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1.
Nat Commun ; 10(1): 5544, 2019 12 05.
Artigo em Inglês | MEDLINE | ID: mdl-31804496

RESUMO

Defects can induce drastic changes of the electronic properties of two-dimensional transition metal dichalcogenides and influence their applications. It is still a great challenge to characterize small defects and correlate their structures with properties. Here, we show that tip-enhanced Raman spectroscopy (TERS) can obtain distinctly different Raman features of edge defects in atomically thin MoS2, which allows us to probe their unique electronic properties and identify defect types (e.g., armchair and zigzag edges) in ambient. We observed an edge-induced Raman peak (396 cm-1) activated by the double resonance Raman scattering (DRRS) process and revealed electron-phonon interaction in edges. We further visualize the edge-induced band bending region by using this DRRS peak and electronic transition region using the electron density-sensitive Raman peak at 406 cm-1. The power of TERS demonstrated in MoS2 can also be extended to other 2D materials, which may guide the defect engineering for desired properties.

2.
J Mol Cell Cardiol ; 121: 242-255, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-30053525

RESUMO

In hypertrophic hearts, autophagic flux insufficiency is recognized as a key pathology leading to maladaptive cardiac remodeling and heart failure. This study aimed to illuminate the cardioprotective role and mechanisms of a new myokine and adipokine, irisin, in cardiac hypertrophy and remodeling. Adult male wild-type, mouse-FNDC5 (irisin-precursor)-knockout and FNDC5 transgenic mice received 4 weeks of transverse aortic constriction (TAC) alone or combined with intraperitoneal injection of chloroquine diphosphate (CQ). Endogenous FNDC5 ablation aggravated and exogenous FNDC5 overexpression attenuated the TAC-induced hypertrophic damage in the heart, which was comparable to the protection of irisin against cardiomyocyte hypertrophy induced by angiotensin II (Ang II) or phenylephrine (PE). Accumulated autophagosome and impaired autophagy flux occurred in the TAC-treated myocardium and Ang II- or PE-insulted cardiomyocytes. Irisin deficiency caused reduced autophagy and aggravated autophagy flux failure, whereas irisin overexpression or supplementation induced protective autophagy and improved autophagy flux, which were reversed by autophagy inhibitors Atg5 siRNA, 3-MA and CQ. Irisin boosted the activity of only AMPK but not Akt and MAPK family members in hypertrophic hearts and cultured cardiomyocytes and further activated ULK1 at Ser555 but not Ser757 and did not affect the mTOR-S6K axis. Blockage of AMPK and ULK1 with compund C and SBI-0206965, respectively, both abrogated irisin's protection against cardiomyocyte hypertrophic injury and reversed its induction of both autophagy and autophagy flux. Our results suggest that irisin protects against pressure overload-induced cardiac hypertrophy by inducing protective autophagy and autophagy flux via activating AMPK-ULK1 signaling.


Assuntos
Proteínas Quinases Ativadas por AMP/genética , Proteína Homóloga à Proteína-1 Relacionada à Autofagia/genética , Cardiomegalia/genética , Fibronectinas/genética , Insuficiência Cardíaca/genética , Proteínas Quinases Ativadas por AMP/antagonistas & inibidores , Angiotensina II/administração & dosagem , Animais , Autofagia/genética , Proteína Homóloga à Proteína-1 Relacionada à Autofagia/antagonistas & inibidores , Benzamidas/administração & dosagem , Cardiomegalia/tratamento farmacológico , Cardiomegalia/patologia , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/patologia , Humanos , Camundongos , Camundongos Transgênicos , Miócitos Cardíacos/efeitos dos fármacos , Fenilefrina/administração & dosagem , Pressão , Pirimidinas/administração & dosagem , Transdução de Sinais , Serina-Treonina Quinases TOR/genética
3.
Nanoscale ; 10(9): 4398-4405, 2018 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-29451566

