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BMP9 induces osteogenic differentiation through up-regulating LGR4 via the mTORC1/ Stat3 pathway in mesenchymal stem cells

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Genes & Diseases 2024年第3期11卷 468-483页

作者： Jie Zhang Jinhai Jiang Hang Liu Shiyu Wang Kaixin Ke Siyuan Liu Yue Jiang Lu Liu Xiang Gao Baicheng He Yuxi Su Department of Pharmacology School of PharmacyChongqing Medical UniversityChongqing 400016China Key Laboratory of Biochemistry and Molecular Pharmacology of Chongqing Chongqing Medical UniversityChongqing 400016China Department of Orthopedics Second Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China orthopedics Department Children's Hospital of Chongqing Medical UniversityChongqing 400014China China International Science and Technology Cooperation Base of Child Development and Critical Disorders Jiangxi Hospital Affiliated Children's Hospital of Chongqing Medical UniversityJiangxi 330000China National Clinical Research Center for Child Health and Disorders China

Bone defects and non-union are prevalent in clinical orthopedy,and the outcomes of current treatments are often suboptimal.Bone tissue engineering offers a promising approach to treating these conditions effectively.Bone morphogenetic protein 9(BMP9)can commit mesenchymal stem cells to osteogenic lineage,and a knowledge of the underlying mechanisms may help advance the field of bone tissue engineering.Leucine-rich repeats con-taining G protein-coupled receptor 4(LGR4),a member of G protein-coupled receptors,is essential for modulating bone development.This study is aimed at investigating the impact of LGR4 on BMP9-induced osteogenesis in mesenchymal stem cells as well as the underlying mechanisms.Bone marrow stromal cells from BMp9-knockout mice exhibited diminished LGR4 expression,and exogenous LGR4 clearly restored the impaired osteogenic potency of the bone marrow stromal cells.Furthermore,LGR4 expression was increased by BMP9 in C3H10T1/2 cells.LGR4 augmented the benefits of BMP9-induced osteogenic markers and bone formation,whereas LGR4 inhibition restricted these effects.Meanwhile,the BMP9-induced li-pogenic markers were increased by LGR4 inhibition.The protein levels of Raptor and p-Stat3 were elevated by BMP9.Raptor knockdown or p-Stat3 suppression attenuated the osteoblastic markers and LGR4 expression brought on by BMP9.LGR4 significantly reversed the blocking ef-fect of Raptor knockdown or p-Stat3 suppression on the BMP9-induced osteoblastic markers.Raptor interacts with p-Stat3,and p-Stat3 activates the LGR4 promoter activity.In conclusion,LGR4 boosts BMP9 osteoblastic potency in mesenchymal stem cells,and BMP9 may up-regulate LGR4 via the mTORC1/Stat3 signal activation.

关键词： BMP9 LGR4 mTORC1 Osteogenic differentiation Stat3

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Microglial depletion impairs glial scar formation and aggravates inflammation partly by inhibiting Stat3 phosphorylation in astrocytes after spinal cord injury

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Neural Regeneration Research 2023年第6期18卷 1325-1331页

作者： Zhi-Lai Zhou Huan Xie Xiao-Bo Tian Hua-Li Xu Wei Li Shun Yao Hui Zhang The Spine Surgery Department Guangdong Second Provincial General HospitalGuangzhouGuangdong ProvinceChina The Second School of Clinical Medicine Southern Medical UniversityGuangzhouGuangdong ProvinceChina Department of Anesthesiology ZhuJiang HospitalSouthern Medical UniversityGuangzhouGuangdong ProvinceChina

