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Sepsis is a life-threatening condition caused by dysregulated host responses to infection. Myeloid cell accumulation and lymphocyte decline are widely recognized phenomena in septic patients. However, the fate of specific immune cells remains unclear. Here, we report the results of a human explorative study of patients with septic peritonitis and patients undergoing abdominal surgery without sepsis. We analyzed pairwise peritoneal fluid and peripheral blood taken 24 h after surgery to characterize immediate immune cell changes. Our results show that myeloid cell expansion and lymphocyte loss occur in all patients undergoing open abdominal surgery, indicating that these changes are not specific to sepsis. However, B1-like lymphocytes were specifically increased in the peritoneal fluid of septic patients, correlating positively with sequential organ failure assessment (SOFA) and acute physiology and chronic health evaluation II (APACHE-II) clinical severity scores. In support of this notion, we identified an accumulation of peritoneal B1b lymphocytes in septic mice.
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Besides the physiological role of histone deacetalylases in maintaining normal cellular integrity, the acetylation landscape is changed in cancer cells, which has been implicated as a potential target in cancer therapy. The overexpression of certain HDACs correlates with specific cancer types. Therefore, the development of specific HDAC inhibitors may extend the therapeutic strategy for cancer therapy. Here, we describe how to investigate the therapeutic potential of specific HDACi by treatment in a mouse model for B-cell lymphoma, exemplified by the HDAC6 inhibitor Marbostat-100.
Assuntos
Inibidores de Histona Desacetilases , Linfoma , Camundongos , Animais , Inibidores de Histona Desacetilases/farmacologia , Inibidores de Histona Desacetilases/uso terapêutico , Histonas , Histona Desacetilases/genética , Acetilação , Linfoma/tratamento farmacológico , Modelos Animais de DoençasRESUMO
Overexpression of MYC is a genuine cancer driver in lymphomas and related to poor prognosis. However, therapeutic targeting of the transcription factor MYC remains challenging. Here, we show that inhibition of the histone deacetylase 6 (HDAC6) using the HDAC6 inhibitor Marbostat-100 (M-100) reduces oncogenic MYC levels and prevents lymphomagenesis in a mouse model of MYC-induced aggressive B-cell lymphoma. M-100 specifically alters protein-protein interactions by switching the acetylation state of HDAC6 substrates, such as tubulin. Tubulin facilitates nuclear import of MYC, and MYC-dependent B-cell lymphoma cells rely on continuous import of MYC due to its high turn-over. Acetylation of tubulin impairs this mechanism and enables proteasomal degradation of MYC. M-100 targets almost exclusively B-cell lymphoma cells with high levels of MYC whereas non-tumor cells are not affected. M-100 induces massive apoptosis in human and murine MYC-overexpressing B-cell lymphoma cells. We identified the heat-shock protein DNAJA3 as an interactor of tubulin in an acetylation-dependent manner and overexpression of DNAJA3 resulted in a pronounced degradation of MYC. We propose a mechanism by which DNAJA3 associates with hyperacetylated tubulin in the cytoplasm to control MYC turnover. Taken together, our data demonstrate a beneficial role of HDAC6 inhibition in MYC-dependent B-cell lymphoma.
Assuntos
Linfoma de Células B , Tubulina (Proteína) , Acetilação , Animais , Proteínas de Choque Térmico HSP40/metabolismo , Proteínas de Choque Térmico/metabolismo , Desacetilase 6 de Histona/metabolismo , Inibidores de Histona Desacetilases/farmacologia , Histona Desacetilases/genética , Histona Desacetilases/metabolismo , Humanos , Linfoma de Células B/tratamento farmacológico , Linfoma de Células B/genética , Camundongos , Fatores de Transcrição/metabolismo , Tubulina (Proteína)/metabolismoRESUMO
Cytotoxic stress activates stress-activated kinases, initiates adaptive mechanisms, including the unfolded protein response (UPR) and autophagy, and induces programmed cell death. Fatty acid unsaturation, controlled by stearoyl-CoA desaturase (SCD)1, prevents cytotoxic stress but the mechanisms are diffuse. Here, we show that 1,2-dioleoyl-sn-glycero-3-phospho-(1'-myo-inositol) [PI(18:1/18:1)] is a SCD1-derived signaling lipid, which inhibits p38 mitogen-activated protein kinase activation, counteracts UPR, endoplasmic reticulum-associated protein degradation, and apoptosis, regulates autophagy, and maintains cell morphology and proliferation. SCD1 expression and the cellular PI(18:1/18:1) proportion decrease during the onset of cell death, thereby repressing protein phosphatase 2 A and enhancing stress signaling. This counter-regulation applies to mechanistically diverse death-inducing conditions and is found in multiple human and mouse cell lines and tissues of Scd1-defective mice. PI(18:1/18:1) ratios reflect stress tolerance in tumorigenesis, chemoresistance, infection, high-fat diet, and immune aging. Together, PI(18:1/18:1) is a lipokine that links fatty acid unsaturation with stress responses, and its depletion evokes stress signaling.
