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ROS-responsive nanoparticle delivery of ferroptosis inhibitor prodrug to facilitate mesenchymal stem cell-mediated spinal cord injury repair

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Bioactive Materials 2024年第8期38卷 438-454页

作者： Renshuai Hua Chenxi Zhao Zhengyu Xu Derong Liu Wenyuan Shen Wenlu Yuan Yan Li Jun Ma Zhishuo Wang Shiqing Feng Department of Orthopedics International Science and Technology Cooperation Base of Spinal Cord InjuryTianjin Key Laboratory of Spine and Spinal Cord InjuryTianjin Medical University General Hospital154 Anshan RoadHeping DistrictTianjin300052China Department of Orthopaedics Qilu Hospital of Shandong UniversityShandong University Centre for OrthopaedicsAdvanced Medical Research InstituteCheeloo College of MedicineShandong UniversityJinanShandong250012China Department of Orthopedics The Second Hospital of Shandong UniversityCheeloo College of MedicineShandong University247 Beiyuan StreetJinanShandong250033China

Spinal cord injury(SCI)is a traumatic condition that results in impaired motor and sensory *** is one of the main causes of neural cell death and loss of neurological function in the spinal cord,and ferroptosis inhibitors are effective in reducing inflammation and repairing *** human umbilical cord mesenchymal stem cells(Huc-MSCs)can ameliorate inflammatory microenvironments and promote neural regeneration in SCI,their efficacy is greatly limited by the local microenvironment after ***,in this study,we constructed a drug-release nanoparticle system with synergistic Huc-MSCs and ferroptosis inhibitor,in which we anchored Huc-MSCs by a Tz-A6 peptide based on the CD44-targeting sequence,and combined with the reactive oxygen species(ROS)-responsive drug nanocarrier mPEG-b-Lys-BECI-TCO at the other end for SCI ***,we also modified the classic ferroptosis inhibitor Ferrostatin-1(Fer-1)and synthesized a new prodrug Feborastatin-1(Feb-1).The results showed that this treatment regimen significantly inhibited the ferroptosis and inflammatory response after SCI,and promoted the recovery of neurological function in rats with *** study developed a combination therapy for the treatment of SCI and also provides a new strategy for the construction of a drug-coordinated cell therapy system.

关键词： Spinal cord injury Huc-MSCs ROS-Responsive nanoparticles Ferroptosis inhibitor

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Chronic lymphocytic leukemia/small lymphocytic lymphoma complicated with skin Langerhans cell sarcoma:A case report

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World Journal of Clinical Cases 2021年第34期9卷 10715-10722页

作者： Shao-Yan Li Yan Wang Li-Hua Wang Department of Dermatology Jinan Central HospitalCheeloo College of MedicineShandong UniversityJinan 250013Shandong ProvinceChina

BACKGROUND Langerhans cell sarcoma(LCS)is a rare malignancy with poor *** and chronic lymphocytic leukemia(CLL)/small lymphocytic lymphoma(SLL)can occur in the same diseased tissues,such as lymph nodes or *** SUMMARY A 48-year-old female Han Chinese patient was admitted for generalized lymph node enlargement for 6 years and abdominal distension for 1 *** was diagnosed with small B-cell lymphoma(stage IV)/CLL(Benet stage B)and received *** started oral ibrutinib in February *** was hospitalized on June 11,2019,and a 1.5 cm×1.5 cm dark-red nodule with ulceration scalp lesion was *** revealed LCS but without CLL/*** was diagnosed with CLL/SLL(Binet stage C,Rai stage IV)accompanied by secondary histiocytic sarcomas and skin LCS and received cyclophosphamide,doxorubicin,vincristine,dexamethasone,and etoposide but developed severe *** ultimately refused treatments and discharged *** died on September 12,*** literature review showed that in patients with CLL/SLL,skin lesions of LCS are accompanied by CLL/*** patient was different from the previously reported cases of skin LCS in patients with CLL/*** In this patient,the skin lesion of LCS showed no concomitant CLL/SLL.

