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Silencing of Jumonji domain-containing 1C inhibits the osteogenic differentiation of bone marrow mesenchymal stem cells via nuclear factor-κb signaling

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World Journal of Stem Cells 2024年第2期16卷 151-162页

作者： Jing-Yi Li Ting-Ting Wang Li Ma Yu Zhang Di Zhu Department of Medical Cosmetology Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070China Department of General Gerontology The First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052Henan ProvinceChina Department of Plastic Surgery China-Japan Friendship HospitalBeijing 100029China Senior Department of Hematology The Fifth Medical CentreGeneral Hospital of Chinese People’s Liberation ArmyBeijing 100071China Department of Orthopaedic Surgery Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070China

bACKGROUND Osteoporosis is a common metabolic bone disorder induced by an imbalance between osteoclastic activity and osteogenic *** osteoporosis,bone mesenchymal stem cells(bMSCs)exhibit an increased ability to differentiate into adipocytes and a decreased ability to differentiate into osteoblasts,resulting in bone *** domain-containing 1C(JMJD1C)has been demonstrated to suppress *** To examine the effect of JMJD1C on the osteogenesis of bMSCs and the potential underlying *** bMSCs were isolated from mouse bone marrow *** Red O staining,Alizarin red staining,alkaline phosphatase staining and the expression of adipo-genic and osteogenic-associated genes were assessed to determine the differen-tiation of *** marrow-derived macrophages(bMMs)were incubated with receptor activator of nuclear factor-kappaΒligand to induce osteoclast differentiation,and osteoclast differen-tiation was confirmed by tartrate-resistant acid phosphatase *** related genes were measured via reverse transcription coupled to the quantitative polymerase chain reaction and western ***-linked immunosorbent assays were used to measure the levels of inflammatory cytokines,including tumor necrosis factor alpha,interleukin-6 and interleukin-1 *** The osteogenic and adipogenic differentiation potential of bMSCs isolated from mouse bone marrow samples was ***1C mRNA and protein expression was upregulated in bMSCs after osteoblast induction,while p-nuclear factor-κb(NF-κb)and inflammatory cytokines were not significantly *** of JMJD1C repressed osteogenic differentiation and enhanced NF-κb activation and inflammatory cytokine release in ***,JMJD1C expression decreased during bMM osteoclast *** The JMJD1C/NF-κb signaling pathway is potentially involved in bMSC osteogenic differentiation and may play vital roles in the pathogenesis of osteoporosis.

关键词： Osteoporosis Mesenchymal stem cells Osteogenesis Jumonji domain-containing 1C nuclear factor-κb

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Down-regulation of peroxisome proliferator-activated receptor γ coactivator-1α expression in fatty acid-induced pancreatic betacell apoptosis involves nuclear factor-κb pathway

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Chinese Medical Journal 2011年第22期124卷 3657-3663页

作者： HE Ting-ting CAO Xiao-pei CHEN Ru-zhu ZHU Xiao-nan WANG Xue-lan LI Yan-bing XIAO Hai-peng Department of Endocrinology First Affiliated Hospital of Sun Yat-sen University Guangzhou Guangdong 510080 China

background Pancreatic beta-cell apoptosis induced by lipotoxicity, to a large extent, contributes to the progression of type 2 diabetes. To investigate the mechanism of free fatty acid induced apoptosis, we aimed to study the effects of palmitic acid （PA） on the apoptosis and peroxisome proliferator-activated receptor y coactivator-1α （PGC-1α） expression in βTC3 cells as well as the possible role of nuclear factor-Kb （NF-Kb） in this process. Methods Hoechst 33258 was used to detect βTC3 cell apoptosis, which was induced by PA stimulation for 12 hours. PGC-1α expression was analyzed by reverse transcription polymerase chain reaction, Iκb kinase β （IKKβ）, Iκbα NF-Kb-inducing kinase （NIK） and ReI-b expressions were analyzed by Western blotting. MGβ2 was employed to block the endogenous Iκbαdegradation before PA administration, and then its effect on PA-inducing cell apoptosis and PGC-1α mRNA expression was analyzed. Results Significant increased cell apoptosis was found at the concentration of 0.5 mmol/L and 1.0 mmol/L PA administration. PA （0.5 mmol/L） could extensively reduced the expression of PGC-1α mRNA. After exposing βTC3 cells to 0.5 mmol/L PA for different time periods （0, 4, 6, 8, 10 and 12 hours）, IKKβ protein expression increased while Iκbα NIK and ReI-b protein expression declined in a time-dependent manner. Pretreatment with MGβ2 to inhibit the degradation of Iκbα partially prevented the down-regulation of PGC-1α mRNA expression after 12-hour PA treatment in accordance with the decrease of PA induced apoptosis. Conclusions NF-Kb canonical pathway was activated in PA-mediated βTC3 cell apoptosis, whereas non-canonical pathway was inhibited. Reduced PGC-1α expression by PA in βTC3 cells could involve the activation of canonical NF-Kb pathway, so as to deteriorate the PA induced apoptosis.