RESUMO

Tip-enhanced Raman spectroscopy (TERS), known as nanospectroscopy, has received increasing interest as it can provide nanometer spatial resolution and chemical fingerprint information of samples simultaneously. Since Ag tips are well accepted to show a higher TERS enhancement than that of gold tips, there is an urgent quest for Ag TERS tips with a high enhancement, long lifetime, and high reproducibility, especially for atomic force microscopy (AFM)-based TERS. Herein, we developed an electrodeposition method to fabricate Ag-coated AFM TERS tips in a highly controllable and reproducible way. We investigated the influence of the electrodeposition potential and time on the morphology and radius of the tip. The radii of Ag-coated AFM tips can be rationally controlled at a few to hundreds nanometers, which allows us to systematically study the dependence of the TERS enhancement on the tip radius. The Ag-coated AFM tips show the highest TERS enhancement under 632.8 nm laser excitation and a broad localized surface plasmon resonance (LSPR) response when coupled to a Au substrate. The tips exhibit a lifetime of 13 days, which is particularly important for applications that need a long measuring time.

4.
Acta Histochem ; 119(3): 244-251, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28233574

RESUMO

Combined pulmonary fibrosis and emphysema (CPFE) is an "umbrella term" encompassing emphysema and pulmonary fibrosis, but its pathogenesis is not known. We established two models of CPFE in mice using tracheal instillation with bleomycin (BLM) or murine gammaherpesvirus 68 (MHV-68). Experimental mice were divided randomly into four groups: A (normal control, n=6), B (emphysema, n=6), C (emphysema+MHV-68, n=24), D (emphysema+BLM, n=6). Group C was subdivided into four groups: C1 (sacrificed on day 367, 7 days after tracheal instillation of MHV-68); C2 (day 374; 14days); C3 (day 381; 21days); C4 (day 388; 28days). Conspicuous emphysema and interstitial fibrosis were observed in BLM and MHV-68 CPFE mouse models. However, BLM induced diffuse pulmonary interstitial fibrosis with severely diffuse pulmonary inflammation; MHV-68 induced relatively modest inflammation and fibrosis, and the inflammation and fibrosis were not diffuse, but instead around bronchioles. Inflammation and fibrosis were detectable in the day-7 subgroup and reached a peak in the day-28 subgroup in the emphysema + MHV-68 group. Levels of macrophage chemoattractant protein-1, macrophage inflammatory protein-1α, interleukin-13, and transforming growth factor-ß1 in bronchoalveolar lavage fluid were increased significantly in both models. Percentage of apoptotic type-2 lung epithelial cells was significantly higher; however, all four types of cytokine and number of macrophages were significantly lower in the emphysema+MHV-68 group compared with the emphysema +BLM group. The different changes in pathology between BLM and MHV-68 mice models demonstrated different pathology subtypes of CPFE: macrophage infiltration and apoptosis of type-II lung epithelial cells increased with increasing pathology score for pulmonary fibrosis.


Assuntos
Enfisema/patologia , Fibrose Pulmonar/patologia , Animais , Apoptose , Modelos Animais de Doenças , Ensaio de Imunoadsorção Enzimática , Imunofluorescência , Inflamação , Pulmão/patologia , Camundongos , Reação em Cadeia da Polimerase em Tempo Real
5.
Basic Res Cardiol ; 111(2): 13, 2016 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-26786260

RESUMO

SIRT6, a member of the NAD(+)-dependent class III deacetylase sirtuin family, has been revealed to play important roles in promoting cellular resistance against oxidative stress. The formation of reactive oxygen species (ROS) and oxidative stress are the crucial mechanisms underlying cellular damage and dysfunction in cardiac ischemia/reperfusion (I/R) injury, but the role of SIRT6 in I/R-induced ROS and oxidative stress is poorly understood. In this study, by using heterozygous SIRT6 knockout (SIRT6(+/-)) mice and cultured neonatal cardiomyocyte models, we investigated how SIRT6 mediates oxidative stress and myocardial injury during I/R. Partial knockout (KO) of SIRT6 aggravated myocardial damage, ventricular remodeling, and oxidative stress in mice subjected to myocardial I/R, whereas restoration of SIRT6 expression by direct cardiac injection of adenoviral constructs encoding SIRT6 reversed these deleterious effects of SIRT6 KO in the ischemic heart. In addition, partial deletion of the SIRT6 gene decreased myocardial functional recovery following I/R in a Langendorff perfusion model. Similarly, the protective effects of SIRT6 were also observed in cultured cardiomyocytes following hypoxia/reoxygenation. Intriguingly, SIRT6 was noticed to up-regulate AMP/ATP and then activate the adenosine 5'-monophosphate-activated protein kinase (AMPK)-forkhead box O3α (FoxO3α) axis and further initiated the downstream antioxidant-encoding gene expression (manganese superoxide dismutase and catalase), thereby decreasing cellular levels of oxidative stress and mediating cardioprotection in the ischemic heart. These results suggest that SIRT6 protects the heart from I/R injury through FoxO3α activation in the ischemic heart in an AMP/ATP-induced AMPK-dependent way, thus upregulating antioxidants and suppressing oxidative stress.