Astrocytes and microglia play an orchestrated role following spinal cord injury;however,the molecular mechanisms through which microglia regulate astrocytes after spinal cord injury are not yet fully understood.Herein,microglia were pharmacologically depleted and the effects on the astrocytic response were examined.We further explored the potential mechanisms involving the signal transducers and activators of transcription 3(Stat3)pathway.For in vivo experiments,we constructed a contusion spinal cord injury model in C57BL/6 mice.To deplete microglia,all mice were treated with colony-stimulating factor 1 receptor inhibitor PLX3397,starting 2 weeks prior to surgery until they were sacrificed.Cell proliferation was examined by 5-ethynyl-2-deoxyuridine(EdU)and three pivotal inflammatory cytokines were detected by a specific Bio-Plex Pro^(TM) Reagent Kit.Locomotor function,neuroinflammation,astrocyte activation and phosphorylated Stat3(pStat3,a maker of activation of Stat3 signaling)levels were determined.For in vitro experiments,a microglia and astrocyte coculture system was established,and the small molecule STA21,which blocks Stat3 activation,was applied to investigate whether Stat3 signaling is involved in mediating astrocyte proliferation induced by microglia.PLX3397 administration disrupted glial scar formation,increased inflammatory spillover,induced diffuse tissue damage and impaired functional recovery after spinal cord injury.Microglial depletion markedly reduced EdU+proliferating cells,especially proliferating astrocytes at 7 days after spinal cord injury.RNA sequencing analysis showed that the JAK/Stat3 pathway was downregulated in mice treated with PLX3397.Double immunofluorescence staining confirmed that PLX3397 significantly decreased Stat3 expression in astrocytes.Importantly,in vitro coculture of astrocytes and microglia showed that microglia-induced astrocyte proliferation was abolished by STA21 administration.These findings suggest that microglial depletion impaired astrocyte proliferation and astro

关键词： astrocytes coculture colony-stimulating factor 1 receptor inhibitor EdU glia scar inflammatory response microglia phosphorylation proliferation spinal cord injury Stat3

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Gp130-dependent Stat3 activation in M-CSF-derived macrophages exaggerates tumor progression

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Genes & Diseases 2024年第3期11卷 51-54页

作者： Yuting Xu Xiaoyu Xu Qianyue Zhang Peizhe Lu Chongjun Xiang Lei Zhang Chunhua Lin Qiaoling Song Key Laboratory of Marine Drugs Ministry of Education of ChinaSchool of Medicine and PharmacyOcean University of ChinaQingdaoShandong 266003China College of Marine Life Sciences Ocean University of ChinaQingdaoShandong 266071China Department of Neuroscience University of MichiganAnn ArborM/48103USA Department of Urology The Affiliated Yantai Yuhuangding Hospital of Qingdao UniversityYantaiShandong 264000China Research Center of Traditional Chinese Medicine and Clinical Pharmacy Shandong Provincial Maternal and Child Health Care Hospital Affiliated to Qingdao UniversityJinanShandong 250014China Innovation Platform of Marine Drug Screening&Evaluation Qingdao National Laboratory for Marine Science and TechnologyQingdaoShandong 266100China

Interleukin-6(IL-6)is a common pluripotent cytokine that is highly expressed in the tumor microenvironment.The IL-6/JAK/Stat3 signaling directly promotes tumor progression,severely hampering antitumor immunity.Macrophages,the richest innate immune cells within the tumor microenvironment,manipulate tumor progression via phenotypic plasticity.

关键词： Stat3 tumor Interleukin

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Novel role of Stat3 in microglia-dependent neuroinflammation after experimental subarachnoid haemorrhage

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Stroke & Vascular Neurology 2022年第1期7卷 62-70页

作者： Zhiyuan Vera Zheng Junfan Chen Hao Lyu Sin Yu Erica Lam Gang Lu Wai Yee Chan George K C Wong Department of Surgery The Chinese University of Hong KongShatinHong Kong Department of Surgery Hainan General HospitalHaikouHainanChina School of Biomedical Science The Chinese University of Hong KongShatinHong Kong

