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The role of Smad signaling in vascular and hematopoietic development revealed by studies using genetic mouse models
Yu Lan,Xiao Yang
Science China Life Sciences , 2010, DOI: 10.1007/s11427-010-0087-3
Abstract: Smads are intracellular mediators of transforming growth factor β (TGF-β) superfamily signaling. In this review, we focus on the genetic mouse models for Smad pathways, which have provided functional evidence regarding the complex circuitry in angiogenesis and hematopoiesis during development. In the early stages of vascular development, TGF-β signaling is a contributing factor in angiogenesis and vascular maturation. Whereas in the later embryogenesis, selected molecules of Smad pathways, such as TGF-β type II receptor (TbRII), ALK5, and Smad5, seem to be dispensable for vessel morphogenesis and integrity. TGF-β signaling is not required in the induction of hematopoietic precursors from mesoderm, but inhibits the subsequent expansion of committed hematopoietic precursors. By contrast, bone morphogenetic protein 4 (BMP4) has long been acknowledged pivotal in mesoderm induction and hematopoietic commitment during development. However, recent genetic evidence shows the BMP4-ALK3 axis is not crucial for the formation of hematopoietic cells from FLK1+ mesoderm. Because of the highly redundant mechanisms within the Smad pathways, the precise role of the Smad signaling involved in vascular and hematopoietic development remains nebulous. The generation of novel cell lineage restricted Cre transgenes would shed new light on the future relevant investigations.
Mesenchymal Stromal Cells Derived from the Bone Marrow of Acute Lymphoblastic Leukemia Patients Show Altered BMP4 Production: Correlations with the Course of Disease  [PDF]
ángeles Vicente López, Miriam Nohemí Vázquez García, Gustavo J. Melen, Ana Entrena Martínez, Isabel Cubillo Moreno, Javier García-Castro, Manuel Ramírez Orellana, Agustín Gregorio Zapata González
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0084496
Abstract: The relevance of tumor microenvironment for the development and progression of tumor cells in hematological malignancies has been extensively reported. Identification of factors involved in the information exchange between the malignant cells and the bone marrow mesenchymal stem cells (BM-MSCs) and the knowledge on their functioning may provide important information to eliminate leukemic cells from protective BM niches. We evaluated changes in BM-MSCs obtained from children with acute lymphoblastic leukemia (ALL) at different times in the course of disease. Whereas ALL-MSCs did not exhibit phenotypic changes compared to BM-derived MSCs isolated from healthy donors, they exhibited increased adipogenic capacity. In addition, the viability of healthy CD34+ hematopoietic progenitors was significantly reduced when co-cultured with ALL-MSCs. ALL-MSCs grow less efficiently, although gradually recover normal growth with treatment. Accordingly, proliferation is particularly low in MSCs obtained at diagnosis and in the first days of treatment (+15 days), recovering to control levels after 35 days of treatment. Correlating these results with bone morphogenetic protein 4 (BMP4) production, a molecule demonstrated to affect MSC biology, we found higher production of BMP4 in ALL-MSCs derived from patients over the course of disease but not in those free of leukemia. However, no significant differences in the expression of different members of the BMP4 signaling pathway were observed. Furthermore, an inverse correlation between high levels of BMP4 production in the cultures and MSC proliferation was found, as observed in MSCs derived from patients at diagnosis that produce high BMP4 levels. In addition, co-culturing ALL-MSC with the REH leukemia cell line, but not CD34+ hematopoietic progenitors, powerfully enhanced BMP4 production, suggesting an intimate crosstalk among ALL-MSCs isolated from BM colonized by ALL cells that presumably also occurs in situ conditions. Our data may support the participation of BMP4 in BM niche, but the mechanism remains to be elucidated.