Assuntos
Fatores de Transcrição Forkhead/metabolismo , Traumatismo por Reperfusão Miocárdica/metabolismo , Sirtuínas/metabolismo , Proteínas Quinases Ativadas por AMP/metabolismo , Monofosfato de Adenosina/metabolismo , Trifosfato de Adenosina/metabolismo , Animais , Animais Recém-Nascidos , Antioxidantes/metabolismo , Apoptose , Catalase/metabolismo , Células Cultivadas , Regulação para Baixo , Proteína Forkhead Box O3 , Técnicas In Vitro , Masculino , Camundongos , Miócitos Cardíacos/metabolismo , Estresse Oxidativo , Ratos Sprague-Dawley , Espécies Reativas de Oxigênio/metabolismo , Sirtuínas/genética , Superóxido Dismutase/metabolismo , Remodelação Ventricular
6.
Biomed Pharmacother ; 69: 82-9, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-25661342

RESUMO

Deacetyl-mycoepoxydiene (DM), a novel secondary metabolite produced by the plant endophytic fungi Phomosis sp., induced the reorganization of cytoskeleton in actively growing MCF-7 cells by promoting polymerization of tubulin. DM could induce cell cycle arrest at G2/M in MCF-7 cells. Additionally, DM-induced apoptosis was characterized with up-regulating caspase-3, Bax, caspase-9, parp, and p21 while down-regulating Bcl-2 activation. DM conferred dose- and time-dependent inhibitory effects upon cell proliferation of MCF-7 cells both in cultured cells and nude mice with human breast carcinoma xenografts. The results obtained from these in vitro and in vivo models provide new data revealing the potential for DM as a novel microtubule inhibitor.


Assuntos
Compostos Bicíclicos Heterocíclicos com Pontes/isolamento & purificação , Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia , Hidrocarbonetos Aromáticos com Pontes/isolamento & purificação , Hidrocarbonetos Aromáticos com Pontes/farmacologia , Endófitos/química , Fungos/química , Microtúbulos/efeitos dos fármacos , Pironas/isolamento & purificação , Pironas/farmacologia , Animais , Compostos Bicíclicos Heterocíclicos com Pontes/química , Hidrocarbonetos Aromáticos com Pontes/química , Pontos de Checagem do Ciclo Celular/efeitos dos fármacos , Morte Celular/efeitos dos fármacos , Divisão Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Relação Dose-Resposta a Droga , Feminino , Fase G2/efeitos dos fármacos , Humanos , Células MCF-7 , Camundongos Endogâmicos BALB C , Camundongos Nus , Microtúbulos/metabolismo , Polimerização , Pironas/química , Ensaios Antitumorais Modelo de Xenoenxerto
7.
J Huazhong Univ Sci Technolog Med Sci ; 34(3): 337-342, 2014 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-24939295

RESUMO

Alveolar epithelial type II (AT II) cells are essential for lung development and remodeling, as they are precursors for type I cells and also produce other non-repair cells (fibroblasts). Progenitor cells are believed to possess capability of multi-potent transdifferentiation, which is closely related to the niche, suggesting the importance of establishment of a lung progenitor cell niche model. We hypothesized that pulmonary surfactant-associated protein A (SPA) suicide gene system would cause AT II cell to kill itself through apoptosis and leave its niche. In vitro, the recombinant adeno-associated virus vectors-SPA-thymidine kinase (rAAV-SPA-TK) system was established to get targeted apoptotic AT II cells. The apoptosis of AT II cells was detected by using MTT. The results showed that cloned SPA gene promoter had specific transcriptional activity in SPA high expression cells, and SPA high expression cells (H441) transfected with TK gene had higher sensitivity to ganciclovir (GCV) than SPA low expression cells (A549). In vivo, increased apoptosis of AT II cells induced by GCV in rAAV-SPA-TK system was observed by TUNEL. Finally, the successful packaging and application of rAAV-SPA-TK system provide experimental basis to get specific lung progenitor cell (AT II) niche in vitro and in vivo.