Background and purpose Signal transducer and activator of transcription 3(Stat3)may contribute to the proinflammation in the central nervous system diseases by modulating the microglial responses.Thus,this study was intended to investigate the effect of Stat3 on microglia-dependent neuroinflammation and functional outcome after experimental subarachnoid haemorrhage(SAH).Methods The SAH model was established by endovascular perforation in the mouse.Real-time PCR(RtPCR)and western blot were used to examine the dynamic Stat3 signalling pathway responses after SAH.To clarify the role of the Stat3 signalling pathway in the microglia-dependent neuroinflammation after SAH,the microglia-specific Stat3 knockout(KO)mice were generated by the Cre-LoxP system.The neurological functions were assessed by Catwalk and Morris water maze tests.Neuronal loss after SAH was determined by immunohistochemistry staining.Microglial polarisation status after Stat3 KO was then examined by RtPCR and immunofluorescence.Results The Stat3 and Janus kinase-signal transducer 2 activated immediately with the upregulation and phosphorylation after SAH.Downstream factors and related mediators altered dynamically and accordingly.Microglial Stat3 deletion ameliorated the neurological impairment and alleviated the early neuronal loss after SAH.To investigate the underlying mechanism,we examined the microglial reaction after Stat3 KO.Stat3 deletion reversed the increase of microglia after SAH.Loss of Stat3 triggered the early morphological changes of microglia and primed microglia from M1 to M2 polarisation.Functionally,microglial Stat3 deletion suppressed the SAH-induced proinflammation and promoted the anti-inflammation in the early phase.Conclusions Stat3 is closely related to the microglial polarisation transition and modulation of microglia-dependent neuroinflammation.Microglial Stat3 deletion improved neurological function and neuronal survival probably through promoting M2 polarisation and anti-inflammatory responses after SAH.Stat3 may serve as

关键词： Stat3 inflammation reversed

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Peroxidase from foxtail millet bran exerts anticolorectal cancer activity via targeting cellsurface GRP78 to inactivate Stat3 pathway

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Acta Pharmaceutica Sinica B 2022年第3期12卷 1254-1270页

作者： Shuhua Shan Jinping Niu Ruopeng Yin Jiangying Shi Lizhen Zhang Caihong Wu Hanqing Li Zhuoyu Li Institute of Biotechnology Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of EducationShanxi UniversityTaiyuan 030006China School of Life Science Shanxi UniversityTaiyuan 030006China

Molecular targeted therapy has become an emerging promising strategy in cancer treatment,and screening the agents targeting at cancer cell specific targets is very desirable for cancer treatment.Our previous study firstly found that a secretory peroxidase of class III derived from foxtail millet bran(FMBP)exhibited excellent targeting anti-colorectal cancer(CRC)activity in vivo and in vitro,whereas its underlying target remains unclear.The highlight of present study focuses on the finding that cell surface glucose-regulated protein 78(cs GRP78)abnormally located on CRC is positively correlated with the anti-CRC effects of FMBP,indicating it serves as a potential target of FMBP against CRC.Further,we demonstrated that the combination of FMBP with the nucleotide binding domain(NBD)of cs GRP78interfered with the downstream activation of signal transducer and activator of transcription 3(Stat3)in CRC cells,thus promoting the intracellular accumulation of reactive oxygen species(ROS)and cell grown inhibition.These phenomena were further confirmed in nude mice tumor model.Collectively,our study highlights cs GRP78 acts as an underlying target of FMBP against CRC,uncovering the clinical potential of FMBP as a targeted agent for CRC in the future.

关键词： Foxtail millet bran FMBP csGRP78 Stat3 ROS Colorectal cancer

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LncRNA-CCAT5-mediated crosstalk between Wnt/β-Catenin and Stat3 signaling suggests novel therapeutic approaches for metastatic gastric cancer with high Wnt activity

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Cancer Communications 2024年第1期44卷 76-100页

作者： Chenchen Liu Aiwen Shen Junquan Song Lei Cheng Meng Zhang Yanong Wang Xiaowen Liu Department of Gastric Surgery Fudan University Shanghai Cancer CenterShanghaiP.R.China Department of Oncology Shanghai Medical CollegeFudan UniversityShanghaiP.R.China Department of Nephrology Shanghai Ninth People’s HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiP.R.China Department of Pulmonary Shanghai Chest HospitalShanghai Jiao Tong UniversityShanghaiP.R.China Department of Pathology Fudan University Shanghai Cancer CenterShanghaiP.R.China