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Transdução de Sinais , Estearoil-CoA Dessaturase , Animais , Apoptose , Ácidos Graxos , Camundongos , Estearoil-CoA Dessaturase/genética , Estearoil-CoA Dessaturase/metabolismo , Resposta a Proteínas não DobradasRESUMO
We provide a descriptive characterization of the unfolded protein response (UPR) in skeletal muscle of human patients with peritoneal sepsis and a sepsis model of C57BL/6J mice. Patients undergoing open surgery were included in a cross-sectional study and blood and skeletal muscle samples were taken. Key markers of the UPR and cluster of differentiation 68 (CD68) as surrogate of inflammatory injury were evaluated by real-time PCR and histochemical staining. CD68 mRNA increased with sepsis in skeletal muscle of patients and animals (p < 0.05). Mainly the inositol-requiring enzyme 1α branch of the UPR was upregulated as shown by elevated X-box binding-protein 1 (XBP1u) and its spliced isoform (XBP1s) mRNA (p < 0.05, respectively). Increased expression of Gadd34 indicated activation of PRKR-Like Endoplasmic Reticulum Kinase (PERK) branch of the UPR, and was only observed in mice (p < 0.001) but not human study subjects. Selected cell death signals were upregulated in human and murine muscle, demonstrated by increased bcl-2 associated X protein mRNA and TUNEL staining (p < 0.05). In conclusion we provide a first characterization of the UPR in skeletal muscle in human sepsis.
Assuntos
Estresse do Retículo Endoplasmático , Músculo Esquelético/metabolismo , Doenças Peritoneais/fisiopatologia , Sepse/fisiopatologia , Resposta a Proteínas não Dobradas , Idoso , Animais , Antígenos CD/genética , Antígenos CD/metabolismo , Antígenos de Diferenciação Mielomonocítica/genética , Antígenos de Diferenciação Mielomonocítica/metabolismo , Feminino , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Pessoa de Meia-Idade , Doenças Peritoneais/genética , Doenças Peritoneais/metabolismo , Proteína Fosfatase 1/genética , Proteína Fosfatase 1/metabolismo , Sepse/genética , Sepse/metabolismo , Proteína 1 de Ligação a X-Box/genética , Proteína 1 de Ligação a X-Box/metabolismoRESUMO
Oncogenic overexpression of MYC leads to the fatal deregulation of signaling pathways, cellular metabolism, and cell growth. MYC rearrangements are found frequently among non-Hodgkin B-cell lymphomas enforcing MYC overexpression. Genetically engineered mouse models (GEMMs) were developed to understand MYC-induced B-cell lymphomagenesis. Here, we highlight the advantages of using Eµ-Myc transgenic mice. We thoroughly compiled the available literature to discuss common challenges when using such mouse models. Furthermore, we give an overview of pathways affected by MYC based on knowledge gained from the use of GEMMs. We identified top regulators of MYC-induced lymphomagenesis, including some candidates that are not pharmacologically targeted yet.
Assuntos
Linfoma de Células B , Linfoma , Camundongos , Animais , Proteínas Proto-Oncogênicas c-myc/genética , Proteínas Proto-Oncogênicas c-myc/metabolismo , Linfoma/patologia , Camundongos Transgênicos , Linfoma de Células B/metabolismo , Linfócitos B/metabolismoRESUMO
The nucleotide analogue azacitidine (AZA) is currently the best treatment option for patients with high-risk myelodysplastic syndromes (MDS). However, only half of treated patients respond and of these almost all eventually relapse. New treatment options are urgently needed to improve the clinical management of these patients. Here, we perform a loss-of-function shRNA screen and identify the histone acetyl transferase and transcriptional co-activator, CREB binding protein (CBP), as a major regulator of AZA sensitivity. Compounds inhibiting the activity of CBP and the closely related p300 synergistically reduce viability of MDS-derived AML cell lines when combined with AZA. Importantly, this effect is specific for the RNA-dependent functions of AZA and not observed with the related compound decitabine that is only incorporated into DNA. The identification of immediate target genes leads us to the unexpected finding that the effect of CBP/p300 inhibition is mediated by globally down regulating protein synthesis.