Assuntos
Células Epiteliais/metabolismo , Genes Transgênicos Suicidas/genética , Proteína A Associada a Surfactante Pulmonar/genética , Timidina Quinase/genética , Antivirais/farmacologia , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Dependovirus/genética , Relação Dose-Resposta a Droga , Eletroforese em Gel de Poliacrilamida , Células Epiteliais/citologia , Células Epiteliais/efeitos dos fármacos , Ganciclovir/farmacologia , Regulação Neoplásica da Expressão Gênica , Vetores Genéticos/genética , Humanos , Marcação In Situ das Extremidades Cortadas , Luciferases/genética , Luciferases/metabolismo , Regiões Promotoras Genéticas/genética , Alvéolos Pulmonares/citologia , Alvéolos Pulmonares/metabolismo , Proteína A Associada a Surfactante Pulmonar/metabolismo , Timidina Quinase/metabolismo
8.
Respir Res ; 15: 33, 2014 Mar 25.
Artigo em Inglês | MEDLINE | ID: mdl-24661402

RESUMO

BACKGROUND: Stem cell transplantation is a promising method for the treatment of chronic obstructive pulmonary disease (COPD), and mesenchymal stem cells (MSCs) have clinical potential for lung repair/regeneration. However, the rates of engraftment and differentiation are generally low following MSC therapy for lung injury. In previous studies, we constructed a pulmonary surfactant-associated protein A (SPA) suicide gene system, rAAV-SPA-TK, which induced apoptosis in alveolar epithelial type II (AT II) cells and vacated the AT II cell niche. We hypothesized that this system would increase the rates of MSC engraftment and repair in COPD rats. METHODS: The MSC engraftment rate and morphometric changes in lung tissue in vivo were investigated by in situ hybridization, hematoxylin and eosin staining, Masson's trichrome staining, immunohistochemistry, and real-time PCR. The expression of hypoxia inducible factor (HIF-1α) and stromal cell-derived factor-1 (SDF-1), and relationship between HIF-1α and SDF-1 in a hypoxic cell model were analyzed by real-time PCR, western blotting, and enzyme-linked immunosorbent assay. RESULTS: rAAV-SPA-TK transfection increased the recruitment of MSCs but induced pulmonary fibrosis in COPD rats. HIF-1α and SDF-1 expression were enhanced after rAAV-SPA-TK transfection. Hypoxia increased the expression of HIF-1α and SDF-1 in the hypoxic cell model, and SDF-1 expression was augmented by HIF-1α under hypoxic conditions. CONCLUSIONS: Vacant AT II cell niches increase the homing and recruitment of MSCs to the lung in COPD rats. MSCs play an important role in lung repair and promote collagen fiber deposition after induction of secondary damage in AT II cells by rAAV-SPA-TK, which involves HIF-1α and SDF-1 signaling.


Assuntos
Quimiocina CXCL12/biossíntese , Subunidade alfa do Fator 1 Induzível por Hipóxia/biossíntese , Transplante de Células-Tronco Mesenquimais/métodos , Células-Tronco Mesenquimais/metabolismo , Doença Pulmonar Obstrutiva Crônica/metabolismo , Doença Pulmonar Obstrutiva Crônica/cirurgia , Animais , Apoptose/fisiologia , Hipóxia Celular/fisiologia , Feminino , Masculino , Doença Pulmonar Obstrutiva Crônica/patologia , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley
10.
Chin Med J (Engl) ; 126(17): 3283-8, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24033950

