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Search Results: 1 - 10 of 221401 matches for " Mari C Sogayar "
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Stem cells in embryonic skin development
Maria F Forni,Marina Trombetta-Lima,Mari C Sogayar
Biological Research , 2012,
Abstract: The skin is a complex stratified organ which acts not only as a permeability barrier and defense against external agents, but also has essential thermoregulatory, sensory and metabolic functions. Due to its high versatility and activity, the skin undergoes continuous self-renewal to repair damaged tissue and replace old cells. Consequently, the skin is a reservoir for adult stem cells of different embryonic origins. Skin stem cell populations reside in the adult hair follicle, sebaceous gland, dermis and epidermis. However, the origin of most of the stem cell populations found in the adult epidermis is still unknown. Far more unknown is the embryonic origin of other stem cells that populate the other layers of this tissue. In this review we attempt to clarify the emergence, structure, markers and embryonic development of diverse populations of stem cells from the epidermis, dermis and related appendages such as the sebaceous gland and hair follicle.
Unveiling novel genes upregulated by both rhBMP2 and rhBMP7 during early osteoblastic transdifferentiation of C2C12 cells
Juan C Bustos-Valenzuela, Andre Fujita, Erik Halcsik, Jose M Granjeiro, Mari C Sogayar
BMC Research Notes , 2011, DOI: 10.1186/1756-0500-4-370
Abstract: BMPs (bone morphogenetic proteins) are members of the TGFβ (transforming growth factor-β) super-family of proteins, which regulate growth and differentiation of different cell types in various tissues, and play a critical role in the differentiation of mesenchymal cells into osteoblasts. In particular, rhBMP2 and rhBMP7 promote osteoinduction in vitro and in vivo, and both proteins are therapeutically applied in orthopaedics and dentistry.Using DNA microarrays and RT-qPCR, we identified both previously known and novel genes which are upregulated by rhBMP2 and rhBMP7 during the onset of osteoblastic transdifferentiation of pre-myoblastic C2C12 cells. Subsequent studies of these genes in C2C12 and mesenchymal or pre-osteoblastic cells should reveal more details about their role during this type of cellular differentiation induced by BMP2 or BMP7. These studies are relevant to better understanding the molecular mechanisms underlying osteoblastic differentiation and bone repair.Bone formation and fracture repair depends on the expression and action of the bone morphogenetic proteins (BMPs), which are members of the transforming growth factor beta (TGF-beta) superfamily of dimeric, disulphide-linked growth factors, comprising more than 15 related proteins. In addition to a crucial role in osteogenesis, BMPs display a myriad of roles in cell proliferation, differentiation, migration and apoptosis, in different cell types [1]. Their role is essential at early phases of development and organogenesis, such as axial embryo determination [2], as well as in limb, eye and kidney development, such that ablation of these genes results in death at very early stages of development, as observed in knock-out mice [3]. In humans, recombinant BMP2 and BMP7 have gained attention in bone repair and in non-union spinal fractures due to their capacity to stimulate the differentiation of mesenchymal stem cells from the periosteum near the lesion site after migration and proliferation induced
GEDI: a user-friendly toolbox for analysis of large-scale gene expression data
André Fujita, Jo?o R Sato, Carlos E Ferreira, Mari C Sogayar
BMC Bioinformatics , 2007, DOI: 10.1186/1471-2105-8-457
Abstract: Here, we introduce an user-friendly toolbox called GEDI (Gene Expression Data Interpreter), an extensible, open-source, and freely-available tool that we believe will be useful to a wide range of laboratories, and to researchers with no background in Mathematics and Computer Science, allowing them to analyze their own data by applying both classical and advanced approaches developed and recently published by Fujita et al.GEDI is an integrated user-friendly viewer that combines the state of the art SVR, DVAR and SVAR algorithms, previously developed by us. It facilitates the application of SVR, DVAR and SVAR, further than the mathematical formulas present in the corresponding publications, and allows one to better understand the results by means of available visualizations. Both running the statistical methods and visualizing the results are carried out within the graphical user interface, rendering these algorithms accessible to the broad community of researchers in Molecular Biology.High-throughput DNA microarray technologies yield up to tens of thousands of gene expression data, which are useful to identify differentially expressed genes, biomarkers and molecular disease profiles. In recent years, microarray platforms have become available at relatively low costs, becoming more popular among research groups which are interested in gene expression analysis. On the other hand, much effort has been spent in developing improved methods to analyze the data derived from these microarrays. These methods involve advanced mathematical and statistical models, which are quite cumbersome to biomedical researchers who attempt to implement these methods. Due to this difficulty, some of these advanced methods are often abandoned and data analysis is carried out using only the classical methods, which are implemented in popular statistical softwares. An user-friendly software could make it possible to use recently developed methods to integrate, qualify, and infer biological insi