Assuntos
Azacitidina/farmacologia , Proteína de Ligação a CREB/antagonistas & inibidores , Proteína de Ligação a CREB/genética , Biossíntese de Proteínas/efeitos dos fármacos , RNA/metabolismo , Antimetabólitos Antineoplásicos/farmacologia , Linhagem Celular Tumoral , Metilação de DNA/efeitos dos fármacos , Humanos , Leucemia Mielomonocítica AgudaRESUMO
In a wide range of lymphoid neoplasms, the process of malignant transformation is associated with somatic mutations in B cells that affect the epigenetic machinery. Consequential alterations in histone modifications contribute to disease-specific changes in the transcriptional program. Affected genes commonly play important roles in cell cycle regulation, apoptosis-inducing signal transduction, and DNA damage response, thus facilitating the emergence of malignant traits that impair immune surveillance and favor the emergence of different B-cell lymphoma subtypes. In the last two decades, the field has made a major effort to develop therapies that target these epigenetic alterations. In this review, we discuss which epigenetic alterations occur in B-cell non-Hodgkin lymphoma. Furthermore, we aim to present in a close to comprehensive manner the current state-of-the-art in the preclinical and clinical development of epigenetic drugs. We focus on therapeutic strategies interfering with histone methylation and acetylation as these are most advanced in being deployed from the bench-to-bedside and have the greatest potential to improve the prognosis of lymphoma patients.
Assuntos
Histonas/metabolismo , Linfoma/metabolismo , Processamento de Proteína Pós-Traducional , Ensaios Clínicos como Assunto , Epigênese Genética , Humanos , Linfoma/genética , Modelos BiológicosRESUMO
A major transcriptional output of cells is ribosomal RNA (rRNA), synthesized by RNA polymerase I (Pol I) from multicopy rRNA genes (rDNA). Constitutive silencing of an rDNA fraction by promoter CpG methylation contributes to the stabilization of these otherwise highly active loci. In cancers driven by the oncoprotein Myc, excessive Myc directly stimulates rDNA transcription. However, it is not clear when during carcinogenesis this mechanism emerges, and how Myc-driven rDNA activation affects epigenetic silencing. Here, we have used the Eµ-Myc mouse model to investigate rDNA transcription and epigenetic regulation in Myc-driven B cell lymphomagenesis. We have developed a refined cytometric strategy to isolate B cells from the tumor initiation, promotion, and progression phases, and found a substantial increase of both Myc and rRNA gene expression only in established lymphoma. Surprisingly, promoter CpG methylation and the machinery for rDNA silencing were also strongly up-regulated in the tumor progression state. The data indicate a dichotomous role of oncogenic Myc in rDNA regulation, boosting transcription as well as reinforcing repression of silent repeats, which may provide a novel angle on perturbing Myc function in cancer cells.
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To gain knowledge about cause-effect relationships for the adhesion of ice on surfaces with different chemical groups, we wanted to study the effect of thin polymer layers on the ice adhesion strength. To minimize the effect of roughness, smooth substrates that have generally relatively low ice adhesion strengths were chosen. To be able to obtain highly reproducible values for the region of low ice adhesion and to measure small differences of ice adhesion at surfaces with different chemical compositions, a new measuring system for the determination of the ice adhesion strength which is based on a modified spin-coater was developed. We show its technical potential on the basis of first results on pure silicon wafers and selected hydrophilic polymer layers. Furthermore, we investigated the effect of the water quality on the ice adhesion strength. The obtained data are discussed in the context of physicochemical properties of the layers and of the chemical characteristics of the used polymers.
