Other Publications (8)
- Arteriosclerosis, Thrombosis, and Vascular Biology
- The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society
- International Journal of Cardiology
- American Journal of Translational Research
- Journal of the American Heart Association
- Journal of Immunology (Baltimore, Md. : 1950)
- Scientific Reports
- Cell Death and Differentiation
Articles by Soenke Weinert in JoVE
隔离和小鼠骨髓的静脉注射单核细胞衍生 Martin Wagner1, Helen Koester1, Christian Deffge1, Soenke Weinert1, Johannes Lauf1, Alexander Francke2, Jerry Lee3, R. C. Braun- Dullaeus1, Joerg Herold1 1Department for Cardiology, Angiology and Pneumology, Otto von Guericke University Magdeburg, 2Herzzentrum Dresden, Universitätsklinikum an der Technischen Universität Dresden, Technische Universität Dresden, 3Department of Public Health and Primary Care, University of Cambridge
小鼠外周动脉疾病模型中单核细胞归巢和肿瘤相关血管生成的活体显微镜观察 Martin Wagner1, Claudia Baer1, Werner Zuschratter2, Monika Riek-Burchardt3, Christian Deffge1, Soenke Weinert1, Jerry C Lee4, Ruediger C Braun-Dullaeus1, Joerg Herold1 1Department of Cardiology and Angiology, University of Magdeburg, 2Leibniz Institute for Neurobiology, 3Institute of Molecular and Clinical Immunology, University of Magdeburg, 4 单核细胞是外周动脉疾病中 arteriogenesis 的重要介质。本协议采用基底膜样基质和活体显微镜, 研究单核细胞注射在股动脉结扎小鼠模型中的单核细胞归巢和肿瘤相关血管生成。
Other articles by Soenke Weinert on PubMed
Time-course Analysis on the Differentiation of Bone Marrow-derived Progenitor Cells into Smooth Muscle Cells During Neointima Formation Arteriosclerosis, Thrombosis, and Vascular Biology. Oct, 2010 | Pubmed ID: 20576944 Bone marrow-derived progenitor cells have been implicated to contribute to neointima formation, but the time course and extent of their accumulation and differentiation into vascular cells and, most importantly, the long-term contribution of bone marrow-derived progenitor cells to the vascular lesion remain undefined.
一代的成熟小鼠单核细胞从异构骨髓和它们的属性的说明。 The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society. Sep, 2011 | Pubmed ID: 21705645 单核细胞参与各种各样的生理和病理过程，其中许多在小鼠模型的研究。当前协议来隔离小鼠单核细胞很少，导致令人不满意细胞产率和纯度。在这里，我们将介绍一种新的方法，以有效地使大批成熟炎症单核细胞区别于异构骨髓细胞悬浮液。骨髓细胞悬浮液被隔离的 Balb/c 从厕股骨和胫骨和 C57Bl/6 小鼠，辅之以巨噬细胞集落刺激因子 (M-CSF)，和被超低附件表面抑制遵守介导的成熟细胞。单元格在指定的时间点收获了、 术的分化过程中，时间线分析和随后被广泛 phenotyped 来验证其 monocytotic 属性。为了确认下游的兼容性，我们测试了典型的单核细胞的行为。我们的协议产生了 24 ± 6 × 10(6) 分化细胞每捐助鼠标，比以前使用获得的收益率所述外周血分离方法高 10 倍。分化的细胞包括大约 47%± 12%单，其余均为成熟巨噬细胞。我们可以上升到 86%± 6%的单核细胞纯度消耗遗民巨噬细胞。我们的研究结果表明骨髓单核细胞 (BMDMs) 是有吸引力的工具，例如，研究先天和自适应的免疫系统、 动脉粥样硬化和细胞迁移期间感染。此外，BMDM 移植可用于测试小说，治疗体内方法在小鼠疾病模型。
The Impact of Rapid Atrial Pacing on ADMA and Endothelial NOS International Journal of Cardiology. Jan, 2012 | Pubmed ID: 20926145 The endothelial nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) is a well-established risk factor for oxidative stress, vascular dysfunction, and congestive heart failure. The aim of the present study was to determine the impact of rapid atrial pacing (RAP) on ADMA levels and eNOS expression.
Transplantation of Bone Marrow Derived Monocytes: a Novel Approach for Augmentation of Arteriogenesis in a Murine Model of Femoral Artery Ligation American Journal of Translational Research. 2013 | Pubmed ID: 23573361 Therapeutic augmentation of collateral artery growth (arteriogenesis) is of tremendous clinical interest. Since monocytes home to areas of arteriogenesis and create a local arteriogeneic milieu by secreting a wide range of growth factors, we followed the idea of utilizing these cells for augmentation of collateral growth. For that purpose, we adoptively transferred both syngeneic (same strain) and allogeneic (different strain) bone marrow derived monocytes (BMDMs) into balb/c mice 24 h after femoral artery ligation. Restoration of hind-limb perfusion was determined by Laser Doppler Perfusion Imaging and histological workup. While syngeneic cell transplantation did not augment arteriogenesis in comparison to non-transplanted animals (PI = 0.56 ± 0.06 vs. 0.48 ± 0.09, respectively, ns), allogeneic monocytes massively promoted the collateralization (PI = 0.85 ± 0.14, p < 0.001). Homed monocytes were visualized near growing collateral vessels by staining the cells with the lipophil fluorochrome DiI prior to transplantation. To analyze whether the effect of allogeneic BMDM transplantations is due to local inflammation triggered by a host-versus-graft reaction, transplant recipients were pre-treated with the immunosuppressive drug cyclosporine A, which completely prevented the effect of allogeineic monocyte transplantation (PI = 0.45 ± 0.06, p < 0.001). Here, we have demonstrated murine allogeneic monocytes to be an attractive way to trigger local inflammatory responses near growing collateral vessels and stimulate their adaption, overcoming the endogenous restriction of collateral vessel growth.