关键词： Skin Langerhans cell sarcomas Chronic lymphocytic leukemia/small lymphocytic lymphoma Ibrutinib Case report

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p66Shc-mediated oxidative stress is involved in gestational diabetes mellitus

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World Journal of Diabetes 2021年第11期12卷 1894-1907页

作者： Ting-Ting Huang Wen-Juan Sun Hai-Ying Liu Hong-Li Ma Bao-Xia Cui cheeloo college of Medicine Shandong UniversityJinan 250000Shandong ProvinceChina Department of Obstetrics Taian City Central HospitalTaian 271000Shandong ProvinceChina Department of Obstetrics The Second HospitalCheeloo College of MedicineShandong UniversityJinan 250000Shandong ProvinceChina Department of Obstetrics and Gynecology Qilu Hospital(Qingdao)Cheeloo College of MedicineShandong UniversityQingdao 266000Shandong ProvinceChina Department of Obstetrics and Gynecology Qilu HospitalCheeloo College of MedicineShandong UniversityJinan 250013Shandong ProvinceChina

BACKGROUND Gestational diabetes mellitus(GDM)is associated with a heightened level of oxidative stress,which is characterized by the overproduction of reactive oxygen species(ROS)from *** studies showed that mitochondrial dysfunction is regulated by dynamin-related protein 1(Drp1)and p66Shc in *** The aim was to investigate the expression of Drp1 and p66Shc and their possible mechanisms in the pathogenesis of *** A total of 30 pregnant women,15 with GDM and 15 without GDM,were *** blood mononuclear cells and placental tissue were *** human JEG3 trophoblast cell line was cultivated in 5.5 mmol/L or 30 mmol/L glucose and transfected with wild-type(wt)-p66Shc and p66Shc siRNA.P66Shc and Drp1 mRNA levels were detected by quantitative real-time polymerase chain *** expression of p66Shc and Drp1 was assayed by immunohistochemistry and western *** was assayed by dihydroethidium *** The p66Shc mRNA level was increased in the serum(P<0.01)and placentas(P<0.01)of women with GDM,and the expression of Drp1 mRNA and protein were also increased in placentas(P<0.05).In JEG3 cells treated with 30 mmol/L glucose,the mRNA and protein expression of p66Shc and Drp1 were increased at 24 h(both P<0.05),48 h(both P<0.01)and 72 h(both P<0.001).ROS expression was also *** levels of Drp1 and ROS expression were detected in JEG3 cells transfected with wt-p66Shc(P<0.01),and low levels were detected in JEG3 cells transfected with p66Shc siRNA(P<0.05).CONCLUSION The upregulated expression of Drp1 and p66shc may contribute to the occurrence and development of *** of the mitochondrial fusion-fission balance could be a novel strategy for GDM treatment.

关键词： p66Shc Dynamin-related protein 1 Gestational diabetes mellitus Oxidative stress Mitochondrial dysfunction

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RGS16 regulated by let-7c-5p promotes glioma progression by activating PI3K-AKT pathway

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Frontiers of Medicine 2023年第1期17卷 143-155页

作者： Chaochao Wang Hao Xue Rongrong Zhao Zhongzheng Sun Xiao Gao Yanhua Qi Huizhi Wang Jianye Xu Lin Deng Gang Li Department of Neurosurgery Qilu HospitalCheeloo College of Medicine and Institute of Brain and Brain-Inspired ScienceShandong UniversityJinan 250012China shandong Key Laboratory of Brain Function Remodeling Jinan 250012China The Second Hospital Cheeloo College of MedicineShandong UniversityJinan 250033China

Gliomas are the most common central nervous system tumours;they are highly aggressive and have a poor prognosis. RGS16 belongs to the regulator of G-protein signalling (RGS) protein family, which plays an important role in promoting various cancers, such as breast cancer, pancreatic cancer, and colorectal cancer. Moreover, previous studies confirmed that let-7c-5p, a well-known microRNA, can act as a tumour suppressor to regulate the progression of various tumours by inhibiting the expression of its target genes. However, whether RGS16 can promote the progression of glioma and whether it is regulated by miR let-7c-5p are still unknown. Here, we confirmed that RGS16 is upregulated in glioma tissues and that high expression of RGS16 is associated with poor survival. Ectopic deletion of RGS16 significantly suppressed glioma cell proliferation and migration both in vitro and in vivo. Moreover, RGS16 was validated as a direct target gene of miR let-7c-5p. The overexpression of miR let-7c-5p obviously downregulated the expression of RGS16, and knocking down miR let-7c-5p had the opposite effect. Thus, we suggest that the suppression of RGS16 by miR let-7c-5p can promote glioma progression and may serve as a potential prognostic biomarker and therapeutic target in glioma.