RESUMO

BACKGROUND: Expression of murine calcium-activated chloride channel family member 3 (mCLCA3) has been reported to be increased in the airway epithelium of asthmatic mice challenged with ovalbumin (OVA). However, its role in asthmatic airway inflammation under no OVA exposure has not yet been clarified. METHODS: mCLCA3 plasmids were transfected into the airways of normal BALB/c mice. mCLCA3 expression and airway inflammation in mouse lung tissue were evaluated. Cell differentials and cytokines in bronchoalveolar lavage fluid (BALF) were analyzed. The expression of mCLCA3 protein and mucus protein mucin-5 subtype AC (MUC5AC) were analyzed by Western blotting. The mRNA levels of mCLCA3, MUC5AC and interleukin-13 (IL-13) were determined quantitatively. RESULTS: mCLCA3 expression was not detected in the control group while strong immunoreactivity was detected in the OVA and mCLCA3 plasmid groups, and was strictly localized to the airway epithelium. The numbers of inflammatory cells in lung tissue and BALF were increased in both mCLCA3 plasmid and OVA groups. The protein and mRNA levels of mCLCA3 and MUC5AC in the lung tissue were significantly increased in the mCLCA3 plasmid and OVA groups compared to the control group. The level of IL-13, but not IL-4, IL-5, IFN-γ, CCL2, CCL5 or CCL11, was significantly increased compared with control group in BALF in the mCLCA3 plasmid and OVA groups. The level of IL-13 in the BALF in the mCLCA3 plasmid group was much higher than that in the OVA group (P < 0.05). The level of mCLCA3 mRNA in lung tissue was positively correlated with the levels of MUC5AC mRNA in lung tissue, IL-13 mRNA in lung tissue, the number of eosinophils in BALF, and the content of IL-13 protein in BALF. The level of IL-13 mRNA in lung tissue was positively correlated with the number of eosinophils in BALF and the level of MUC5AC mRNA in lung tissue. CONCLUSION: These findings suggest that increased expression of a single-gene, mCLCA3, could simulate an asthma attack, and its mechanism may involve mCLCA3 overexpression up-regulating IL-13 expression.


Assuntos
Inflamação/metabolismo , Mucina-5AC/metabolismo , Alérgenos , Animais , Asma , Canais de Cloreto , Feminino , Inflamação/induzido quimicamente , Interleucina-13/metabolismo , Interleucina-4/genética , Interleucina-4/metabolismo , Interleucina-5/genética , Interleucina-5/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Mucina-5AC/genética , Ovalbumina/farmacologia
11.
PLoS One ; 7(6): e39770, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22761896

RESUMO

BACKGROUND: Precise coordination of the hypothalamic-pituitary-gonadal axis orchestrates the normal reproductive function. As a central regulator, the appropriate synthesis and secretion of gonadotropin-releasing hormone I (GnRH-I) from the hypothalamus is essential for the coordination. Recently, emerging evidence indicates that histone deacetylases (HDACs) play an important role in maintaining normal reproductive function. In this study, we identify the potential effects of HDACs on Gnrh1 gene transcription. METHODOLOGY/PRINCIPAL FINDINGS: Inhibition of HDACs activities by trichostatin A (TSA) and valproic acid (VPA) promptly and dramatically repressed transcription of Gnrh1 gene in the mouse immortalized mature GnRH neuronal cells GT1-7. The suppression was connected with a specific region of Gnrh1 gene promoter, which contains two consensus Otx2 binding sites. Otx2 has been known to activate the basal and also enhancer-driven transcription of Gnrh1 gene. The transcriptional activity of Otx2 is negatively modulated by Grg4, a member of the Groucho-related-gene (Grg) family. In the present study, the expression of Otx2 was downregulated by TSA and VPA in GT1-7 cells, accompanied with the opposite changes of Grg4 expression. Chromatin immunoprecipitation and electrophoretic mobility shift assays demonstrated that the DNA-binding activity of Otx2 to Gnrh1 gene was suppressed by TSA and VPA. Overexpression of Otx2 partly abolished the TSA- and VPA-induced downregulation of Gnrh1 gene expression. CONCLUSIONS/SIGNIFICANCE: Our data indicate that HDAC inhibitors downregulate Gnrh1 gene expression via repressing Otx2-driven transcriptional activity. This study should provide an insight for our understanding on the effects of HDACs in the reproductive system and suggests that HDACs could be potential novel targets for the therapy of GnRH-related diseases.