Smad5双等位基因剔除ES细胞的建立及其初步研究*  [PDF]
中国科学 生命科学 , 2000,
Abstract: Smad5是TGF-β信号的细胞质内信号转导分子.Smad5的定位剔除导致小鼠胚胎期死亡.为了进一步研究Smad5在组织器官发育中的功能,利用同源重组技术获得了Smad5双等位基因剔除的胚胎干(ES)细胞.首先利用Cre-LoxP系统删除了Smad5中靶ES细胞的抗性基因,再用相同的打靶载体进行转染,经Southern杂交筛选获得了Smad5双等位基因剔除的ES细胞.嵌合体研究的结果表明,Smad5在心脏和神经管的正常发育中可能起重要的作用.Smad5双等位基因剔除ES细胞在裸鼠皮下可以形成畸胎瘤,并可分化成包括神经细胞、肌肉细胞、软骨细胞、内皮细胞等在内的多种细胞,因而Smad5双等位基因剔除的ES细胞可用于研究Smad5介导的TGF-?信号在多种组织器官发育和ES细胞体外定向分化中的作用.
Infrared Radiation Drying of Mint Leaves  [PDF]
B. S. Demirturk,H. Kocabiyik,B. S. Demirturk
Journal of Tekirdag Agricultural Faculty , 2008,
Abstract: The effects of air velocity on the drying characteristics, drying time and drying rate of mint leaves were investigated at infrared drying. Specific energy consumption and color properties of dried mint leaves were examined. Experiments were conducted using four levels of air velocity (0.5, 1.0, 1.5 and 2.0 m/s) at 1080 W/m2 of infrared radiation density. The drying time ranged from 64 to 180 minutes for all the drying conditions. The drying rate increased with decreasing of air velocity. The specific energy consumption values varied between 37.04 and 106.58 MJ/kg-evaporated water for all the drying conditions. Colour parameters were found to be affected by process variables.
Mint Water - the Science Behind the Tradition !
Khawla S.H. Al-Haddad,Rasha A.S. Al-Qassemi,R.K. Robinson
Pakistan Journal of Nutrition , 2003,
Abstract: When cultures of three common pathogens, namely Salmonella infantis, Salmonella hadar and Pseudomonas aeruginosa were added individually to a commercial sample of Mint Water at levels of ~ 500 colony-forming units ml-1, no viable cells could be detected after 10 minutes exposure. It is suggested that D-carvone is the active ingredient and that there is a sound scientific basis for the use of this traditional Middle Eastern remedy for bacterial infections.
SPOC1-Mediated Antiviral Host Cell Response Is Antagonized Early in Human Adenovirus Type 5 Infection  [PDF]
Sabrina Schreiner,Sarah Kinkley,Carolin Bürck,Andreas Mund,Peter Wimmer,Tobias Schubert,Peter Groitl,Hans Will,Thomas Dobner
PLOS Pathogens , 2013, DOI: 10.1371/journal.ppat.1003775
Abstract: Little is known about immediate phases after viral infection and how an incoming viral genome complex counteracts host cell defenses, before the start of viral gene expression. Adenovirus (Ad) serves as an ideal model, since entry and onset of gene expression are rapid and highly efficient, and mechanisms used 24–48 hours post infection to counteract host antiviral and DNA repair factors (e.g. p53, Mre11, Daxx) are well studied. Here, we identify an even earlier host cell target for Ad, the chromatin-associated factor and epigenetic reader, SPOC1, recently found recruited to double strand breaks, and playing a role in DNA damage response. SPOC1 co-localized with viral replication centers in the host cell nucleus, interacted with Ad DNA, and repressed viral gene expression at the transcriptional level. We discovered that this SPOC1-mediated restriction imposed upon Ad growth is relieved by its functional association with the Ad major core protein pVII that enters with the viral genome, followed by E1B-55K/E4orf6-dependent proteasomal degradation of SPOC1. Mimicking removal of SPOC1 in the cell, knock down of this cellular restriction factor using RNAi techniques resulted in significantly increased Ad replication, including enhanced viral gene expression. However, depletion of SPOC1 also reduced the efficiency of E1B-55K transcriptional repression of cellular promoters, with possible implications for viral transformation. Intriguingly, not exclusive to Ad infection, other human pathogenic viruses (HSV-1, HSV-2, HIV-1, and HCV) also depleted SPOC1 in infected cells. Our findings provide a general model for how pathogenic human viruses antagonize intrinsic SPOC1-mediated antiviral responses in their host cells. A better understanding of viral entry and early restrictive functions in host cells should provide new perspectives for developing antiviral agents and therapies. Conversely, for Ad vectors used in gene therapy, counteracting mechanisms eradicating incoming viral DNA would increase Ad vector efficacy and safety for the patient.