Cloning and characterization of a novel alternatively spliced transcript of the human CHD7 putative helicase
Christian Colin, Flávia S Tobaruella, Ricardo G Correa, Mari C Sogayar, Marcos A Demasi
BMC Research Notes , 2010, DOI: 10.1186/1756-0500-3-252
Abstract: Here, we report the cloning and characterization by experimental and computational studies of a novel alternative transcript of the human CHD7 (named CHD7 CRA_e), which lacks most of its coding exons. We confirmed by overexpression of CHD7 CRA_e alternative transcript that it is translated into a protein isoform lacking most of the domains displayed by the canonical isoform. Expression of the CHD7 CRA_e transcript was detected in normal liver, in addition to the DU145 human prostate carcinoma cell line from which it was originally isolated.Our findings indicate that the splicing event associated to the CHD7 CRA_e alternative transcript is functional. The characterization of the CHD7 CRA_e novel isoform presented here not only sets the basis for more detailed functional studies of this isoform, but, also, contributes to the alternative splicing annotation of the CHD7 gene and the design of future functional studies aimed at the elucidation of the molecular functions of its gene products.The CHD7 (Chromodomain Helicase DNA binding protein 7) gene encodes a member of the chromodomain family of ATP-dependent chromatin remodeling enzymes. In 2004, CHD7 was described as the major gene involved in the CHARGE syndrome [1], a complex genetic disorder related to multiple birth malformations and functional disorders, including ocular coloboma (C), heart disease (H), choanal atresia (A), retarded growth and/or anomalies of the central nervous system (R), genito-urinary defects and/or hypogonadism (G), and ear anomalies and/or deafness (E) [2]. De novo mutations in the CHD7 gene, especially nonsense and frameshift mutations, are found in approximately 60% of the individuals with CHARGE [1-4]. Embryonic lethality at E10.5-E11.5 in mice which are homozygous for null mutations in Chd7 support the haplo-insufficiency model as the most likely mechanism involved in this syndrome. Additionally, mice which are heterozygous for null mutations in Chd7 recapitulate many of the traits found
TGF-β1 modulates the homeostasis between MMPs and MMP inhibitors through p38 MAPK and ERK1/2 in highly invasive breast cancer cells
Luciana R Gomes, Letícia F Terra, Rosangela AM Wailemann, Leticia Labriola, Mari C Sogayar
BMC Cancer , 2012, DOI: 10.1186/1471-2407-12-26
Abstract: The mRNA expression levels of TGF-β isoforms and their receptors were analyzed by qRT-PCR in a panel of five human breast cancer cell lines displaying different degrees of invasiveness and metastatic potential. The highly invasive MDA-MB-231 cell line was treated with different concentrations of recombinant TGF-β1 and also with pharmacological inhibitors of p38 MAPK and ERK1/2. The migratory and invasive potential of these treated cells were examined in vitro by transwell assays.In general, TGF-β2, TβRI and TβRII are over-expressed in more aggressive cells, except for TβRI, which was also highly expressed in ZR-75-1 cells. In addition, TGF-β1-treated MDA-MB-231 cells presented significantly increased mRNA expression of MMP-2, MMP-9, MMP-14, TIMP-2 and RECK. TGF-β1 also increased TIMP-2, MMP-2 and MMP-9 protein levels but downregulated RECK expression. Furthermore, we analyzed the involvement of p38 MAPK and ERK1/2, representing two well established Smad-independent pathways, in the proposed mechanism. Inhibition of p38MAPK blocked TGF-β1-increased mRNA expression of all MMPs and MMP inhibitors analyzed, and prevented TGF-β1 upregulation of TIMP-2 and MMP-2 proteins. Moreover, ERK1/2 inhibition increased RECK and prevented the TGF-β1 induction of pro-MMP-9 and TIMP-2 proteins. TGF-β1-enhanced migration and invasion capacities were blocked by p38MAPK, ERK1/2 and MMP inhibitors.Altogether, our results support that TGF-β1 modulates the mRNA and protein levels of MMPs (MMP-2 and MMP-9) as much as their inhibitors (TIMP-2 and RECK). Therefore, this cytokine plays a crucial role in breast cancer progression by modulating key elements of ECM homeostasis control. Thus, although the complexity of this signaling network, TGF-β1 still remains a promising target for breast cancer treatment.Breast cancer is a worldwide health problem for women, since it is the first in incidence and the second in mortality among cancer types [1]. Similarly to the majority of solid tumors, the mai