关键词： beta-cell apoptosis peroxisome proliferator-activated receptor 7 coactivator-1α nuclear factor-κb

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Interleukin-1 inhibits Sox9 and collagen type Ⅱ expression via nuclear factor-κb in the cultured human intervertebral disc cells

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Chinese Medical Journal 2009年第20期122卷 2483-2488页

作者： YU Zhan-ge XU Ning WANG Wen-bo PAN Shang-ha LI Ke-shen LIU Jia-kun Department of Orthopaedic Surgery the First Affiliated Hospital of Harbin Medical University Harbin Heilongjiang 150001 China Central Laboratory the First Affiliated Hospital of Harbin Medical University Harbin Heilongjiang 150001 China Department of biomedical Engineering Harbin Engineering University Harbin Heilongjiang 150001 China

background The most significant biological change in intervertebral disc degeneration is the decrease of chondrocyte specific gene and protein expression of Sox9 and collagen type Ⅱ. Interleukin-1 （IL-1） is not expressed in the normal intervertebral disc tissue but increases in the degenerated intervertebral disc tissue. This suggests that IL-1 may play a role in regulation of the expression of Sox9 and collagen type Ⅱ. Methods Human intervertebral disc cells were isolated and cultured. Sox9 and collagen type Ⅱ expression during treatment with IL-1, with or without the nuclear factor-κb （NF-κb） activity inhibitor curcumin, were detected by using reverse transcription-polymerase chain reaction （RT-PCR） and Western blotting, and the activity of the NF-κb signaling pathway was detected by the electrophoretic mobility shift assay （EMSA）. Results IL-1 lowered the mRNA level and protein expression of Sox9 and collagen type Ⅱ in the cultured intervertebral disc cells in a dose dependent manner （P 〈0.05）, and this effect was attenuated by curcumin. Curcumin alone had no effect on Sox9 and collagen type Ⅱ expression （P 〉0.05）. IL-1 at concentrations of 0.1 ng/ml, 1 ng/ml and 10 ng/ml could stimulate the activity of NF-κb in the intervertebral disc cells in a dose dependent manner （P 〈0.05） that was inhibited by curcumin. Conclusions We demonstrated the previously unknown function of IL-1 in inhibiting Sox9 and collagen type Ⅱ via NF-κb in the intervertebral disc cells. This inhibition can be attenuated by curcumin, which is an effective NF-κb activity inhibitor.

关键词： interleukin-1 Sox9 collagen type Ⅱ nuclear factor-κb intervertebral disc cells

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Inhibition of nuclear factor-κb activity enhanced chemosensitivity to cisplatin in human lung adeno-carcinoma A549 cells under chemical hypoxia conditions

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Chinese Medical Journal 2013年第17期126卷 3276-3282页