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Acute lymphoblastic leukemia (ALL) is an aggressive blood cancer that mainly affects children. Relapse rates are high and toxic chemotherapies that block DNA replication and induce DNA damage lead to health problems later in life, underlining the need for improved therapies. MYC is a transcription factor that is hyperactive in a large proportion of cancers including leukemia but is difficult to target in therapy. We show that ablation of the function of the BTB/POZ domain factor Zbtb17 (Miz-1), an important cofactor of c-Myc, significantly delayed T- and B-ALL/lymphoma in mice and interfered with the oncogenic transcriptional activity of c-Myc. Leukemic cells that still emerged in this system activated DNA replication pathways that could be targeted by current chemotherapeutic drugs such as cytarabine. Acute ablation of the Miz-1 POZ domain enhanced the effect of cytarabine treatment. The combined treatment was effective in both Eµ-Myc and Notch ICN-driven leukemia models and prolonged survival of tumor-bearing animals by accelerating apoptosis of leukemic cells. These observations suggest that targeting MIZ-1 could render current ALL chemotherapies more effective, with a better outcome for patients. SIGNIFICANCE: Ablation of the POZ domain of Miz-1 perturbs its interaction with c-MYC and delays the generation of T- and B-cell leukemias and lymphomas.
Assuntos
Citarabina/farmacologia , Leucemia-Linfoma Linfoblástico de Células Precursoras B/tratamento farmacológico , Leucemia-Linfoma Linfoblástico de Células T Precursoras/tratamento farmacológico , Proteínas Inibidoras de STAT Ativados/genética , Ubiquitina-Proteína Ligases/genética , Animais , Antimetabólitos Antineoplásicos/farmacologia , Feminino , Regulação Neoplásica da Expressão Gênica , Genes myc , Camundongos Transgênicos , Leucemia-Linfoma Linfoblástico de Células Precursoras B/genética , Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética , Domínios Proteicos , Proteínas Inibidoras de STAT Ativados/metabolismo , Proteína Supressora de Tumor p53/genética , Proteína Supressora de Tumor p53/metabolismo , Ubiquitina-Proteína Ligases/metabolismoRESUMO
The tuberous sclerosis complex (TSC) 1/2 is a negative regulator of the nutrient-sensing kinase mechanistic target of rapamycin complex (mTORC1), and its function is generally associated with tumor suppression. Nevertheless, biallelic loss of function of TSC1 or TSC2 is rarely found in malignant tumors. Here, we show that TSC1/2 is highly expressed in Burkitt's lymphoma cell lines and patient samples of human Burkitt's lymphoma, a prototypical MYC-driven cancer. Mechanistically, we show that MYC induces TSC1 expression by transcriptional activation of the TSC1 promoter and repression of miR-15a. TSC1 knockdown results in elevated mTORC1-dependent mitochondrial respiration enhanced ROS production and apoptosis. Moreover, TSC1 deficiency attenuates tumor growth in a xenograft mouse model. Our study reveals a novel role for TSC1 in securing homeostasis between MYC and mTORC1 that is required for cell survival and tumor maintenance in Burkitt's lymphoma. The study identifies TSC1/2 inhibition and/or mTORC1 hyperactivation as a novel therapeutic strategy for MYC-driven cancers.
Assuntos
Linfoma de Burkitt/metabolismo , Regulação Neoplásica da Expressão Gênica , Proteínas Proto-Oncogênicas c-myc/metabolismo , Proteína 1 do Complexo Esclerose Tuberosa/metabolismo , Proteína 2 do Complexo Esclerose Tuberosa/metabolismo , Animais , Linfoma de Burkitt/genética , Linfoma de Burkitt/patologia , Células HEK293 , Xenoenxertos , Humanos , Células MCF-7 , Alvo Mecanístico do Complexo 1 de Rapamicina/genética , Alvo Mecanístico do Complexo 1 de Rapamicina/metabolismo , Camundongos , Camundongos Endogâmicos NOD , Camundongos SCID , MicroRNAs/genética , MicroRNAs/metabolismo , Transplante de Neoplasias , Proteínas Proto-Oncogênicas c-myc/genética , RNA Neoplásico/genética , RNA Neoplásico/metabolismo , Proteína 1 do Complexo Esclerose Tuberosa/genética , Proteína 2 do Complexo Esclerose Tuberosa/genéticaRESUMO
Histone deacetylase inhibitors (HDACi) are used as therapeutics for several B cell-derived malignancies. Furthermore, they have been shown to modulate the response of the immune system, like the B cell function. HDACi treatment affects differentiation, proliferation, and survival of B cells. Here we describe how to investigate the effects of HDACi treatment on naïve B cells regarding class-switch recombination (CSR) in vitro using flow cytometry.