Correlation between MMPs and their inhibitors in breast cancer tumor tissue specimens and in cell lines with different metastatic potential
Rita CS Figueira, Luciana R Gomes, Jo?o S Neto, Fabricio C Silva, Ismael DCG Silva, Mari C Sogayar
BMC Cancer , 2009, DOI: 10.1186/1471-2407-9-20
Abstract: We analyzed the expression levels of MMP-2, MMP-9 and MMP-14 and their inhibitors (TIMP-1, TIMP-2 and RECK) by quantitative RT-PCR (qRT-PCR) in five human breast cancer cell lines presenting increased invasiveness and metastatic potential, 72 primary breast tumors and 30 adjacent normal tissues. Moreover, the role of cell-extracellular matrix elements interactions in the regulation of expression and activity of MMPs and their inhibitors was analyzed by culturing these cell lines on plastic or on artificial ECM (Matrigel).The results demonstrated that MMPs mRNA expression levels displayed a positive and statistically significant correlation with the transcriptional expression levels of their inhibitors both in the cell line models and in the tumor tissue samples. Furthermore, the expression of all MMP inhibitors was modulated by cell-Matrigel contact only in highly invasive and metastatic cell lines. The enzyme/inhibitor balance at the transcriptional level significantly favors the enzyme which is more evident in tumor than in adjacent non-tumor tissue samples.Our results suggest that the expression of MMPs and their inhibitors, at least at the transcriptional level, might be regulated by common factors and signaling pathways. Therefore, the multi-factorial analysis of these molecules could provide new and independent prognostic information contributing to the determination of more adequate therapy strategies for each patient.Among diverse cancer types, breast carcinoma stands out for its increasing incidence rates and high mortality worldwide [1]. Like most solid tumors, metastatic disease rather than the primary tumor itself is responsible for death [2-4]. The metastatic process involves a complex cascade of events, including the organized breakdown of the extracellular matrix (ECM) by matrix metalloproteinases (MMPs) [5,6]. Together, the MMPs are able to process or degrade all ECM components. Each ECM element is cleaved by a specific MMP or MMP group [7]. The acti
Toll-like receptor 4 (TLR4) expression in human and murine pancreatic beta-cells affects cell viability and insulin homeostasis
Humberto M Garay-Malpartida, Roberta F Mour?o, Marluce Mantovani, Icaro A Santos, Mari C Sogayar, Anna C Goldberg
BMC Immunology , 2011, DOI: 10.1186/1471-2172-12-18
Abstract: CD11b positive macrophages were practically absent from isolated human islets obtained from non-diabetic brain-dead donors, and TLR4 mRNA and cell surface expression were restricted to β-cells. A significant loss of cell viability was observed in these β-cells indicating a possible relationship with TLR4 expression. Monitoring gene expression in β-cells exposed for 48h to the prototypical TLR4 ligand LPS showed a concentration-dependent increase in TLR4 and CD14 transcripts and decreased insulin content and secretion. TLR4-positive MIN6 cells were also LPS-responsive, increasing TLR4 and CD14 mRNA levels and decreasing cell viability and insulin content.Taken together, our data indicate a novel function for TLR4 as a molecule capable of altering homeostasis of pancreatic β-cells.Islets are small organ-like structures, which are rich in vasculature and are predominantly constituted of insulin-secreting β-cells and glucagon-producing α-cells. As the main target of autoimmunity that results in type 1 diabetes, β-cells have been the subject of numerous studies aiming to identify the mechanisms which cause the massive cell death that ultimately leads to overt disease. In the setting of autoimmunity, β-cells respond to the onslaught of proinflammatory cytokines produced by immune cells, such as interleukin (IL)-1β, tumor necrosis factor (TNF) -α and interferon- γ, which trigger the NF-κB pathway and promote transcription of genes that ultimately cause β-cell dysfunction and cell death [1].A promising treatment for type 1 diabetes is islet cell transplantation [2]. To this end, pancreata from brain-dead non-diabetic donors are selected and islets are harvested and purified in clean room facilities for infusion into the portal vein of diabetic patients. However, the isolation procedure employed to obtain purified islets is time-consuming and frequently fails to produce sufficient good quality islets to enable a successful engraftment. The low yield during the isolation proc
Androgen responsive intronic non-coding RNAs
Rodrigo Louro, Helder I Nakaya, Paulo P Amaral, Fernanda Festa, Mari C Sogayar, Aline M da Silva, Sergio Verjovski-Almeida, Eduardo M Reis
BMC Biology , 2007, DOI: 10.1186/1741-7007-5-4