作者： LI Fang HUANG Li SU Xiao-li GU Qi-hua HU Cheng-ping Department of Respiratory Diseases Xiangya Hospital Central South University Changsha Hunan 410007 China

background Tumor hypoxia, one of the features of solid tumors, is associated with chemo-resistance. Recently, nuclear factor-Kb （NF-κb） was found to be activated during hypoxia. However, the impact of NF-κb activation on chemo-resistance during hypoxia remains unknown. Methods Human lung adenocarcinoma A549 cells were transfected with NF-κb p65siRNA and treated with cobalt chloride （COCI2） to mimic hypoxia in the presence or absence of cisplatin. NF-Kb expression was measured by Western blotting, immune-fluorescence and real-time PCR. Hypoxia-inducible factor-1α （HIF-1α） and bcl-2 expression were determined by Western blotting. Cell apoptosis and survival with half-maximum inhibitory concentration （IC50） of cisplatin were determined by Annexin V-FITC/PI and 3-（4, 5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT）, respectively. Results Exposure ofA549 cells to COCl2 increased nuclear HIF-1α protein expression, and enhanced NF-Kb p65 protein nuclear accumulation （the mark of NF-κb activation） in a time and dose dependant manner. COCI2 did not promote apoptosis in A549 cells; on the contrary, it reduced cisplatin-induced apoptosis and increased the IC50 of cisplatin. However, when we inhibited CoCI2-induced activation of NF-κb through NF-κb p65siRNA, cisplatin-induced apoptosis was increased and IC50 of cisplatin was reduced to levels similar to those in control cells. Meanwhile, CoCI2-induced bcl-2 over- expression was down-regulated in the presence of cisplatin when NF-κb activity was inhibited. Conclusion Up-regulating bcl-2 might be involved in NF-κb activation induced resistance to cisplatin in A549 cells under CoCl2-induced chemical hypoxia.

关键词： lung adenocarcinoma nuclear factor-κb chemical hypoxia chemotherapy bcl-2

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Toll-like receptor 4-mediated nuclear factor-κb activation in spinal cord contributes to chronic morphine-induced analgesic tolerance and hyperalgesia in rats

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Neuroscience bulletin 2014年第6期30卷 936-948页

作者： Liying bai Caihong Zhai Kun Han Zhisong Li Junliang Qian Ying Jing Wei Zhang Ji-Tian Xu Department of Anesthesiology The First Affiliated HospitalZhengzhou University Department of Physiology Medical School of Zhengzhou University

nuclear factor kappa b（NF-κb） in the spinal cord is involved in pro-infl ammatory cytokine-mediated pain facilitation. However, the role of NF-κb activation in chronic morphine-induced analgesic tolerance and the underlying mechanisms remain unclear. In the present study, we found that the level of phosphorylated NF-κb p65（p-p65） was increased in the dorsal horn of the lumbar 4–6 segments after intrathecal administration of morphine for 7 consecutive days, and the p-p65 was co-localized with neurons and astrocytes. The expression of TNF-α and IL-1β was also increased in the same area. In addition, pretreatment with pyrrolidinedithiocarbamate（PDTC） or SN50, inhibitors of NF-κb, prevented the development of morphine analgesic tolerance and alleviated morphine withdrawal-induced allodynia and hyperalgesia. The increase in TNF-α and IL-1β expression induced by chronic morphine exposure was also partially blocked by PDTC pretreatment. In another experiment, rats receiving PDTC or SN50 beginning on day 7 of morphine injection showed partial recovery of the anti-nociceptive effects of morphine and attenuation of the withdrawal-induced abnormal pain. Meanwhile, intrathecal pretreatment with lipopolysaccharide from Rhodobacter sphae-roides, an antagonist of toll-like receptor 4（TLR4）, blocked the activation of NF-κb, and prevented the development of morphine tolerance and withdrawal-induced abnormal pain. These data indicated that TLR4-mediated NF-κb activation in the spinal cord is involved in the development and maintenance of morphine analgesic tolerance and withdrawalinduced pain hypersensitivity.

关键词： nuclear factor-κb pro-inflammatory cytokines Toll-like receptor 4 morphine tolerance hyperalgesia

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Clinical significance of SQSTM1/P62 and nuclear factor-κb expression in pancreatic carcinoma

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World Journal of Gastrointestinal Oncology 2020年第7期12卷 719-731页

