[보고서]스마트에이징 융복합연구센터

김재룡

보고서 정보

주관연구기관

영남대학교
YeungNam University

연구책임자

김재룡

참여연구자

박범찬 , 최용훈 , 배영경 , 최형철 , 우창훈 , 조두형 , 박소영 , 정대원 , 김종오 , 정지헌 , 장성호 , 도준영 , 김일국

보고서유형

최종보고서

발행국가

대한민국

언어

한국어

발행년월

2020-02

과제시작연도

2019

주관부처

과학기술정보통신부
Ministry of Science and ICT

등록번호

TRKO202300013183

과제고유번호

1711091413

사업명

집단연구지원(R&D)

DB 구축일자

2023-10-25

키워드

노화.노화질환.노화극복.산화스트레스.세노테라퓨틱스.약물전달체.스마트에이징.Aging.Age-related disease.Aging intervention.CD9.Oxidative stress.Senotherapeutics.Drug delivery.Smart aging.

표 CD9 induces cellular senescence and aggravates atherosclerosis in mice. A. CD9 knockdown in senescent cells rescues cellular senescence. B. CD9 overexpression accelerates cellular senescence in young cells. C. Signal pathway of cellular senescence by CD9. D. Cd9 ablation ameliorates atherosclerosis in ApoE-/- mice. E. and F. Cd9 blocking antibody mitigates atherosclerosis in ApoE-/- mice
표 Distribution of CD9-HMSN@Cy5.5 in the atherosclerotic lesions of ApoE-/- . (A) Distribution of IgG-HMSN@Cy5.5 and CD9-HMSN@Cy5.5 in the organs of ApoE-/- . (B) Quantitative analysis of fluorescence distribution. (C) Immunofluorescence staining of CD9-HMSN@Cy5.5 and IgG-HMSN@Cy5.5 with PECAM in frozen tissue sections of atherosclerotic lesions. (D) Immunofluorescence staining of CD9-HMSN@Cy5.5 and IgG-HMSN@Cy5.5 with F4/80 in frozen tissue sections of atherosclerotic lesions
표 In vivo therapeutic efficacy of CD9-HMSN@RSV on alleviating the progression of atherosclerotic senescent plaques in ApoE-/- mice. (A) Experimental scheme. (B) Measurement of body weight. (C) Evaluation of total cholesterol levels. (D) Images of isolated aortas stained with SA-β-gal staining. (E) Quantitative analysis of areas with SA-β-gal staining. (F) Images of isolated aortas stained with Oil red O. (G) Quantitative analysis of areas with Oil red O staining. (H) Immunofluorescence staining of CD9 with SPiDER-βGal in endothelial cells of atheroslcerotic lesions, (I) Immunofluorescence staining of CD9 with SPiDER-βGal in macrophages of atherosclerotic lesions
표 Protein typing of human-plasma-driven EVs extracted from prostate-cancer patients and healthy donors. (A) Heat map for CD81, CD63, CD9, and cancer markers. (B) Eight markers validated for 43 prostate-cancer patients and 30 healthy donors using direct ELISA. (C) ROC curves obtained for eight markers. (D) AUCs calculated for eight markers. (E) HSP90 expression in patient-plasma-driven EV (red) and healthy-donor-plasma-drive n EV (black) demonstrated as waterfall plot. Cut-off (OD = 0.087) was obtained based on negative likelihood ratio
표 Effects of CD9 vaccine on atherosclerosis in ApoE-/- mice. A. Selection of CD9 peptides by antigenicity prediction. B. Antibody formation in mouse sera immunized with CD9 vaccine. C. Analysis of antibody titer. D. Effect of CD9 vaccine on atherosclerosis in ApoE-/- mice. **, p<0.01 (One way-ANOVA)
표 Senotherapeutic activity of ESC-conditioned media
표 Target exploration of senotherapeutic candidate (HHT). A. Scheme of DART method. B. Silver staining of proteins treated with pronase in HDFs. C. Validation of binding of HHT to several target proteins. D. Effects of knockdown of target proteins on senescent cell survival of HHT. E. Effects of knockdown of target proteins on apoptosis induced by HHT
표 Effects of HHT on clearance of senescent cells in p16Luc mice. A. Luminescence analysis. B. SAβG staining in lung tissues. C. Immunofluorescence analysis of p53 and p16 in lung tissues. D. Western blotting of senescence-associated proteins in lung tissues
표 Effects of HHT on bleomycin-induced lung fibrosis. A. Experimental scheme. B. Body weight change. C. Pulmonary resistance measured by phlethysmography. D. Histological analysis of lung tissues. E. SAβG staining in lung tissues. F. Immunofluorescence analysis of p53 and p16 in lung tissues. G. Western blotting of senescence-associate d proteins in lung tissues
