGF-β)signaling drives metastasis and is strongly enhanced during cancer ***,the use of on-target TGF-βsignaling inhibitors in the treatment of cancer patients remains unsuccessful,highlighting a gap in the understanding of TGF-βbiology that limits the establishment of efficient anti-metastatic ***,we show that TGF-βsignaling hyperactivation in breast cancer cells is required for metastasis and relies on increased small extracellular vesicle(sEV)*** sEV’s unique role,TGF-βsignaling levels induced by sEVs exceed the activity of matching concentrations of soluble ligand TGF-β.Further,genetic disruption of sEV secretion in highlymetastatic breast cancer cells impairs cancer cell aggressiveness by reducing TGF-βsignaling to nearly-normal ***,TGF-βsignaling activity in non-invasive breast cancer cells is inherently low,but can be amplified by sEVs,enabling invasion and metastasis of poorly-metastatic breast cancer *** the translational potential of inhibiting sEV trafficking in advanced breast cancers,treatment with dimethyl amiloride(DMA)decreases sEV secretion,TGF-βsignaling activity,and breast cancer progression in *** both the sEV trafficking and TGF-βsignaling by combining DMA and SB431542 at suboptimal doses potentiated this effect,normalizing the TGF-βsignaling in primary tumors to potently reduce circulating tumor cells,metastasis,and tumor ***,this study establishes sEVs as critical elements in TGF-βbiology,demonstrating the feasibility of inhibiting sEV trafficking as a new therapeutic approach to impair metastasis by normalizing TGF-βsignaling levels in breast cancer cells.

关键词： metastasis doses invasion

MSC-derived exosomes attenuate hepatic fibrosis in primary sclerosing cholangitis through inhibition of Th17 differentiation

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Asian Journal of Pharmaceutical Sciences 2024年第1期19卷 119-134页

作者： Wenyi Chen Feiyan Lin Xudong Feng Qigu Yao Yingduo Yu Feiqiong Gao Jiahang Zhou Qiaoling Pan Jian Wu Jinfeng Yang Jiong Yu Hongcui Cao Lanjuan Li State Key laboratory for the Diagnosis and Treatment of Infectious Diseases National Clinical Research Center for Infectious DiseasesCollaborative Innovation Center for Diagnosis and Treatment of Infectious DiseasesNational Medical Center for Infectious DiseasesThe First Affiliated HospitalZhejiang University School of MedicineHangzhou 310003China Jinan Microecological Biomedicine Shandong laboratory Jinan 250117China Key laboratory of Diagnosis and Treatment of Aging and Physic-chemical Injury Diseases of Zhejiang Province Hangzhou 310003China

Primary sclerosing cholangitis(PSC)is an autoimmune cholangiopathy characterized by chronic inflammation of the biliary epithelium and periductal fibrosis,with no curative treatment available,and liver transplantation is inevitable for end-stage *** placentalmesenchymal stem cell(hpMSC)-derived exosomes have demonstrated the ability to prevent fibrosis,inhibit collagen production and possess immunomodulatory properties in autoimmune liver ***,we prepared hpMSC-derived exosomes(Exo^(MSC))and further investigated the anti-fibrotic effects and detailed mechanism on PSC based on Mdr2^(−/−)mice and multicellular organoids established from PSC *** results showed that Exo^(MSC) ameliorated liver fibrosis in Mdr2^(−/−)mice with significant collagen reduction in the preductal area where Th17 differentiation was inhibited as demonstrated by RNAseq analysis,and the percentage of CD4+IL-17A+T cells was reduced both in Exo^(MSC)-treated Mdr2^(−/−)mice(Mdr2^(−/−)-Exo)in vivo and Exo^(MSC)-treated Th17 differentiation progressed in ***,Exo^(MSC) improved the hypersecretory phenotype and intercellular interactions in the hepatic Th17 microenvironment by regulating PERK/CHOP signaling as supported by multicellular ***,our data demonstrate the antifibrosis effect of Exo^(MSC) in PSC disease by inhibiting Th17 differentiation,and ameliorating the Th17-induced microenvironment,indicating the promising potential therapeutic role of Exo^(MSC) in liver fibrosis of PSC or Th17-related diseases.

