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Ectopic expression of clusterin/apolipoprotein J or Bcl-2 decreases the sensitivity of HaCaT cells to toxic effects of ropivacaine

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Cell Research 2004年第5期14卷 415-422页

作者： Evangelos KONTARGIRIS,Evangelos KOLETTAS,Athina VADALOUCA,Ioannis P. TROUGAKOS,Efstathios S. GONOS,Vasiliki KALFAKAKOU Laboratory of Experimental physiology University of Ioannina Medical School 45110 Ioannina Greece Laboratory of Experimental physiology University of Ioannina Medical School 45110 Ioannina Greece Department of Anesthesia Pain Relief and Palliative Care University Clinic Areteion Hospital Athens Greece Laboratory of molecular and cellular Aging Institute of Biological Research and Biotechnology National Hellenic Research Foundation 11635 Athens Greece Laboratory of molecular and cellular Aging Institute of Biological Research and Biotechnology National Hellenic Research Foundation 11635 Athens Greece Laboratory of Experimental physiology University of Ioannina Medical School 45110 Ioannina Greece

Local anesthetics inhibit cell proliferation and induce apoptosis in various cell types. Ropivacaine, a unique, novel tertiary amine-type anesthetic, was shown to inhibit the proliferation of several cell types including keratinocytes. We found that Ropivacaine could inhibit the proliferation and induce apoptosis in an immortalized human keratinocyte line, HaCaT, in a dose- and time-dependent manner and with the deprivation of serum. The dose-dependent induction of apoptosis by ropivacaine was demonstrated by DNA fragmentation analysis and the proteolytic cleavage of a caspase-3 substrate — poly (ADP-ribose) polymerase (PARP). In addition, ropivacaine downregulated the expression of clusterin/ apoliporotein J, a protein with anti-apoptotic properties, in a dose-dependent manner, which well correlated with the induction of apoptosis of HaCaT cells. To investigate the role of clusterin/apoliporotein J in ropivacaine-induced apoptosis, HaCaT cells overexpressing clusterin/apoliporotein J were generated and compared to cells expressing the well estab- lished anti-apoptotic Bcl-2 protein. Ectopic overexpression of the secreted form of clusterin/apoliporotein J or Bcl-2 decreased the sensitivity of HaCaT cells to toxic effects of ropivacaine as demonstrated by DNA fragmentation, the proteolytic cleavage of PARP and by a reduction in procaspase-3 expression. Furthermore, the downregulation of endogenous clusterin/apolipoprotein J levels by ropivacaine suggested that this might be one mechanism by which ropivacaine induced cell death in HaCaT cells. In conclusion, the ability of ropivacaine to induce antiproliferative responses and to suppress the expression of the anti-apoptotic protein clusterin/apolipoprotein J, combined with previ- ously reported anti-inflammatory activity and analgesic property of the drug, suggests that ropivacaine may have poten- tial utility in the local treatment of tumors.

关键词： keratinocytes ropivacaine clusterin/Apolipoprotein J Bcl-2 apoptosis.

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Trivalent Chromium Modulates Hexosamine Biosynthesis Pathway Transcriptional Activation of Cholesterol Synthesis and Insulin Resistance

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Open Journal of Endocrine and Metabolic Diseases 2013年第4期3卷 1-8页

作者： Brent A. Penque Lixuan Tackett Jeffrey S. Elmendorf departments of cellular and Integrative physiology and Biochemistry and molecular Biology Centers for Diabetes Research and Membrane Biosciences Indiana University School of Medicine Indianapolis USA