关键词： RGS16 let-7c-5p glioma proliferation migration

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The miR-9-5p/CXCL11 pathway is a key target of hydrogen sulfide-mediated inhibition of neuroinflammation in hypoxic ischemic brain injury

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Neural Regeneration Research 2024年第5期19卷 1084-1091页

作者： Yijing Zhao Tong Li Zige Jiang Chengcheng Gai Shuwen Yu Danqing Xin Tingting Li Dexiang Liu Zhen Wang Department of Physiology School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Neurosurgery Qingdao Municipal HospitalQingdaoShandong ProvinceChina Department of medical Psychology and Ethics School of Basic Medicine SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Key Laboratory of Birth Regulation and Control Technology of National Health Commission of China Maternal and Child Health Care Hospital of Shandong Province Affiliated to Qingdao UniversityJinanShandong ProvinceChina

We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal ***,the precise mechanism underlying the role of H2S in this situation remains *** this study,we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine,a H2S precursor,attenuated the cerebral infarction and cerebral atrophy induced by hypoxia and ischemia and increased the expression of miR-9-5p and cystathionineβsynthase(a major H2S synthetase in the brain)in the prefrontal *** also found that an miR-9-5p inhibitor blocked the expression of cystathionineβsynthase in the prefrontal cortex in mice with brain injury caused by hypoxia and ***,miR-9-5p overexpression increased cystathionine-β-synthase and H2S expression in the injured prefrontal cortex of mice with hypoxic ischemic brain injury.L-cysteine decreased the expression of CXCL11,an miR-9-5p target gene,in the prefrontal cortex of the mouse model and in lipopolysaccharide-stimulated BV-2 cells and increased the levels of proinflammatory cytokines BNIP3,FSTL1,SOCS2 and SOCS5,while treatment with an miR-9-5p inhibitor reversed these *** findings suggest that H2S can reduce neuroinflammation in a neonatal mouse model of hypoxic ischemic brain injury through regulating the miR-9-5p/CXCL11 axis and restoringβ-synthase expression,thereby playing a role in reducing neuroinflammation in hypoxic ischemic brain injury.

关键词： chemokine(C-X-C motif)ligand 11 cystathionineβsynthase H2S hypoxic ischemic brain injury inflammation L-cysteine lipopolysaccharide microglia miR-9-5p neuroprotection

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Child with adenylosuccinate lyase deficiency caused by a novel complex heterozygous mutation in the ADSL gene:A case report

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World Journal of Clinical Cases 2022年第30期10卷 11082-11089页

作者： Xing-Chen Wang Ting Wang Rui-Han Liu Yan Jiang Dan-Dan Chen Xin-Yu Wang Qing-Xia Kong cheeloo college of Medicine Shandong UniversityJinan 250012Shandong ProvinceChina Department of Neurology Affiliated Hospital of Jining Medical UniversityJining 272000Shandong ProvinceChina Department of Pediatrics Affiliated Hospital of Jining Medical UniversityJining 272000China college of TCM Shandong University of Traditional Chinese MedicineJinan 250012Shandong ProvinceChina Clinical medical college Jining Medical UniversityJining 272000Shandong ProvinceChina

BACKGROUND Adenylosuccinate lyase(ADSL)deficiency is a rare autosomal-recessive defect of purine metabolism caused by mutation of the ADSL *** can cause severe neurological impairment and diverse clinical manifestations,including *** SUMMARY Here,we describe a 3-year-old Chinese boy who had both psychomotor retardation and refractory *** resonance imaging showed myelin *** findings supported a diagnosis of ***-exon sequencing revealed the presence of a novel complex heterozygous mutation in the ADSL gene:The splicing mutation c.154-3C>G and the missense mutation c.71C>T(***24Leu).Considering the patient’s clinical presentation and genetic test results,the complex heterozygous mutation was predicted to prevent both ADSL alleles from producing normal ADSL,which may have led to ADSL ***,the child was diagnosed with ADSL *** We identified a novel complex heterozygous mutation in the ADSL gene associated with ADSL deficiency,thus expanding the known spectrum of pathogenic mutations that cause ADSL ***,we describe epilepsy that occurs in patients with ADSL deficiency.