A New Mint1 Isoform, but Not the Conventional Mint1, Interacts with the Small GTPase Rab6  [PDF]
Anika Thyrock, Edith Ossendorf, Martin Stehling, Mark Kail, Tanja Kurtz, Gottfried Pohlentz, Dieter Waschbüsch, Simone Eggert, Etienne Formstecher, Johannes Müthing, Klaus Dreisewerd, Stefan Kins, Bruno Goud, Angelika Barnekow
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0064149
Abstract: Small GTPases of the Rab family are important regulators of a large variety of different cellular functions such as membrane organization and vesicle trafficking. They have been shown to play a role in several human diseases. One prominent member, Rab6, is thought to be involved in the development of Alzheimer’s Disease, the most prevalent mental disorder worldwide. Previous studies have shown that Rab6 impairs the processing of the amyloid precursor protein (APP), which is cleaved to β-amyloid in brains of patients suffering from Alzheimer’s Disease. Additionally, all three members of the Mint adaptor family are implied to participate in the amyloidogenic pathway. Here, we report the identification of a new Mint1 isoform in a yeast two-hybrid screening, Mint1 826, which lacks an eleven amino acid (aa) sequence in the conserved C-terminal region. Mint1 826, but not the conventional Mint1, interacts with Rab6 via the PTB domain. This interaction is nucleotide-dependent, Rab6-specific and influences the subcellular localization of Mint1 826. We were able to detect and sequence a corresponding proteolytic peptide derived from cellular Mint1 826 by mass spectrometry proving the absence of aa 495–505 and could show that the deletion does not influence the ability of this adaptor protein to interact with APP. Taking into account that APP interacts and co-localizes with Mint1 826 and is transported in Rab6 positive vesicles, our data suggest that Mint1 826 bridges APP to the small GTPase at distinct cellular sorting points, establishing Mint1 826 as an important player in regulation of APP trafficking and processing.
SPOC: A widely distributed domain associated with cancer, apoptosis and transcription
Luis Sánchez-Pulido, Ana M Rojas, Karel H van Wely, Carlos Martinez-A, Alfonso Valencia
BMC Bioinformatics , 2004, DOI: 10.1186/1471-2105-5-91
Abstract: We describe undetected members of the Spen family in other lineages (Plasmodium and Plants) and localise SPOC in a new domain context, in a family that is common to all eukaryotes using profile-based sequence searches and structural prediction methods.The widely distributed DIO (Death inducer-obliterator) family is related to cancer and apoptosis and offers new clues about SPOC domain functionality.The aim of this study was to characterize the Spen family at the sequence level. The Spen family of proteins participates in various biological processes. It is involved in neuronal cell fate, survival and axonal guidance [1-3], cell cycle regulation [4], and repression of head identity in the embryonic trunk [5]. More recently it has been shown that the split ends gene participates in Wingless signalling in the eye, wing and leg imaginal discs [6] in the fly. The human Spen protein SHARP (SMRT/HDAC1-associated repressor protein) has been identified as a component of transcriptional repression complexes in both nuclear receptor and Notch/RBP-Jkappa signalling pathways [7-9]. Therefore, the Spen family of proteins appears to regulate transcription in several signalling pathways. In addition, the human Spen protein RBM15 (RNA-binding motif protein 15) is involved in the recurrent t(1;22) translocation whose product