作者： Zhao-Yang Zhang Sen Guo Rui Zhao Zhi-Peng Ji Zhuo-Nan Zhuang Department of Emergency Surgery Qilu HospitalShandong UniversityJinan 250012Shandong ProvinceChina Department of General Surgery Qilu HospitalShandong UniversityJinan 250012Shandong ProvinceChina Department of General Surgery Second Affiliated Hospital of Shandong UniversityJinan 250033Shandong ProvinceChina Department of Gastrointestinal Surgery Beijing Tsinghua Changgung HospitalSchool of Clinical MedicineTsinghua UniversityBeijing 102200China

bACKGROUND Overexpression of SQSTM1(sequestosome 1,P62)and nuclear factor-κb(NF-κb)plays an important role in the invasion and metastasis of a variety of malignant *** To explore the expression of P62 and NF-κb in pancreatic cancer and their relationship with clinicopathological *** The expression levels of P62 and NF-κb were analyzed by immunohistochemistry with a tissue chip containing 40 cases of human pancreatic *** we analyzed the correlation among P62 expression,phospho-P65 expression,and clinicopathological features of pancreatic carcinoma *** P62 expression was mainly observed in the cytoplasm of pancreatic carcinoma *** P65(phospho-P65)was mainly expressed in the nucleus and cytoplasm of pancreatic carcinoma *** was a significant difference in P62 expression among T *** a significant difference in phosphor-P65 expression among pathology types was *** the cases with strongly positive P62 expression,significant differences were found in *** there were significant differences in T stage and tumor-node-metastasis stage in the cases with strongly positive phosphor-P65 *** In pancreatic carcinoma,P62 expression is significantly correlated with T *** may be a valuable malignant indicator for human pancreatic carcinoma.

关键词： Pancreatic carcinoma Phosphorylated P65 P62 SQSTM1 nuclear factor-κb Malignant

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Iguratimod promotes transformation of mononuclear macrophages in elderly patients with rheumatoid arthritis by nuclear factor-κb pathway

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World Journal of Clinical Cases 2021年第10期9卷 2181-2191页

作者： Sha Liu Li-Ping Song Rong-bin Li Le-Heng Feng Hui Zhu Department of Rheumatism The First Hospital of QiqiharAffiliated Qiqihar Hospital of Southern Medical UniversityQiqihar 161005Heilongjiang ProvinceChina

bACKGROUND The role of macrophages in rheumatoid arthritis(RA)and its mechanism have attracted much attention in RA *** accumulate in the synoviums of RA,and the proportion of M1 type pro-inflammatory macrophages is higher than that of M2 type anti-inflammatory macrophages,leading to the secretion of inflammatory molecules and the aggravation of inflammatory reaction,which has made macrophages a potential target of RA *** is a kind of cyclo-oxygenase-2 inhibitor that affects macrophage *** is speculated that its anti-inflammatory and anti-rheumatic effects may be related to the regulation of macrophage M1/M2 *** To investigate the effects of Iguratimod on the polarity of mononuclear macrophages in elderly patients with *** Elderly patients with RA and joint effusion were selected,including 10 men and 25 women,with an average age of 66.37±4.42 *** were treated with oral administration of 25 mg Iguratimod(Iremod,State Food and Drug Administration Approval No.H20110084)twice daily for 12 *** Activity Score 28 and Health Assessment Questionnaire score were collected according to the disease severity before and after *** blood and joint effusion fluid were collected,mononuclear macrophages were extracted and expression of cell surface markers CD86,CD64,CD163,and CD206 was analyzed by flow *** concentration of inflammatory factors interleukin(IL)-6,IL-1β,transforming growth factor-β,and IL-4 in the joint effusion fluid was analyzed by enzyme-linked immunosorbent *** of mononuclear cells inhibitor of nuclear factor-κb(Iκb)and phosphorylated Iκb in peripheral blood was analyzed by western *** Disease Activity Score 28 score and Health Assessment Questionnaire score of patients treated with Iguratimod decreased *** percentage of cell surface markers CD86 and CD64 decreased significantly,and the percentage of CD163 and CD206 increased signifi

关键词： Rheumatoid arthritis Iguratimod Macrophage Polarity nuclear factor-κb

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Changes of sulfur dioxide, nuclear factor-κb, and interleukin-8 levels in pediatric acute lymphoblastic leukemia with bacterial inflammation

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Chinese Medical Journal 2014年第23期127卷 4110-4113页