Trivalent chromium has long been recognized to benefit carbohydrate and lipid metabolism. Given emerging evidence that suggests chromium improves insulin sensitivity through the maintenance of an optimal level of plasma membrane (PM) cholesterol, we delineated the role of this micronutrient in attenuating hyperinsulinemia-induced cholesterol biosynthesis and insulin resistance. Exposing 3T3-L1 adipocytes to physiological hyperinsulinemia (500 pM 12 h), resulted in a marked impairment in insulin-stimulated glucose transport. Concurrent treatment with chromium in the picolinate form (CrPic, 10 nM 16 h) prevented against glucose transport dysfunction. Insulin signaling was neither impaired by hyperinsulinemia nor amplified by chromium to promote this protective action. Instead, it was found that hyperinsulinemia promoted an increase in PM cholesterol content that was observed to impair the acute ability of insulin to stimulate GLUT4 redistribution to the PM. Chromium prevented against the accumulation of PM cholesterol. Mechanistically, hyperinsulinemia promoted increases in O-GlcNAc modification of specificity protein 1 (Sp1), known to engage a cholesterolgenic response. Subsequent chromatin immunoprecipitation and luciferase assays revealed that hyperinsulinemia increased the binding affinity of Sp1 to the promoter region of Hmgcr, encoding 3-hydroxy 3-methyl-glutaryl-CoA reductase (HMGR), as well as HMGR promoter activity. This resulted in gains in mRNA and protein content of HMGR, with resulting elevations in PM cholesterol content. Moreover, treatment with chromium prevented this transcriptional response. Together, these data suggest a mechanism whereby CrPic affords glycemic health through inhibition of a transcriptional cholesterolgenic program detrimental to insulin action.

关键词： 3T3-L1 Adipocytes GLUT4 HMG-CoA Reductase Hyperinsulinemia Sp1

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Sulfur Dioxide Inhibits Extracellular Signal-regulated Kinase Signaling to Attenuate Vascular Smooth Muscle Cell Proliferation in Angiotensin II-induced Hypertensive Mice

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Chinese Medical Journal 2016年第18期129卷 2226-2232页

作者： Hui-Juan Wu Ya-Qian Huang Qing-Hua Chen Xiao-Yu Tian Jia Liu Chao-Shu Tang Hong-Fang Jin Jun-Bao Du Department of Pediatrics Peking University First Hospital Beijing 100034 China Department of physiology and Pathophysiology Peking University Health Science Centre Beijing 100191 China Key Laboratory of molecular cardiology Ministry of Education Beijing 100091 China

Background： Clarifying the mechanisms underlying vascular smooth muscle cell （VSMC） proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide （SO2） inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin Ⅱ （Angll）-induced VSMC proliferation by SO, has not been fully elucidated. This study was designed to investigate if SO2 inhibited VSMC proliferation in mice with hypertension induced by Angll. Methods： Thirty-six male C57 mice were randomly divided into control, Angll, and Angll ＋ SO2 groups. Mice in Angll group and Angl I ＋ SO2 group received a capsule-type Angll pump implanted under the skin of the back at a slow-release dose of 1000 ng-kg^-1min In addition, mice in Angll ＋ SO2 received intraperitoneal injections of SO., donor. Arterial blood pressure of tail artery was determined. The thickness of the aorta was measured by elastic fiber staining, and proliferating cell nuclear antigen （PCNA） and phosphorylated-extracellular signal-regulated kinase （P-ERK） were detected in aortic tissues. The concentration of SO~ in serum and aortic tissue homogenate supernatant was measured using high-performance liquid chromatography with fluorescence determination. In the in vio＇o study, VSMC of A7R5 cell lines was divided into six groups： control, Angll, Angll ＋ SO2 PD98059 （an inhibitor of ERK phosphorylation）, Angll ＋ PD98059, and Angll ＋ SO, ＋ PD98059. Expression of PCNA, ERK, and P-ERK was determined by Western blotting. Results： In animal experiment, compared with the control group, Angll markedly increased blood pressure （P 〈 0.01 ） and thickened the aortic wall in mice （P 〈 0.05） with an increase in the expression of PCNA （P 〈 0.05）. SO2 however, reduced the systemic hypertension and the wall thickness induced by AnglI （P 〈 0.05）. It inhibited the increased expression of PCNA and P-ERK induced by A

关键词： Angiotensin II Hypertension Proliferation Sulfur Dioxide Vascular Smooth Muscle Cell

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Antisense Oligodeoxynucleotide Inhibits Expression of Re-com binantPorcine Follicle-Stim ulating Horm one Receptor

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Journal of Huazhong University of Science and Technology(Medical Sciences) 1999年第3期19卷 175-180页