is the RBM15-MKL1 fusion protein. This aberrant protein is related to the megakaryoblastic leukemia 1 (MKL1) [10,11].On the other hand, DIO and its homologue PHF3 (PHD finger protein 3) are human proteins that contain a PHD (Plant Homeodomain) finger and a TFIIS (Transcription Factor S-II) domain: both domains are usually associated with transcription [12,13]. The DIO-1 protein regulates the early stages of cell death in mouse and humans [14,15]. Experimental evidence shows that the PHF3 protein is ubiquitously expressed in normal tissues, including brain. However, its expression is dramatically reduced or lost in glioblastoma, the most frequent tumour reported i
Regulation of BMP4 on the proliferation and differentiation in SVZa neural stem cells
Shiyong Liu,Zhiyuan Zhang,Yechun Song,Kejun Qiu,Kecheng Zhang,Ning An,Zheng Zhou,Wenqin Cai,Hui Yang
Chinese Science Bulletin , 2004, DOI: 10.1360/03wc0607
Abstract: The neural stem cells in the anterior subventricular zone (SVZa) mainly generate the progenitors that will differentiate into neurons, and along a highly circumscribed migratory access — Rostral migratory stream (RMS), they migrate to the olfactory bulbs (OB). To understand the effects of BMPs on SVZa neural stem cells, in this study BMP4 at various concentrations was used to induce SVZa neural stem cells, and the living cell labeling using BMP4 promotor conjugated with red fluorescence protein showed the expression of BMP4 dynamically. The results demonstrated that low BMP4 doses (1– 5 ng/mL) promoted while high doses (10– 100 ng/mL) inhibited the proliferation of SVZa neural stem cells, and BMP4 promoted neuron differentiation in the early stage (1– 3 d), howeverm, it inhibited the neuron commitment after 4 d. Noggin, the antagonist of BMP4, blocked the physiological effects of BMP4. In OB, BMP4 is mainly to accelerate the progenitors to withdraw from the cell cycle and trigger the differentiation, and in RMS, it promotes the proliferation of committed progenitors and not differentiation, further in SVZa, BMP4 enhances astrocyte commitment.
Regulation of BMP4 on the proliferation and differentiation in SVZa neural stem cells
Shiyong Liu,Zhiyuan Zhang,Yechun Song,Kejun Qiu,Kecheng Zhang,Ning An,Zheng Zhou,Wenqin Cai,Hui Yang,
LIUShiyong
,ZHANGZhiyuan,SONGYechun,QIUKejun,ZHANGKecheng,ANNing,ZHOUZheng,CAIWenqin,YANGHui

科学通报(英文版) , 2004,
Abstract: The neural stem cells in the anterior subventricula zone (SVZa) mainly generate the progenitors that will differentiate into neurons, and along a highly circumscribed migratory access-Rostral migratory stream (RMS), they migrate to the olfactory bulbs (OB). To understand the effects of BMPs on SVZa neural stem cells, in this study BMP4 at various concentrations was used to induce SVZa ,neural stem cells, aud the living cell labeling using BMP4 pronmtor conjugated with red fluorescence protein showed the expression of BMP4 dynamically. The results demonstrated that low BMP4 doses (1-5 ng/mL) promoted while high doses(10-100 ng/mL) inhibited the proliferation of SVZa neural stem cells, and BMP4 promoted neuron differentiation in the early stage (1-3 d), howeverm, it inhibited the neuron commitment after 4 d. Noggin, the antagonist of BMP4, blocked the physiological effects of BMP4. In OB, BMP4 is mainly to accelerate the progenitors to withdraw from the cell cycle and trigger the differentiation, and in RMS, it promotes the proliferation of committed progenitors and not differentiation, further in SVZa, BMP4 enhances astrocyte commitment.
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