Tetanus Toxoid-pulsed Monocyte Vaccination for Augmentation of Collateral Vessel Growth Journal of the American Heart Association. 2014 | Pubmed ID: 24732919 The pathogenesis of collateral growth (arteriogenesis) has been linked to both the innate and adaptive immune systems. While therapeutic approaches for the augmentation of arteriogenesis have focused on innate immunity, exploiting both innate and adaptive immune responses has not been examined. We hypothesized that tetanus toxoid (tt) immunization of mice followed by transplantation of monocytes (Mo) exposed ex vivo to tt augments arteriogenesis after ligation of the hind limb.
CD4+ T Cells from Human Neonates and Infants Are Poised Spontaneously to Run a Nonclassical IL-4 Program Journal of Immunology (Baltimore, Md. : 1950). Jun, 2014 | Pubmed ID: 24778440 Senescence or biological aging impacts a vast variety of molecular and cellular processes. To date, it is unknown whether CD4(+) Th cells display an age-dependent bias for development into specific subpopulations. In this study, we show the appearance of a distinct CD4(+) T cell subset expressing IL-4 at an early stage of development in infant adenoids and cord blood that is lost during aging. We identified by flow cytometric, fluorescent microscopic, immunoblot, and mass spectrometric analysis a population of CD4(+) T cells that expressed an unglycosylated isoform of IL-4. This T cell subpopulation was found in neonatal but not in adult CD4(+) T cells. Furthermore, we show that the mRNA of the Th2 master transcription factor GATA3 is preferentially expressed in neonatal CD4(+) T cells. The Th2 phenotype of the IL-4(+)CD4(+) T cells could be reinforced in the presence of TGF-β. Although the IL-4(+)CD4(+) T cells most likely originate from CD31(+)CD4(+) T recent thymic emigrants, CD31 was downregulated prior to secretion of IL-4. Notably, the secretion of IL-4 requires a so far unidentified trigger in neonatal T cells. This emphasizes that cytokine expression and secretion are differentially regulated processes. Our data support the hypothesis of an endogenously poised cytokine profile in neonates and suggest a link between cytokine production and the developmental stage of an organism. The determination of the IL-4 isoform-expressing cells in humans might allow the identification of Th2 precursor cells, which could provide novel intervention strategies directed against Th2-driven immunopathologies such as allergies.
GSK-3β Controls NF-kappaB Activity Via IKKγ/NEMO Scientific Reports. Dec, 2016 | Pubmed ID: 27929056 The NF-κB signaling pathway is central for the innate immune response and its deregulation is found in multiple disorders such as autoimmune, chronic inflammatory and metabolic diseases. IKKγ/NEMO is essential for NF-κB activation and NEMO dysfunction in humans has been linked to so-called progeria syndromes, which are characterized by advanced ageing due to age-dependent inflammatory diseases. It has been suggested that glycogen synthase kinase-3β (GSK-3β) participates in NF-κB regulation but the exact mechanism remained incompletely understood. In this study, we identified NEMO as a GSK-3β substrate that is phosphorylated at serine 8, 17, 31 and 43 located within its N-terminal domain. The kinase forms a complex with wild-type NEMO while point mutations of NEMO at the specific serines abrogated GSK-3β binding and subsequent phosphorylation of NEMO resulting in its destabilization. However, K63-linked polyubiquitination was augmented in mutated NEMO explaining an increased binding to IKKα and IKKβ. Even IκBα was found degraded. Still, TNFα-stimulated NF-κB activation was impaired pointing towards an un-controlled signalling process. Our data suggest that GSK-3β is critically important for ordered NF-κB signalling through modulation of NEMO phosphorylation.
RSK-mediated Nuclear Accumulation of the Cold-shock Y-box Protein-1 Controls Proliferation of T Cells and T-ALL Blasts Cell Death and Differentiation. Feb, 2017 | Pubmed ID: 28009354 Deregulated proliferation is key to tumor progression. Although unrestricted proliferation of solid tumor cells correlates with the cold-shock protein Y-box (YB)-binding protein-1 accumulation in the nuclei, little is known about its expression and function in hematopoietic malignancies, such as T-cell acute lymphoblastic leukemia (T-ALL). Here we show that YB-1 protein is highly enriched in the nuclei of activated T cells and malignant human T-ALL cell lines but not in resting T cells. YB-1 S(102) mutations that either mimic (S102D) or prevent phosphorylation (S102N) led to accumulation of YB-1 in the nucleus of T cells or strictly excluded it, respectively. Inactivation of ribosomal S6 kinase (RSK) was sufficient to abrogate T-cell and T-ALL cell proliferation, suggesting that RSK mediates cell-cycle progression, possibly dependent on YB-1-phosphorylation. Indeed, phosphomimetic YB-1(S102D) enhanced proliferation implying that S(102) phosphorylation is a prerequisite for malignant T-cell proliferation. At initial diagnosis of T-ALL, YB-1 localization was significantly altered in the nuclei of tumor blasts derived from bone marrow or peripheral blood. Our data show deregulated YB-1 in the nucleus as a yet unreported characteristic of T-ALL blasts and may refine strategies to restrict progression of hematopoietic tumors.