作者： ZHU Changhong 1, Mark D. Nixon 2, WANG Yifang 1, Andrew R. LaBarbera 3 1 Center of Reproductive Medicine, Tongji Hospital, Tongji Medical University, Wuhan 430030 2 Department of Obstetrics and Gynecology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0526 3 Department of molecular and cellular physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0526 Center of Reproductive Medicine Tongji Hospital Tongji Medical University Wuhan Department of Obstetrics and Gynecology University of Cincinnati College of Medicine Cincinnati Department of molecular and cellular physiology University of Cincinnati College of Medicine Cincinnati

To assess the role of follicle stimulating hormone receptor(FSHR) gene expression in regulating expression of FSHR protein in the plasma membrane, the effects of a porcine FSHR cDNA antisense oligodeoxynucleotide (ODN) on FSHR mRNA levels and 125 I FSH binding were determined in Chinese hamster ovary cells expression recombinant porcine FSHR (pFSHR CHO cells). An 18 mer phosphorothioate endcapped antisense ODN that corresponded to the region surrounding the translation initiation codon of the porcine FSHR cDNA was synthesized. An 18 mer nonsense sequence of identical nucleotide composition, which had little homology to known DNA sequences, was synthesized for use as a control. pFSHR CHO cells were cultured in 24 well plates (10 5 cells/well) in the absence or presence of 1 20 μmol/L antisense or nonsense ODN for 24 h and then assayed for porcine FSHR mRNA, using quantitative reverse transcription and competitive polymerase chain reaction, and for 125 I FSH binding activity. Treatment with 10 μmol/L antisense ODN caused a paradoxical increase in porcine FSHR mRNA from 0.89±0.06 to 1.64±0.08 ng/mg total RNA ( P <0.05). Transfection with lipofectamine and 0.33 μmol/L antisense ODN caused an increase in porcine mRNA from 0.95±0.08 to 1.53±0.07 ng/mg total RAN. This was probably due to upregulation of mRNA synthesis resulting from inhibition of porcine FSHR protein translation. The nonsense ODN had no effect on porcine FSHR mRNA. Antisense, but not nonsense, ODN (10 μmol/L) inhibited membrane binding of 125 I FSH by 13.6± 0.8 % ( P <0.05) in 24 h. Treatment of cells with antisense ODN (10 μmol/L) for 48 h resulted in a 76±1.5 % ( P <0.05) inhibition of 125 I FSH binding. In contrast, transfection with lipofectamine and 0.33 μmol/L antisense ODN at 0 h caused a 76.1±1.3 % ( P <0.05) reduction in binding within 24 h. Binding had returned to 52.3±2.3 % ( P < 0.05) of normal by 48 h. These results indicate

关键词： follicle stimulating hormone antisense oligodeoxynucleotide folliculogenesis mRNA spermatogenesis

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LonP1 Links Mitochondria–ER Interaction to Regulate Heart Function

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Research 2024年第1期2023卷 595-609页

作者： Yujie Li Dawei Huang Lianqun Jia Fugen Shangguan Shiwei Gong Linhua Lan Zhiyin Song Juan Xu Chaojun Yan Tongke Chen Yin Tan Yongzhang Liu Xingxu Huang Carolyn K.Suzuki Zhongzhou Yang Guanlin Yang Bin Lu The Affiliated Nanhua Hospital and School of Basic Medical Sciences Hengyang Medical SchoolUniversity of South ChinaHengyangHunan 421001China School of Laboratory Medicine and Life Sciences Wenzhou Medical UniversityWenzhouZhejiang 325035China National Health Commission Key Laboratory of Birth Defect Research and Prevention Hunan Provincial Maternal and Child Health Care HospitalChangshaHunan 410008China Key Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications Ministry of Education of ChinaLiaoning University of Traditional Chinese MedicineShenyangLiaoning 110847China Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province The First Affiliated Hospital of Wenzhou Medical UniversityWenzhouZhejiangChina Hubei Key Laboratory of Cell Homeostasis College of Life SciencesWuhan UniversityWuhanHubei 430072China Nanjing Maternity and Child Health Care Hospital Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical UniversityNanjing 210004China Animal Center Wenzhou Medical UniversityWenzhouZhejiang 325035China Department of cardiology The First Affiliated Hospital of University of South ChinaHengyangHunanChina School of Life Science and Technology Shanghai Tech UniversityShanghai 201210China Department of Microbiology Biochemistry and Molecular GeneticsNew Jersey Medical School-RutgersThe State University of New JerseyNewarkNJUSA State Key Laboratory of Pharmaceutical Biotechnology Department of CardiologyNanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical School and MOE Key Laboratory of Model Animal for Disease StudyModel Animal Research CenterNanjing UniversityNanjing 210061China