Background:Although the constitutively activated Wnt/β-catenin signaling pathway plays vital roles in gastric cancer(GC)progression,few Wnt inhibitors are approved for clinical use.Additionally,the clinical significance of long non-coding RNAs(lncRNAs)in GC intraperitoneal dissemination(IPD)remains elusive.Here,we investigated the function and therapeutic potential of Wnt-transactivated lncRNA,colon cancer-associated transcript 5(CCAT5),in GC metastasis.Methods:LncRNA-sequencing assay was performed to document abun-dance changes of lncRNAs induced by Wnt family member 3A(Wnt3a)and degradation-resistantβ-catenin(S33Y mutated)in ascites-derived GC cells with low Wnt activity.Luciferase reporter,Chromatin immunoprecipitation(ChIP)-re-ChIP assays were performed to determine how CCAT5 was tran-scribed.The clinical significance of CCAT5 was examined in 2 cohorts of GC patients.The biological function of CCAT5 was investigated through gain-and loss-of-function studies.The molecular mechanism was explored through RNA-sequencing,mass spectrometry,and CRISPR/Cas9-knocknout system.The therapeutic potential of CCAT5 was examined through RNAi-based cell xenograft model and patient-derived xenograft(PDX)model of IPD.Results:WeidentifiedanovelWnt-regulatedlncRNA,CCAT5,whichwastrans-activated by theβ-catenin/transcription factor 3(TCF3)complex.CCAT5 was significantly upregulated in GC and predicted poor prognosis.Functional studies confirmed the promotive role of CCAT5 in GC growth and metastasis.Mechanis-tically,CCAT5 bound to the C-end domain of signal transducer and activator of transcription 3(Stat3)and blocks Src homology 2 domain-containing protein tyrosine phosphatase 1(SHP-1)-mediated Stat3 Y705 dephosphorylation,leading to Stat3 nuclear entry and transactivation,thus accelerating GC progression.Furthermore,we demonstrated that both Wnt3a andβ-catenin acted as activa-tor of Stat3 signaling pathway,and the interplay between CCAT5 and Stat3 was functionally essential for Wnt-drived Stat3 signaling and tumor evolu-tion.Fina

关键词： CCAT5 gastric cancer intraperitoneal dissemination Stat3 Wnt/β-catenin

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The delivery of miR-21a-5p by extracellular vesicles induces microglial polarization via the Stat3 pathway following hypoxia-ischemia in neonatal mice

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Neural Regeneration Research 2022年第10期17卷 2238-2246页

作者： Dan-Qing Xin Yi-Jing Zhao Ting-Ting Li Hong-Fei Ke Cheng-Cheng Gai Xiao-Fan Guo Wen-Qiang Chen De-Xiang Liu Zhen Wang Department of Physiology School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Neurology Loma Linda University HealthLoma LindaCAUSA Department of Cardiology Qilu HospitalCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Medical Psychology and Ethics School of Basic Medicine SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina

Extracellular vesicles(EVs)from mesenchymal stromal cells(MSCs)have previously been shown to protect against brain injury caused by hypoxia-ischemia(HI).The neuroprotective effects have been found to relate to the anti-inflammatory effects of EVs.However,the underlying mechanisms have not previously been determined.In this study,we induced oxygen-glucose deprivation in BV-2 cells(a microglia cell line),which mimics HI in vitro,and found that treatment with MSCs-EVs increased the cell viability.The treatment was also found to reduce the expression of pro-inflammatory cytokines,induce the polarization of microglia towards the M2 phenotype,and suppress the phosphorylation of selective signal transducer and activator of transcription 3(Stat3)in the microglia.These results were also obtained in vivo using neonatal mice with induced HI.We investigated the potential role of miR-21a-5p in mediating these effects,as it is the most highly expressed miRNA in MSCs-EVs and interacts with the Stat3 pathway.We found that treatment with MSCs-EVs increased the levels of miR-21a-5p in BV-2 cells,which had been lowered following oxygen-glucose deprivation.When the level of miR-21a-5p in the MSCs-EVs was reduced,the effects on microglial polarization and Stat3 phosphorylation were reduced,for both the in vitro and in vivo HI models.These results indicate that MSCs-EVs attenuate HI brain injury in neonatal mice by shuttling miR-21a-5p,which induces microglial M2 polarization by targeting Stat3.