Assuntos
Regulação da Expressão Gênica/fisiologia , Hormônio Liberador de Gonadotropina/genética , Histona Desacetilases/metabolismo , Fatores de Transcrição Otx/fisiologia , Animais , Western Blotting , Linhagem Celular , Imunoprecipitação da Cromatina , Ensaio de Desvio de Mobilidade Eletroforética , Ensaio de Imunoadsorção Enzimática , Histona Desacetilases/fisiologia , Ácidos Hidroxâmicos/farmacologia , Camundongos , Regiões Promotoras Genéticas , Transcrição Genética/fisiologia , Ácido Valproico/farmacologia
12.
DNA Cell Biol ; 30(10): 809-19, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21563965

RESUMO

Oxidative stress induces serious tissue injury in cardiovascular diseases. Salidroside, with its strong antioxidative and cytoprotective actions, is of particular interest in the development of antioxidative therapies for oxidative injury in cardiac diseases. We examined the pharmacological effects of salidroside on H9c2 rat cardiomyoblast cells under conditions of oxidative stress induced by hydrogen peroxide (H2O2) challenge. Salidroside attenuated H2O2-impaired cell viability in a concentration-dependent manner, and effectively inhibited cellular malondialdehyde production, lethal sarcolemmal disruption, cell necrosis, and apoptosis induced by H2O2 insult. Salidroside significantly augmented Akt phosphorylation at Serine 473 in the absence or presence of H2O2 stimulation; wortmannin, a specific inhibitor of PI3K, abrogated salidroside protection. Salidroside increased the intracellular mRNA expression and activities of catalase and Mn-superoxide dismutases in a PI3K-dependent manner. Our results indicated that salidroside protected cardiomyocytes against oxidative injury through activating the PI3K/Akt pathway and increasing the expression and activities of endogenous PI3K dependent antioxidant enzymes.


Assuntos
Antioxidantes/farmacologia , Citoproteção , Glucosídeos/farmacologia , Miócitos Cardíacos , Estresse Oxidativo/efeitos dos fármacos , Fenóis/farmacologia , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Androstadienos/farmacologia , Animais , Apoptose/efeitos dos fármacos , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Citometria de Fluxo , Expressão Gênica , Peróxido de Hidrogênio/efeitos adversos , Peróxido de Hidrogênio/farmacologia , Peroxidação de Lipídeos/efeitos dos fármacos , Malondialdeído/análise , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/enzimologia , Fosfatidilinositol 3-Quinases/genética , Fosforilação , Reação em Cadeia da Polimerase , Proteínas Proto-Oncogênicas c-akt/genética , Ratos , Transdução de Sinais/efeitos dos fármacos , Wortmanina
13.
Peptides ; 30(10): 1816-21, 2009 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-19619601

RESUMO

Peptide aptamers are molecules which can specifically bind to a given target protein and have the potential to selectively block the function of the target protein. It has been reported that a peptide aptamer (C1-1) identified from a randomized expression library specifically bound to the core protein of hepatitis B virus and inhibited viral capsid formation and DNA replication in vitro. Adenoviral systems are popular platforms for reliable gene delivery and high-level transient expression in any mammalian cell type in vitro, and have a natural tropism for the liver after systemic administration. In the present study, we explored the feasibility of gene therapy against HBV infection with adenoviral system, and found that systematic administration of recombinant adenovirus encoding the peptide aptamer (C1-1) significantly inhibited viral capsid formation, HBV DNA replication and virion production in vivo. These results suggest an efficient antiviral treatment against HBV infection by delivery of anti-HBV peptide aptamer with recombinant adenovirus.


Assuntos
Adenoviridae/genética , Aptâmeros de Peptídeos , Replicação do DNA , DNA Viral/metabolismo , Vírus da Hepatite B/fisiologia , Proteínas do Core Viral/metabolismo , Adenoviridae/metabolismo , Animais , Aptâmeros de Peptídeos/genética , Aptâmeros de Peptídeos/metabolismo , Linhagem Celular , DNA Viral/genética , Terapia Genética/métodos , Vetores Genéticos , Vírus da Hepatite B/genética , Humanos , Camundongos , Camundongos Transgênicos , Proteínas do Core Viral/genética
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