Interorganelle contacts and communications are increasingly recognized to play a vital role in cellular function and *** particular,the mitochondria–endoplasmic reticulum(ER)membrane contact site(MAM)is known to regulate ion and lipid transfer,as well as signaling and organelle ***,the regulatory mechanisms of MAM formation and their function are still ***,we identify mitochondrial Lon protease(LonP1),a highly conserved mitochondrial matrix protease,as a new MAM tethering *** removal of LonP1 substantially reduces MAM formation and causes mitochondrial ***,deletion of LonP1 in the cardiomyocytes of mouse heart impairs MAM integrity and mitochondrial fusion and activates the unfolded protein response within the ER(UPR^(ER)).Consequently,cardiac-specific LonP1 deficiency causes aberrant metabolic reprogramming and pathological heart *** findings demonstrate that LonP1 is a novel MAM-localized protein orchestrating MAM integrity,mitochondrial dynamics,and UPR^(ER),offering exciting new insights into the potential therapeutic strategy for heart failure.

关键词： offering programming insight

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Endothelin-1 induces intracellular [Ca^(2+)] increase via Ca^(2+) influx through the L-type Ca^(2+) channel, Ca^(2+)-induced Ca^(2+) release and a pathway involving ET_A receptors, PKC, PKA and AT1 receptors in cardiomyocytes

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Science China(Life Sciences) 2009年第4期52卷 360-370页

作者： ZENG QingHua1, LI XingTing1, ZHONG GuoGan2, ZHANG WenJie2 & SUN ChengWen3 1 Laboratory of molecular & cellular physiology, School of Life Sciences, Northeast Normal University, Changchun 130024, China 2 Department of physiology, School of Basic Medical Sciences, Jilin University, Changchun 130021, China 3 Department of Pharmaceutical Sciences, North Dakota State University, Fargo, NorthDakota, USA Laboratory of molecular & cellular physiology School of Life Sciences Northeast Normal University Changchun China Department of physiology School of Basic Medical Sciences Jilin University Changchun China Department of Pharmaceutical Sciences North Dakota State University Fargo USA

Using fura-2-acetoxymethyl ester (AM) fluorescence imaging and patch clamp techniques, we found that endothelin-1 (ET-1) significantly elevated the intracellular calcium level ([Ca2+]i) in a dose-dependent manner and activated the L-type Ca2+ channel in cardiomyocytes isolated from rats. The effect of ET-1 on [Ca2+]i elevation was abolished in the presence of the ETA receptor blocker BQ123, but was not affected by the ETB receptor blocker BQ788. ET-1-induced an increase in [Ca2+]i, which was inhibited 46.7% by pretreatment with a high concentration of ryanodine (10 μmol/L), a blocker of the ryanodine receptor. The ET-1-induced [Ca2+]i increase was also inhibited by the inhibitors of protein kinase A (PKA), protein kinase C (PKC) and angiotensin type 1 receptor (AT1 receptor). We found that ET-1 induced an enhancement of the amplitude of the whole cell L-type Ca2+ channel current and an increase of open-state probability (NPo) of an L-type single Ca2+ channel. BQ123 completely blocked the ET-1-induced increase in calcium channel open-state probability. In this study we demonstrated that ET-1 regulates calcium overload through a series of mechanisms that include L-type Ca2+ channel activation and Ca2+-induced Ca2+ release (CICR). ETA receptors, PKC, PKA and AT1 receptors may also contribute to this pathway.