표 DNA chip assay in bleomycin-induced lung tissues treated with or without HHT. A. Hierarchical clustering analysis. B. Gene ontology analysis. C. Expression of senescence-associated genes
표 Effects of HHT on renal fibrosis induced by ischemia-reperfusion injury. A. Experimental scheme. B. Plasma creatinine level. C. Lipofuscin staining in renal tissues. D. Histological analysis of renal tissues. E. Immunofluorescence analysis of p53 and p16 in renal tissues. F. Western blotting of senescence-associated proteins in renal tissues
표 Effects of HHT on peritoneal fiboris induced by chlorhexidine. A. Experimental scheme. B. Body weigth change. C. Histological analysis of peritonium. D. Immunofluorescen ce analysis of p53 and p16 in peritoneal tissues. E. Western blotting of senescence-asso ciated proteins in peritoneal tissues
표 Effects of Hht, Cer, and Tra on radiation-induced lung fibrosis A. Experimental scheme. B. whole lung explants. C. Histological analysis of whole lung tissues. D. Hitological analysis of lung fibrosis. E. Qunatification of inflammatory index. F. Quantification of collagen deposition. G. Realtime PCR of fibrosis-associated genes. Rap, rapamycin as a positive control
표 Effects of uPAR-LMSN/DX on senescent tumor cells. (A) Schematic illustration of uPAR-LMSN/DX. (B) Size, PDI and zeta potential of uPAR-LMSN/DX. (C) TEM images of MSN and uPAR-LMSN/DX. (D) Selective clearance of senescent cells in tumor by uPAR-LMSN/DX. (E) In vivo antitumor study in HCT116-bearing Balb/c nude mice
표 Representative immunohistochemical results for CD9 expression. A, Non-neoplastic epithelial cells of mammary glands (thick arrows) and ducts (thin arrows) are negative or weakly positive for CD9 expression. Stromal immune cells, but not all, show strong immunoreactivity for CD9. B, The tumour cells are negative for CD9 expression, but most of the stromal immune cells show strong immunoreactivity for CD9. C, In this case, CD9 is strongly expressed on tumour cells, but positive stromal immune cells are scanty. D, This case shows strong CD9 expression in both tumour cells and stromal immune cells
표 Kaplan-Meier survival curves according to CD9 expression in patients with invasive lobular carcinoma. (A) OS. (B) DFS.OS = overall survival; DFS = disease-free survival
표 Kaplan-Meier survival analysis with log-rank test of CD9 expression. (A) Survival curves of the T-CD9 (−) versus T-CD9 (+) in all cases. (B) Survival curves of the T-CD9 (−) versus T-CD9 (+) in left-sided tumors. (C) Survival curves of the T-CD9 (−) versus T-CD9 (+) in right-sided tumors. (D) Survival curves of the I-CD9 (−) versus I-CD9 (+) in all cases. (E) Survival curves of the I-CD9 (−) versus I-CD9 (+) in left-sided tumors. (F) Survival curves of the I-CD9 (−) versus I-CD9 (+) in right-sided tumors. T-CD9, CD9 expression in tumor cells; I-CD9, CD9 expression in immune cells
표 Survival analysis according to presence or absence of SASP. Breast cancer-specific survival (BCSS), and disease-free survival (DFS) for all 1,140 breast cancer patients (A-B) and patients with the luminal A subtype (C-D) or triple-negative breast cancer (E-F)
표 Distribution of intravenously injected DsRed adipose-derived stromal cells by immunofluorescent staining. A high number of DsRed adipose-derived stromal cells were recruited to grafted green fluorescent protein (GFP) fat (above, left), whereas very few DsRed adipose-derived stromal cells were observed in subcutaneous fat (above, right) at postoperative week 1. (Below) These results were similar in grafted and subcutaneous fat at postoperative week 4. Scale bars = 100 μm
표 Reduction in adipocyte size in response to MLN4924 (MLN) treatment for 4 days. (A) Representative images of adipose tissues with hematoxylin and eosin (H ###P < 0.001 vs low-MLN4924 group. Scale bars = 100 μm