关键词： extracellular vesicles hypoxia-ischemia mesenchymal stromal cells microglia miR-21a-5p neuroinflammation oxygen-glucose deprivation Stat3

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Alantolactone-loaded chitosan/hyaluronic acid nanoparticles suppress psoriasis by deactivating Stat3 pathway and restricting immune cell recruitment

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Asian Journal of Pharmaceutical Sciences 2022年第2期17卷 268-283页

作者： Ruijie Chen Yuan-Yuan Zhai Lining Sun Zeqing Wang Xing Xia Qing Yao Longfa Kou Department of Pharmacy the Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhou 325027China School of Pharmaceutical Sciences Wenzhou Medical UniversityWenzhou 325035China

Psoriasis is a common chronic immune-mediated skin disease characterized by hyperproliferation and aberrant differentiation of keratinocytes and massive infiltration of inflammatory immune cells.Recent studies showed that Signal Transducer and Activator of Transcription 3(Stat3),which plays an important role in cell survival,proliferation,differentiation,angiogenesis,and immune responses,is constitutively activated in epidermal keratinocytes of human psoriatic skin lesions.In addition,Stat3 promotes the differentiation and expansion of T cells and facilitates cytokine production,thereby exacerbating the condition of psoriasis.Alantolactone(ALT)is a sesquiterpene lactone compound that could selectively suppress Stat3 activation,but its effectiveness and application in psoriasis treatment have not been determined.In this study,we developed ALT loaded chitosan/hyaluronic acid nanoparticles(CHALT),and investigated its therapeutic potential for psoriasis therapy.CHALT effectively abrogated the hyperproliferation by inducing ROS-mediated apoptosis with loss of mitochondrialmembrane potential,and also inhibited IL-6-induced Stat3 signaling activation and inflammatory reaction in HaCaT cell line.In an Imiquimod(IMQ)-induced psoriasis model,the topical treatment of psoriasis lesions with CHALT effectively attenuated the Stat3 hyperactivation within keratinocytes and ameliorated the symptoms of psoriasis.In addition,it was found that CHALT restricted the recruitment of immune cells.These results indicated that ALT-based nanoformulation CHALT holds great potential for psoriasis therapy.

关键词： Psoriasis Alantolactone Stat3 Chitosan Nanoparticle

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MicroRNAs and JAK/Stat3 signaling:A new promising therapeutic axis in blood cancers

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Genes & Diseases 2022年第4期9卷 849-867页

作者： Mehdi Sajjadi-Dokht Talar Ahmad Merza Mohamad Heshu Sulaiman Rahman Marwah Suliman Maashi Svetlana Danshina Navid Shomali Saeed Solali Faroogh Marofi Elham Zeinalzadeh Morteza Akbari Ali Adili Ramin Aslaminabad Majid Farshdousti Hagh Mostafa Jarahian Immunology Research Center Tabriz University of Medical SciencesTabriz ***Iran Department of Pharmacology College of PharmacyHawler Medical UniversityErbil 44001Iraq Department of Physiology College of MedicineUniversity of SulaymaniyahSulaymaniyah 46001Iraq Department of Medical Laboratory Sciences Komar University of Science and TechnologySulaymaniyah 46002Iraq Department of Propaedeutics of Dental Diseases I.M.Sechenov First Moscow State Medical UniversityMoscow 119991Russia Department of Immunology Faculty of MedicineTabriz University of Medical SciencesTabriz ***Iran Department of Oncology Tabriz University of Medical SciencesTabriz ***Iran German Cancer Research Center(DKFZ) Toxicology and Chemotherapy Unit(G401)Heidelberg 69120Germany Stem Cells and Regenerative Medicine Unit at King Fahad Medical Research Centre Jeddah 21589Saudi Arabia