关键词： endothelin-1(ET-1) cardiomyocytes intracellular calcium concentration ([Ca2+]i) L-type Ca2+ channel current (ICaL) Ca2+-induced Ca2+ release (CICR) ETA receptors PKC PKA AT1 receptors

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Pathology-induced NG2 proteoglycan expression in microglia

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Neural Regeneration Research 2023年第4期18卷 801-802页

作者： Erika Meyer Anja Scheller molecular physiology Center for Integrative Physiology and Molecular MedicineUniversity of SaarlandHomburgGermany(Meyer EScheller A)Laboratory of Brain Ischemia and NeuroprotectionDepartment of Pharmacology and TherapeuticsState University of MaringáMaringáBrazil

Oligodendrocyte precursor cells(OPCs)and microglia are two very fascinating cell types with a multitude of important but different *** a first glance,they appear not to share many cellular properties,nor are directly related to one another or derived from a common *** all differences,emerging data show that both cell types express the protein nerve/glial antigen 2(NG2)after pathological insults(Figure 1).For years,it remained controversial whether microglia really could express NG2 upon injury,with contradictory results reported among different disease *** this question,we could recently show by using triple transgenic knock-in mice and either an acute injury model(stab wound injury)or the middle cerebral artery occlusion combined with immunohistochemistry that a subset of microglia activates the cspg4 gene in a disease dependent manner leading to a bonafide microglia-specific NG2 protein expression besides OPCs and *** data show that the cspg4 gene not only gets transcribed in microglia based on reporter expression after recombination,but also the protein itself is expressed(Huang et al.,2020).

关键词： NG2 wound Figure

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Hibernation with rhythmicity:the circadian clock and hormonal adaptations of the hibernating Asiatic toads(Bufo gargarizans)

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Integrative Zoology 2022年第4期17卷 656-669页

作者： Zhigang XIE Ibrahim M.AHMAD Lirong ZUO Feng XIAO Yongpeng WANG Dongming LI Zhejiang Academy of Agricultural Sciences HangzhouChina College of Chemistry and Life Science Zhejiang Normal UniversityJinhuaChina Ministry of Education Key Laboratory of molecular and cellular Biology Key Laboratory of Animal PhysiologyBiochemistry and Molecular Biology of Hebei ProvinceCollege of Life SciencesHebei Normal UniversityShijiazhuangChina

Hibernation is one of the fundamental strategies in response to cold environmental *** hibernation,the endocrine and circadian systems ensure minimal expenditure of energy for *** circadian rhythms of key hormones,melatonin(MT),corticosterone(CORT),triiodothyronine(T3),and thyroxine(T4),and the underlying molecular regulatory mechanisms of hibernation have been well determined in mammals but not in ***,a terrestrial hibernating species,Asiatic toad(Bufo gargarizans),was employed to investigate the plasma CORT,MT,T3,and T4;and the retina,brain,and liver mRNA expression of the core clock genes,including circadian locomotor output cycles kaput(Clock),brain and muscle ARNT-like 1(Bmal1),cryptochrome(Cry)1 and 2,and period(Per)1 and 2,at 7-time points over a 24-h period under acute cold(1 day at 4℃),and hibernation(45 days at 4℃).Our results showed that the circadian rhythms of the core clock genes were rather unaffected by acute cold exposure in the retina,unlike the brain and *** contrast,during hibernation,the liver clock genes displayed significant circadian oscillations,while those in the retina and brain stopped ***,plasma CORT expressed circadian oscillations in both groups,and T3 in acute cold exposure group,whereas T4 and MT did *** results reveal that the plasma CORT and the liver sustain rhythmicity when the brain was not,indicating that the liver clock along with the adrenal clock synergistically maintains the metabolic requirements to ensure basic survival in hibernating Asiatic toads.