표 Diagram depicting viable zone of fat grafts and the hypothesis of this study. Reducing the size of adipocytes was hypothesized to increase the number of adipocytes within the viable zone compared to control grafts. MLN4924 inhibits the expression of adipogenic proteins and genes. (Left) Protein expression of PPARγ and perilipin in mouse fat tissues was analyzed by western blotting. (Right) qPCR was performed to evaluate the expression of adipogenic genes. Gene expression levels were quantified relative to 18S rRNA
표 폴리코사놀-HDL의 조직재생 촉진
표 흡연 경력 산모의 모유에서 콜레스테롤 변화
표 Cellular uptake of (V)LDL by macrophages from mothers with small neonates
표 Schematic model of blood pressure regulation via lipoprotein
표 Regulation of vascular smooth muscle cell proliferation by gliclazide
표 The regulation of nifedipine on [Ca2+]i level and autophagic activation through AMPK. Cells were treated with H2O2 and then treated with nifedipine and/or compound C (C.C; 10 μM, 1 h). (A) Intracellular Ca2+ was stained with Fluo-4 AM. (B) Western blot analysis indicated that autophagy activity was increased by the nifedipine-induced activation of AMPK
표 Inhibitory effects of SRT1720 on inflammatory cytokine and cellular senescence via the potentiation of autophagy induced by the SIRT1-facilitated deacetylation of NF-κB in senescent HDFs. (A, B) Expression of SIRT1, Ac-NF-kB, LC3, and Beclin-1. (C) LC3 immunofluorescent staining. (D, E) Protein and mRNA levels of IL-6 and IL-8. (F) The phenotypes of HDFs were determined by indirect immunofluorescent staining with antibodies for IL-6 (green) and IL-8 (red). (G) SA-β-gal staining and expression of p53 and p21
표 Metformin increases the expression of SIRT3 and attenuates mitochondrial oxidative stress in ADR-induced senescent VSMCs. (A) VSMCs were pretreated with 500 nM ADR for 4 hr and incubated with 2 mM Met for 1 hr, and protein expression levels were analyzed by immunoblotting. (B) VSMCs were treated with ADR and Met, and SIRT3 mRNA levels were assessed by real-time PCR. (C) After treatment with ADR and Met, the phenotypes of fixated VSMCs were identified by indirect immunofluorescent staining
표 The effects of fisetin on PTEN, PKCδ, and NOX1 subunits in VSMCs. (A) The protein levels of PTEN and p-PKCδ (Tyr311). (B) H2O2-increased p22phox expression. (C) Immunoprecipitation analysis of p47phox phosphorylation at serine. (D) The levels of ROS production
표 Telmisartan-induced
표 Aphidicolin accumulates one active form of the eNOS protein, p-eNOS-Ser1179, in the nucleus, which mediates the cytoprotective effects of aphidicolin-increased NO. (A) Levels of p-eNOS-Ser1179 and eNOS protein. (B) Subcellular localization of WT-eNOS protein. (C) Using confocal microscopic data, RFP dye co-localized in the nucleus was assessed in WT-eNOS gene-transfected cells at 100× magnification. (D) Cell viability
표 FIR irradiation inhibits cell proliferation and colony formation in MDA-MB-231 breast cancer cells
표 CHOP deficiency inhibits MGO-induced aortic endothelial dysfunction and endothelial apoptosis. (A) Isomeric tension assay for vessels, (B) en face immunostaining
표 ERK5 inhibition exacerbates STZ-induced diabetes via ER stress regulation
표 Role of ER stress in statin-induced myopathy in vivo
표 Effects of a p90RSK inhibitor in high glucose-induced TXNIP regulation and β cell dysfunction. (A) Western blot, (B) TXNIP promoter, (C) ChREBP nuclear translocation
표 Apelin-13 protects aortic vessels from MGO-induced endothelial dysfunction
표 Potential candidates for ER stress-related miRNA in endothelial cells
표 Potential candidates for miR-616 based on RNA sequencing array
표 miR-616 reduces TXNIP and CHOP-dependent ER stress responses
표 miR-616 targets CXCL5 and TNFSF14, and reduces inflammatory responses
표 MsrB3 deletion prevents high-fat diet induced insulin resistance via increased mitochondrial biogenesis in mice. A. Body weight B. Whole body insulin resistance. C. Skeletal muscle insulin resistance. D. Grp78 protein levels. E. Ubiquitinated protein levels F&G. Mitochondrial complex I & III. H. Graphical abstract