作者： Wu Wanshui Jia Yongrui Du Shuxu Tang Hong Sun Yangling Sun Liming J Department of Pediatrics Shijitan Hospital Capital Medical University Beijing 100038 China Health Science Center Peking University Beijing 100191 China

background bacterial inflammation is a common complication in patients with leukemia,and sulfur dioxide （SO2） is a bioactive molecule in modulating Gram-negative bacilli *** study aimed to examine the changes in SO2,nuclear factor-κb （NF-κb）,and interleukin-8 （IL-8） levels in pediatric acute lymphoblastic leukemia （ALL） with Gram-negative bacterial *** Fifty-five ALL children were enrolled in this study,including 30 males and 25 females,aged 3-13 years,and the median age was 7.8 *** these children who accepted chemotherapy for ALL were divided into the control group （before chemotherapy）,the infection group （after chemotherapy with infection）,and the recovery group （the infection was controlled after 1 week）.The serum level of SO2 was detected using high performance liquid chromatography with fluorescence assay,and NF-κb and IL-8 levels were measured by enzyme-linked immunosorbent assay （ELISA）.Human THP-1 cells were cultured,induced,and differentiated into macrophages,which were divided into five groups and each group was cultured with different stimulators：lipopolysaccharide （LPS） group,LPS＋L-aspartate-β-hydroxamate （HDX） group,LPS＋SO2 group,SO2,and control ***-κb level and IL-8 protein contents by ELISA were examined in each *** In comparison with those of the control group,levels of serum SO2,NF-κb,and IL-8 of the infection group were significantly increased （P ＜0.05）,while those of the recovery group were significantly decreased （P ＜0.05）.A positive correlation was found between levels of serum SO2 and intracellular NF-κb/IL-8,and the correlation coefficients were 0.671 and 0.798 （P ＜0.05）,*** to the results found in human THP-1 cells,levels of NF-κb and IL-8 in LPS group were significantly increased compared with those of the control group （P ＜0.05）; when compared with those in LPS group,levels of NF-κb in LPS＋HDX group further increased significantly （P ＜0.05）; however,the NF-κb levels of LP

关键词： acute lymphoblastic leukemia child sulfur dioxide nuclear factor-κb interleukin-8

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Expression of nuclear factor-κb in Mouse Uterus during Peri-implantation

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第4期24卷 361-364页

作者：谢青贞辛志敏曹路敏李万 Family Planning Research Institute Tongji Medical College Huazhong University of Science and Technology

To investigate the expression of the subunit p65 of NF-κb and inhibitor kappa b alpha (Iκbα) in mouse uterus during peri-implantation, thereby investigating whether transient activation of nuclear factor-κb (NF-κb) takes place during embryo implantation in mice. Immunohistochemical technique was used to examine the expression and localization of p65 in endometrium or deciduas, and Western blot analysis was employed to detect the levels of Iκbα protein in mouse endometrium or deciduas. P65 protein was detected in stromal cells, epithelial cells of endometrium as well as in myometrium. Staining was predominately seen in the cytoplasm of the cells. Staining intensity for p65 was stronger in the epithelial compartment than the stromal compartment and myometrium. Staining intensity increased slightly during pregnancy, and it reached a high level on pregnancy day 5 and day 8. In contrast to p65, the level of Iκbα protein was lowest on pregnancy day 5 in all groups. Our results suggested that NF-κb may regulate embryo implantation by its transient activation in mice.

关键词： nuclear factor-κb embryo implantation endometrium

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Effect of Propofol on nuclear factor-κb Signal Pathway and Cardiomyocytes Apoptosis in Myocardium Ischemia/Reperfusion Injury in Rats

Effect of Propofol on Nuclear Factor-κB Signal Pathway and ...

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中国药理学会第十次全国学术会议

作者： XIE Li-jun,ZHANG Jian-xin,LI Lan-fang (Hebei Academy of Medical Sciences,Shijiazhuang 050021)

background and Objective Myocardium ischemia/reperfusion injury(I/R) is a commonly perioperative cardiac *** signaling pathways are activated in response to myocardium I/R including nuclear factor-κb(NF-κb) *** has been proved that NF-κb is a pivotal transcription factor playing a key role in oxidative stress and inflammatory ***,2,6-diisopropylphenol,an intravenous anaesthetic with a rapid and short an-

关键词： propofol ischaemia/reperfusion nuclear factor-κb apoptosis rat

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