Blood disorders include a wide spectrum of blood-associated malignancies resulting from inherited or acquired defects.The ineffectiveness of existing therapies against blood disorders arises from different reasons,one of which is drug resistance,so different types of leukemia may show different responses to treatment.Leukemia occurs for a variety of genetic and acquired reasons,leading to uncontrolled proliferation in one or more cell lines.Regarding the genetic defects,oncogene signal transducer and activator of transcription(stat)family transcription factor,especially Stat3,play an essential role in hematological disorders onset and progress upon mutations,dysfunction,or hyperactivity.Besides,microRNAs,as biological molecules,has been shown to play a dual role in either tumorigenesis and tumor suppression in various cancers.Besides,a strong association between Stat3 and miRNA has been reported.For example,miRNAs can regulate Stat3 via targeting its upstream mediators such as IL6,IL9,and JAKs or directly binding to the Stat3 gene.On the other hand,Stat3 can regulate miRNAs.In this review study,we aimed to determine the role of either microRNAs and Stat3 along with their effect on one another's activity and function in hematological malignancies.

关键词： Interleukin JAKs Leukemia miRNAs Stat3

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M2型巨噬细胞来源的外泌体lncRNA NR_028113.1通过激活JAK2/Stat3通路促进巨噬细胞的极化

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南方医科大学学报 2023年第3期43卷 393-399页

作者：张梦莹李志裴纬亚李雪琴杨辉朱小龙吕坤皖南医学院重大疾病非编码RNA转化研究安徽普通高校重点实验室安徽芜湖241001 皖南医学院弋矶山医院中心实验室安徽芜湖241001 皖南医学院弋矶山医院风湿免疫科安徽芜湖241001

目的探究M2型巨噬细胞来源的外泌体lncRNA NR_028113.1对巨噬细胞极化的影响及机制。方法体外分离并培养BALB/c小鼠骨髓来源的巨噬细胞(BMDMs),IL-4诱导其向M2型巨噬细胞极化后,提取并鉴定M2细胞上清液所分泌的外泌体exosome(M2-exo),qR... 详细信息

目的探究M2型巨噬细胞来源的外泌体lncRNA NR_028113.1对巨噬细胞极化的影响及机制。方法体外分离并培养BALB/c小鼠骨髓来源的巨噬细胞(BMDMs),IL-4诱导其向M2型巨噬细胞极化后,提取并鉴定M2细胞上清液所分泌的外泌体exosome(M2-exo),qRT-PCR检测M2外泌体中lncRNA的表达。将100μg/mL的M2-exo,对照组用等体积的PBS分别与M0巨噬细胞共孵育48 h后,qRT-PCR及Western blot检测各组细胞中Arg1、YM-1、FIZZ1、iNOS和TNF-α的表达,流式细胞术检测CD206^(+)细胞比例,Western blot检测各组细胞JAK2/Stat3蛋白磷酸化水平。设计、合成lncRNA smart silencer特异性抑制lncRNA NR_028113.1的表达,转染M2细胞48 h后提取各组细胞(exo+NC和exo+smart silencer)上清液分泌的外泌体再与M0型巨噬细胞共孵育,检测孵育后各组细胞中Arg1、YM-1、FIZZ1、iNOS和TNF-α的表达以及CD206^(+)细胞比例和JAK2/Stat3信号通路蛋白磷酸化水平。结果lncRNA NR_028113.1在M2型巨噬细胞外泌体中高表达(PStat3蛋白磷酸化水平显著增加(P3.1的表达后,共培养的M0巨噬细胞中Arg1、YM-1和FIZZ1表达显著下调(PStat3蛋白磷酸化水平显著减少(P3.1可显著促进巨噬细胞向M2型极化,其机制可能与激活JAK2/Stat3信号通路相关。

关键词：外泌体 lncRNA 巨噬细胞极化 JAK2 Stat3

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