Assuntos
Linfócitos B/efeitos dos fármacos , Inibidores de Histona Desacetilases/farmacologia , Histona Desacetilases/imunologia , Switching de Imunoglobulina/efeitos dos fármacos , Separação Imunomagnética/métodos , Recombinação Genética/efeitos dos fármacos , Animais , Linfócitos B/citologia , Linfócitos B/imunologia , Benzamidas/farmacologia , Carbazóis/farmacologia , Ciclo Celular , Diferenciação Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Citocinas/farmacologia , Citometria de Fluxo/métodos , Histona Desacetilases/genética , Ácidos Hidroxâmicos/farmacologia , Imunoglobulinas/genética , Indóis/farmacologia , Lipopolissacarídeos/farmacologia , Camundongos , Camundongos Endogâmicos C57BL , Panobinostat , Cultura Primária de Células , Piridinas/farmacologia , Recombinação Genética/imunologiaRESUMO
Impaired T lymphopoiesis is associated with immunosuppression of the adaptive immune response and plays a role in the morbidity and mortality of patients and animal models of sepsis. Although previous studies examined several intrathymic mechanisms that negatively affect T lymphopoiesis, the extrathymic mechanisms remain poorly understood. Here, we report a dramatic decrease in the percentage of early T lineage progenitors (ETPs) in three models of sepsis in mice (cecal ligation and puncture, lipopolysaccharide continuous injection, and poly I:C continuous injection). However, septic mice did not show a decrease in the number of bone marrow (BM) precursor cells. Instead, the BM progenitors for ETPs expressed reduced mRNA levels of CC chemokine receptor (CCR) 7, CCR9 and P-selectin glycoprotein ligand 1, and exhibited impaired homing capacity in vitro and in vivo. Furthermore, RNA-Seq analysis and real-time PCR showed a marked downregulation of several lymphoid-related genes in hematopoietic stem and progenitor cells. Hematopoietic stem and progenitor cells differentiated into myeloid cells but failed to generate T lymphocytes in vitro and in vivo. Our results indicate that the depletion of ETPs in septic mice might be a consequence of an impaired migration of BM progenitors to the thymus, as well as a defect in lymphoid lineage commitment. Stem Cells 2016;34:2902-2915.
Assuntos
Linfopoese , Sepse/complicações , Timo/patologia , Animais , Atrofia , Células da Medula Óssea/citologia , Células da Medula Óssea/efeitos dos fármacos , Linhagem da Célula/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Perfilação da Expressão Gênica , Hematopoese Extramedular/efeitos dos fármacos , Células-Tronco Hematopoéticas/citologia , Células-Tronco Hematopoéticas/efeitos dos fármacos , Lipopolissacarídeos/farmacologia , Contagem de Linfócitos , Linfopoese/efeitos dos fármacos , Masculino , Camundongos Endogâmicos C57BL , Mielopoese/efeitos dos fármacos , Poli I-C/farmacologia , Receptores de Quimiocinas/metabolismo , Sepse/genética , Sepse/patologia , Linfócitos T/efeitos dos fármacos , Linfócitos T/patologia , Timo/efeitos dos fármacos , Receptores Toll-Like/agonistas , Receptores Toll-Like/metabolismoRESUMO
PURPOSE: SIRT1-activating compounds (STACs) may have potential in the management of cancer. However, the best-studied STAC, the naturally occurring compound resveratrol, is reported to have contradictory effects in combination chemotherapy regimens: It has been shown both to increase and to decrease the action of anticancer agents. To shed more light on this issue, we comparatively investigated the impact of resveratrol and the synthetic STAC SRT1720 on the responsiveness of Ewing's sarcoma (ES) cells to the chemotherapeutic drugs etoposide and vincristine. METHODS: Because the effects of STACs can depend on the functionality of the tumor suppressor protein p53, we used three ES cell lines differing in their p53 status, i.e., wild-type p53 WE-68 cells, mutant p53 SK-ES-1 cells and p53 null SK-N-MC cells. Single agent and combination therapy effects were assessed by flow cytometric analyses of propidium iodide uptake and mitochondrial depolarization, by measuring caspase 3/7 activity and by gene expression profiling. RESULTS: When applied as single agents, both STACs were effective in ES cells irrespective of their p53 status. Strikingly, however, when applied in conjunction with cytostatic agents, the STACs displayed reverse effects: SRT1720 largely enhanced etoposide- and vincristine-induced cell death, while resveratrol inhibited it. Combination index analyses validated the antipodal impact of the STACs on the effectiveness of the chemotherapeutics. CONCLUSION: These findings suggest that the synthetic STAC SRT1720 may be useful to enhance the efficacy of anticancer therapy in ES. But they also suggest that the dietary intake of the natural STAC resveratrol may be detrimental during chemotherapy of ES.
Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia , Neoplasias Ósseas/tratamento farmacológico , Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia , Sarcoma de Ewing/tratamento farmacológico , Sirtuína 1/metabolismo , Estilbenos/farmacologia , Apoptose/efeitos dos fármacos , Neoplasias Ósseas/metabolismo , Neoplasias Ósseas/patologia , Caspases/genética , Caspases/metabolismo , Proliferação de Células/efeitos dos fármacos , Etoposídeo/administração & dosagem , Citometria de Fluxo , Humanos , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Resveratrol , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Sarcoma de Ewing/metabolismo , Sarcoma de Ewing/patologia , Sirtuína 1/genética , Células Tumorais Cultivadas , Vincristina/administração & dosagemRESUMO
The molecular dynamics of poly(2-vinyl-pyridine) (P2VP) brushes is measured by Broadband Dielectric Spectroscopy (BDS) in a wide temperature (250 K to 440 K) and broad spectral (0.1 Hz to 1 MHz) range. This is realized using nanostructured, highly conductive silicon electrodes being separated by silica spacers as small as 35 nm. A "grafting-to"-method is applied to prepare the P2VP-brushes with five different grafting densities (0.030 nm(-2) to 0.117 nm(-2)), covering the "true-brush" regime with highly stretched coils and the "mushroom-to-brush" transition regime. The film thickness ranges between 1.8 to 7.1 (±0.2) nm. Two relaxations are observed, an Arrhenius-like process being attributed to fluctuations in the poly(glycidyl-methacrylate) (PGMA) linker used for the grafting reaction and the segmental dynamics (dynamic glass transition) of the P2VP brushes. The latter is characterized by a Vogel-Fulcher-Tammann dependence similar to bulk P2VP. The results can be comprehended considering the length scale on which the dynamic glass transition (≤1 nm) takes place.
RESUMO
Thin films with tunable properties are very interesting for potential applications as functional coatings with, for example, anti-icing or improved easy-to-clean properties. A novel "reactive layer stack" approach was developed to create covalently grafted mono- and multilayers of poly(glycidyl methacrylate)/poly(tert-butyl acrylate) diblock copolymers. Because these copolymers contain poly(glycidyl methacrylate) blocks they behave as self-cross-linking materials after creation of acrylic acid functionalities by splitting off the tert-butyl units. The ellipsometrically determined coating thickness of the resulting hydrophilic multilayers depended linearly on the number of applied layers. Amphiphilic films with tunable wettability were prepared using triblock terpolymers with an additional poly(methyl methacrylate) block. The mechanism of the formation of the (multi)layers was investigated in detail by studying the acidolysis of the surface-linked tert-butyl acrylate blocks by infrared reflection absorbance spectroscopy, accompanied by surface analysis using atomic force microscopy and contact angle measurements. In the case of the amphiphilic and switchable terpolymer layers this reaction was very sensitive to the used acidic reagent.
RESUMO
The adsorption of poly(vinylformamide) (PVFA) and its derivative statistical copolymer poly(vinyl-formamide-co-vinylamine) (PVFA-co-PVAm) on metallic copper and copper oxide particles as well as planar copper surfaces was studied as a function of the degree of hydrolysis of PVFA, the pH, and the polymer concentration in solution. The chemical composition and molecular structure of the PVFA-co-PVAm layers were investigated by surface-sensitive spectroscopic methods such as XPS, DRIFT spectroscopy, and ellipsometry. The findings allowed us to explain the adsorption mechanisms and the forces driving the PVFA-co-PVAm adsorption. It was shown that PVFA-co-PVAm layers thicker than 30 nm are able to protect the planar copper surface against corrosive attack.