关键词： Mesenchymal stem cell Exosomes Primary sclerosing cholangitis Fibrosis Organoids Th17

BFP1:One of 700 Arabidopsis F-box proteins mediates degradation of JA oxidases to promote plant immunity

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Molecular Plant 2024年第3期17卷 375-376页

作者： Claus Wasternack Bettina Hause Department of Molecular Signal Processing Leibniz Institute of Plant Biochemistry7 Weinberg 306120 Halle(Saale)Germany Department of cell and Metabolic Biology Leibniz Institute of Plant Biochemistry06120 Halle(Saale)Germany

A switch off in jasmonate(JA)signaling by hydroxylation upon wounding was described in 2008(Miersch et al.,2008).This initiated the cloning of CYP450 enzymes involved in hydroxylation and carboxylation of JA and its amino acid conjugate JA-le,the most active form of JA compounds(reviewed by Wasternack and Feussner[2018]and Heitz et al.[2019]).Due to the central role of JA and JA-lle in plant stress responses and development(Wasternack and Hause,2013),catabolism of JA and its derivatives is an essential component in the sustainment of homeostasis of active JA compounds(Howe et al.,2018;Heitz et al.,2019).Catabolism of JA and JAIle takes place by JA-induced oxygenases(JOXs),also named JA-oxidases(JAOs),and by hydroxylation(CYP94B3/B1)followed by carboxylation(CYP94C1),respectively(Heitz et al.,2019).Another reaction performed by IAR3/ILL6 results in the deconjugation of JA-lle and 12-OH-JA-le to JA and 12-OH-JA,respectively(Heitz et al.,2019;Wasternack and Feussner,2018).

关键词： conjugate initiated media

LH-Nts Neurons Regulate VTA Calcium Dynamics Via Releasing GABA and Nts

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Neuroscience Bulletin 2024年第4期40卷 550-552页

作者： Danni Chen Yinfeng Yuan Zhihui Huang Yongjie Wang School of Pharmacy Hangzhou Normal UniversityHangzhou311121ZhejiangChina Key laboratory of Element Class Anti-Cancer Chinese Medicines Engineering Laboratory of Development and Application of Traditional Chinese MedicinesCollaborative Innovation Center of Traditional Chinese Medicines of Zhejiang ProvinceHangzhou Normal UniversityHangzhou311121ZhejiangChina

The peripheral and central nervous systems have numerous examples of two or more neuroactive products co-existing in the same neuron[1],which can simultaneously be released as both fast-acting neurotransmitters and slow-acting regulatory neuropeptides[2].For example,neurons in the lateral hypothalamus(LH)release both irritant neurotensin(Nts)and inhibitory-aminobutyric acid(GABA),two counterproductive substances[3].LH-Nts neurons project to the ventral tegmental area(VTA)and form synaptic connections with dopamine(DA)neurons to regulate reward[4-6].More critically,VTA-DA neurons express the Nts receptor Ntsrl and play a crucial role in cognition,anesthesia,reward,and disgust[4,7,8].Nevertheless,a mechanistic understanding of how stimulation and inhibition work together to control the output of neural circuits remains *** is very difficult to selectively isolate these signaling pathways in cell and circuit-specific manners.