표 SelW deletion does not affect high-fat diet induced insulin resistance A. SelW expression in tissues B. Body weight C. Whole body insulin resistance. D. Skeletal muscle insulin resistance
표 Prx2 deletion aggravates aging-associated insulin resistance in mice. A. Whole body insulin resistance. B. Skeletal muscle insulin resistance. Phosphorylation of Akt (C) and AS160 (D). Protein levels of 4HNE (E), nitrotyrosine (NT)(F), heme oxygenase (HO)1(G) and p53 (H)
표 Clusterin deletion aggravates high-fat diet-induced renal lipid accumulation and fibrosis A. Periodic acid-Schiff staining for the mesangial matrix area. B. trichrome staining for interstitial fibrosis. C. Collagen 4A protein levels. D. Fibronectin1 mRNA levels. E. LAMP 1 expression. F. Renal cholesterol uptake. G. Renal palmitate uptake
표 Effect of a new senotherapeutic on high-fat diet-induced obesity and insulin resistance. A. Body weight B. Fat pad weight. C. Glucose tolerance test. D. Glucose area under the curve E. p16 expression in adipose tissue in p16 luciferase knockin mice F&G. SA-β Gal staining in adipose tissue H&I. Crown-like structure in adipose tissue. J. Distribution of adipocyte size
표 The effect of senotherapeutics on insulin resistance in aged mice. A. Glucose tolerance test. B. Insulin tolerance test. C. SAβgal staining D. Cytokine expression
표 The effect of senotherapeutics on obesity and insulin resistance induced by high-fat diet. A. Body weight B. Food intake. C. Glcuose tolerance test. D. Area under the curve (AUC) for glucose E. Insulin tolerance test. F. AUC for glucose
표 Selenoprotein W ensures physiological bone remodeling by preventing hyperactivity of osteoclasts. A. Downregulation of SELENOW during osteoclastogenesis. B, C. Increased bone mass phenotypes in mice with SELENOW deficiency. μCT analysis of age/sex-matched SELENOW−/− mice (B) and osteoclast-specific SELENOW knockout mice (SELENOWtm/c/tm1c:LysM-Cre; SeWfl/fl;LysM-Cre). (C). D. Osteoporotic phenotypes in mice with SELENOW overexpression. E. RANKL-dependent repression of SELENOW blocks osteoporosis caused by overactive osteoclasts
표 Roles of Mitogen-Activated Protein Kinases in Osteoclast Biology. A. Osteoclastogenic signaling cascade controlled by upstream activators and inhibitors of extracellular signal-regulated kinase (ERK). B. Osteoclastogenic signaling cascade controlled by upstream activators and inhibitors of c-Jun N-terminal kinase (JNK). C. Osteoclastogenic signaling cascade controlled by upstream activators and inhibitors of p38 mitogen-activated protein kinases (MAPK)
표 MsrA−/− female mice exhibit increased bone mass. A. DAX analysis. B. μCT analysis. C. Analysis of osteoclasts and osteoclasts in bone tissue. D. Increased differentiation marker genes expression of osteoblasts from MsrA−/− female mice. E. Increased differntiation of osteoblasts originated from MsrA−/− female mice
표 Surface engineering of pancreatic islet surface by multilayered deposition of FK506/DOPA–NPs A. PLGA–PEG–DOPA copolymer.B. construction of FK506/DOPA–NPs. C.Particles to interact with amine groups of collagen. D&E. Form a multilayer on the islet surface
표 The inhibitory mechanisms of cellular senescence by polymeric microshere -facilitated site specific delivery
표 Inhibition of cellular senescence in transplanted islets
표 Mechanistic evaluation of the interaction between islet surface components and PD-MS. A Schematic illustration B. Immunofluoresce nce staining of islet. C. Macroscopic images of ECM. D&E. ECM coated surface
표 The inhibitory effect of rapamycin microsphere on immune activation in dendritic cells. A.CD40. B. CD80. C. CCR7
표 Synergic effect ot rapamycin microsphere and PEG islets on diabetes

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