关键词： Asiatic toad circadian rhythm clock genes cold exposure hibernation metabolic hormones

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Non-celiac gluten sensitivity: All wheat attack is not celiac

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World Journal of Gastroenterology 2017年第40期23卷 7201-7210页

作者： Samuel O Igbinedion Junaid Ansari Anush Vasikaran Felicity N Gavins Paul Jordan Moheb Boktor Jonathan S Alexander Department of Internal Medicine Louisiana State University Health Sciences Center Department of molecular and cellular physiology Louisiana State University School of Medicine Department of Gastroenterology and Hepatology Louisiana State University Health Sciences Center

Currently,1% of the United States population holds a diagnosis for celiac disease(CD),however,a more recently recognized and possibly related condition,"non-celiac gluten sensitivity"(NCGS)has been suggested to affect up to 6%of the United States *** reliable clinical tests for CD exist,diagnosing individuals affected by NCGS is still complicated by the lack of reliable biomarkers and reliance upon a broad set of intestinal and extra intestinal symptoms possibly provoked by *** has been proposed to exhibit an innate immune response activated by gluten and several other wheat *** present,an enormous food industry has developed to supply gluten-free products(GFP)with GFP sales in 2014 approaching$1 billion,with estimations projecting sales to reach$2 billion in the year *** enormous demand for GFP also reflects a popular misconception among consumers that gluten avoidance is part of a healthy lifestyle *** of NCGS and other gluten related disorders(e.g.,irritable bowel syndrome)call for a review of current distinctive diagnostic criteria that distinguish each,and identification of biomarkers selective or specific for *** aim of this paper is to review our current understanding of NCGS,highlighting the remaining challenges and questions which may improve its diagnosis and treatment.

关键词： Non-celiac gluten sensitivity Celiac disease Gluten Wheat Gluten related disorder Gluten free diet

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Collagen type Ⅲ is an important linking molecule between generated renal tubules and an artificial polyester interstitium--Reticulin as a linker between generated tubules and the interstitium

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中国组织工程研究与临床康复 2008年第32期12卷 6201-6208页

作者： W.W. Minuth L. Denk A. Blattmann Ho Castrop Department of molecular and cellular Anatomy University of RegensburgUniversity Strect 31D-93053 RegensburgGermany Department of physiology University of RegensburgUniversity Strect 31D-93053 RegensburgGermany

在再生医学领域,已经有很多人考虑在将来用干/祖细胞治疗急慢性肾功能衰竭。但是,要使这种治疗方案行之有效,需要了解关于患病肾脏肾小管发育的细胞生物学信息。与干/祖细胞治疗急慢性肾功能衰竭相关尚待明晰的细胞生物学问题包括:①干... 详细信息

在再生医学领域,已经有很多人考虑在将来用干/祖细胞治疗急慢性肾功能衰竭。但是,要使这种治疗方案行之有效,需要了解关于患病肾脏肾小管发育的细胞生物学信息。与干/祖细胞治疗急慢性肾功能衰竭相关尚待明晰的细胞生物学问题包括:①干/祖细胞的整合。②干/祖细胞的定向分化类型。③新形成肾小管的空间构成。为了更好的了解这项技术的相关机制,文章应用了先进的培养技术在人工非细胞外基质材料界面条件下构建肾小管。将新生兔肾来源的干/祖细胞用多层聚酯纤维网覆盖,放置在灌注培养器中,用含1×10-7mol/L醛固酮的新鲜合成的在DMEM基础上改良的IMDM培养基诱导培养13d。扫描电镜下,在大豆凝集素、银染和抗Ⅲ型胶原或层粘连蛋白γ1单克隆抗体标记的全标本包埋爬片或冰冻切片上观察肾小管的生长情况。扫描电镜观察结果显示,新生成的肾小管完全被基底膜覆盖,纤维网状板有大量的纤维与生成的肾小管基底面和周围人工聚酯材料相互交联。抗Ⅲ型胶原染色和银染结果表明,在新生成的肾小管的基底膜和邻近的人工聚酯材料间有大量的纤维交织,在发育成熟的肾小管中有与新生成肾小管相同排列形式的Ⅲ型胶原纤维。以上实验结果说明,Ⅲ胶原是联系新生成的肾小管基底面和人工基质聚酯纤维的分子纽带。

关键词：组织工程学灌注培养干/祖细胞肾小管人工间质基底膜 Ⅲ型胶原聚酯

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