关键词： anesthesia stimulation dopamine

PIM1-HDAC2 axis modulates intestinal homeostasis through epigenetic modification

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Acta Pharmaceutica Sinica B 2024年第7期14卷 3049-3067页

作者： Jianming Yang Yawen Xiao Ningning Zhao Geng Pei Yan Sun Xinyu Sun Kaiyuan Yu Chunhui Miao Ran Liu Junqiang Lv Hongyu Chu Lu Zhou Bangmao Wang Zhi Yao Quan Wang Key laboratory of Immune Microenvironment and Disease(Ministry of Education) Tianjin Institute of ImmunologyState Key Laboratory of Experimental Hematologythe Province and Ministry Co-sponsored Collaborative Innovation Center for Medical EpigeneticsDepartment of ImmunologySchool of Basic Medical SciencesTianjin Institute of Urologythe Second Hospital of Tianjin Medical UniversityTianjin Key Laboratory of Cellular and Molecular ImmunologyTianjin Medical UniversityTianjin 300070China Department of Pathology Tianjin Medical University Cancer Institute and Hospital/National Clinical Research Center of Cancer/Key Laboratory of Cancer Prevention and TherapyTianjin/Tianjin’s Clinical Research Center of CancerTianjin 30060China Department of Gastroenterology and Hepatology Tianjin Medical University General HospitalTianjin Medical UniversityTianjin 300070China

The mucosal barrier is crucial for intestinal homeostasis,and goblet cells are essential for maintaining the mucosal barrier *** proviral integration site for Moloney murine leukemia virus-1(PIM1)kinase regulates multiple cellular functions,but its role in intestinal homeostasis during colitis is ***,we demonstrate that PIM1 is prominently elevated in the colonic epithelia of both ulcerative colitis patients and murine models,in the presence of intestinal *** PIM1 leads to decreased goblet cells,thus impairing resistance to colitis and colitis-associated colorectal cancer(CAC)in ***,PIM1 modulates goblet cell differentiation through the Wnt and Notch signaling ***,PIM1 interacts with histone deacetylase 2(HDAC2)and downregulates its level via phosphorylation,thereby altering the epigenetic profiles of Wnt signaling pathway ***,these findings investigate the unknown function of the PIM1-HDAC2 axis in goblet cell differentiation and ulcerative colitis/CAC pathogenesis,which points to the potential for PIM1-targeted therapies of ulcerative colitis and CAC.

关键词： PIM1 HDAC2 Goblet cell Gut microbiota Intestinal homeostasis Epigenetic modification Ulcerative colitis CAC

Nuclear Factor-κB signaling Pathway Constitutively Activated in Esophageal Squamous cell Carcinoma cell Lines and Inhibition of Growth of cells by Small Interfering RNA

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Acta Biochimica et Biophysica Sinica 2006年第5期38卷 318-326页

作者： Fang TIAN Wei-Dong ZANG Wei-Hong HOU Hong-Tao LIU Le-Xun XUE laboratory for cell Biology,Medical College,Zhengzhou University,Zhengzhou 450052,China laboratory for cell Biology Medical College Zhengzhou UniversityZhengzhou 450052 China

Although constitutive nuclear factor(NF)-kB activation has been reported in many humantumors,the role of the NF-kB pathway in esophageal squamous cell carcinoma(ESCC)has not been *** this study,NF-kB pathway in two ESCC cell lines was investigated using immunocytochemistry,Westernblot and reverse transciiption-polymerase chain *** activation of NF-kB DNA binding was determinedby electrophoretic mobility-shift *** interference was used to specifically inhibit the expression *** of cells Was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide *** results showed that p50,p65,IkBα,p-IkBα and IkB kinase β were expressed and mainly localized in *** transcription-polymerase chain reaction results showed the constitutive expressions ofp50,p65 and IkBα mRNA in the two ESCC cell ***,the nuclear extracts revealed that p50and p65 translocated to the nucleus had DNA-binding ***,small interfering RNA of p65 decreasedthe expression of p65,and the viability of ceils transfected with p65 small interfering RNA was significantlysuppressed at the same concentration of 5-fluorouracil(Psignaling pathway in the ESCC *** interference targeting at p65 increased the sensitivity of the ESCC cell lines to 5-fluorouracil,suggesting that NF-kB might be a good target for cancer treatment.

关键词： NF-κB RNA interference esophageal squamous cell carcinoma IκBα IκBα kinase