关键词： Adenylosuccinate lyase deficiency Compound heterozygous mutations Epilepsy Pathogenic mutation Case report

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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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Neurotoxicity due to dimethylamine borane poisoning via skin absorption:a case report

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World Journal of Emergency Medicine 2022年第6期13卷 500-503页

作者： Guang-cai Yu Ya-qian Li Tian-zi Jian Bao-tian Kan Si-qi Cui Ping Han Xiang-dong Jian Department of Poisoning and Occupational Diseases Emergency MedicineQilu Hospital of Shandong UniversityCheeloo College of MedicineShandong UniversityJinan 250012China shandong university of Traditional Chinese Medicine Jinan 250012China Department of Geriatric Medicine Qilu Hospital of Shandong UniversitySchool of NursingCheeloo College of MedicineShandong UniversityJinan 250012China School of Public Health Cheeloo College of MedicineShandong UniversityJinan 250012China

Dear editor,Dimethylamine borane(DMAB,CAS no.74-94-2),also called boron-dimethylamine complex,is a white crystalline *** has an amine odour under mild conditions.[1]As an excellent reducing agent,DMAB is widely used in the semiconductor industry,pharmaceutical manufacturing,[2]oligomer and polymer production,and hydrogen storage.[3]Acute DMAB exposure may cause eye or respiratory irritation,throat discomfort,vomiting,diarrhoea,and pulmonary oedema.[1,4]Isolated reports indicated that DMAB exposure causes acute cerebellar oedema and peripheral neuropathy.[1,5,6]Herein,we report a case of DMAB poisoning via dermal absorption in which the central and peripheral nervous systems were the primary sites of toxic *** highlight the use of brain magnetic resonance imaging(MRI)and electromyography(EMG)for evaluation after exposure.

关键词： conditions. absorption boron

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The hepatic macrophage pool in NASH

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Cellular & Molecular Immunology 2021年第8期18卷 2059-2060页

作者： Tixiao Wang Chunhong Ma Key Laboratory for Experimental Teratology of Ministry of Education Key Laboratory of Infection and Immunity of Shandong Provinceand Department of ImmunologySchool of Basic Medical SciencesCheeloo Medical College of Shandong UniversityJinanShandongChina Advanced medical Research Institute Shandong UniversityJinanShandongChina

Nonalcoholic fatty liver disease(NAFLD)and its inflammatory subtype nonalcoholic steatohepatitis(NASH)are currently the most common chronic liver diseases worldwide and emerging risk factors for hepatocellular carcinoma.1 Numerous studies have demonstrated the critical involvement of hepatic macrophages,including resident Kupffer cells(KCs)and recruited monocyte-derived macrophages(MoMFs).

关键词： liver NAFLD NASH

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Macrophage exosomes modified by miR-365-2-5p promoted osteoblast osteogenic differentiation by targeting OLFML1

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Regenerative Biomaterials 2024年第3期3卷 134-147页

作者： Caiyao Hou Yujue Zhang Zhaoyong Lv Yurun Luan Jun Li Chunxiu Meng Kun Liu Xin Luo Liyu Chen Fengzhen Liu Department of Materials Science and Engineering Liaocheng UniversityLiaocheng 252000China Liaocheng People's Hospital Liaocheng Hospital Affliated Shandong First Medical UniversityLiaocheng 252000China The Second Hospital Cheeloo College of MedicineShandong UniversityJinan 250023China

In the bone immune microenvironment,immune cells can regulate osteoblasts through a complex communication *** play a central role in mediating immune osteogenesis,exosomes derived from them have osteogenic regulation and can be used as cariers in bone tissue ***,there are problems with exosomal therapy alone,such as poor targeting,and the content of loaded molecules cannot reach the therapeutic *** this study,macrophage-derived exosomes modified with miR-365-2-5p were developed to accelerate bone ***3T3-E1 cells were incubated with the culture supermatants of Mo,M1 and M2 macrophages,and it was found that the culture medium of M2 macrophages had the most significant effects in contributing to ***-throughput sequencing identified that miR-365-2-5p was significantly expressed in exosomes derived from M2 *** incubated MC3T3-E1 with exosomes overexpressing or kmocking down miR-365-2-5p to examine the biological function of exosome miR-365-2-5p on MC3T3-E1 *** findings suggested that miR-365-2-5p secreted by exosomes increased the osteogenesis of ***,miR-365-2-5p had a direct influence over osteogenesis for *** analysis combined with dual luciferase detection indicated that miR-365-2-5p binded to the 3'-UTR of *** summary,exosomes secreted by M2 macrophages targeted OLFML1 through miR-365-2-5p to facilitate osteogenesis.

关键词： macrophage exosomes osteogenesis osteoimmunology

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