Abstract: Using a custom-built cDNA microarray enriched in intronic transcribed sequences, we found 39 intronic non-coding RNAs for which levels were significantly regulated by androgen exposure. Orientation-specific reverse transcription-PCR indicated that 10 of the 13 were transcribed in the antisense direction. These transcripts are long (0.5–5 kb), unspliced and apparently do not code for proteins. Interestingly, we found that the relative levels of androgen-regulated intronic transcripts could be correlated with the levels of the corresponding protein-coding gene (asGAS6 and asDNAJC3) or with the alternative usage of exons (asKDELR2 and asITGA6) in the corresponding protein-coding transcripts. Binding of the androgen receptor to a putative regulatory region upstream from asMYO5A, an androgen-regulated antisense intronic transcript, was confirmed by chromatin immunoprecipitation.Altogether, these results indicate that at least a fraction of naturally transcribed intronic non-coding RNAs may be regulated by common physiological signals such as hormones, and further corroborate the notion that the intronic complement of the transcriptome play functional roles in the human gene-expression program.Non-coding RNAs (ncRNAs), particularly those transcribed from genomic regions spanning introns of spliced genes, have been proposed as a fundamental advance in the genetic operating system of higher organisms by influencing the genomic program of differentiation and development in individuals and species [1,2]. Many functions, such as transcriptional or translational regulation, RNA splicing, gene silencing, imprinting and dosage compensation, have been assigned to mammalian ncRNAs [3]. Most functionally characterized ncRNAs belong to classes of small RNAs such as microRNAs [4] and small nucleolar RNAs (snoRNAs) [5]. While several novel long ncRNAs have been described in mammalian organisms [6,7] few have been characterized in more detail, the ~15 kb Xist RNA involved in inactivatio
Modeling gene expression regulatory networks with the sparse vector autoregressive model
André Fujita, Jo?o R Sato, Humberto M Garay-Malpartida, Rui Yamaguchi, Satoru Miyano, Mari C Sogayar, Carlos E Ferreira
BMC Systems Biology , 2007, DOI: 10.1186/1752-0509-1-39
Abstract: We have applied the Sparse Vector Autoregressive model to estimate gene regulatory networks based on gene expression profiles obtained from time-series microarray experiments. Through extensive simulations, by applying the SVAR method to artificial regulatory networks, we show that SVAR can infer true positive edges even under conditions in which the number of samples is smaller than the number of genes. Moreover, it is possible to control for false positives, a significant advantage when compared to other methods described in the literature, which are based on ranks or score functions. By applying SVAR to actual HeLa cell cycle gene expression data, we were able to identify well known transcription factor targets.The proposed SVAR method is able to model gene regulatory networks in frequent situations in which the number of samples is lower than the number of genes, making it possible to naturally infer partial Granger causalities without any a priori information. In addition, we present a statistical test to control the false discovery rate, which was not previously possible using other gene regulatory network models.In order to understand cell functioning as a whole, it is necessary to describe, at the molecular level, how gene products interact with each other. This could help to identify new target genes and to design new drugs for treatment of several diseases [1-3]. Due to the high number of genes involved in these networks, activating or suppressing feedback loops, the dynamics of their interactions is very complex and difficult to infer.With the development of high-throughput technologies, such as DNA microarrays, it is possible to simultaneously analyze the expression of up to thousands of genes and to construct gene networks based on inferences over gene expression data.Several methods to model genetic networks were proposed in the last few years, such as the Bayesian networks [4-8], Structural Equation Models [9], Probabilistic Boolean Networks [10-12],
Generation and characterization of human insulin-releasing cell lines
Leticia Labriola, Maria G Peters, Karin Krogh, Iván Stigliano, Letícia F Terra, Cecilia Buchanan, Marcel CC Machado, Elisa Joffé, Lydia Puricelli, Mari C Sogayar
BMC Cell Biology , 2009, DOI: 10.1186/1471-2121-10-49
Abstract: We generated ex-vivo primary cultures from two independent human insulinomas and from a human nesidioblastosis, all of which were cultured up to passage number 20. All cell lines secreted human insulin and C-peptide. These cell lines expressed neuroendocrine and islets markers, confirming the expression profile found in the biopsies. Although all beta cell lineages survived an anchorage independent culture, none of them were able to invade an extracellular matrix substrate.We have established three human insulin-releasing cell lines which maintain antigenic characteristics and insulin secretion profiles of the original tumors. These cell lines represent valuable tools for the study of molecular events underlying beta cell function and dysfunction.A major obstacle in beta cell research has been the lack of a human pancreatic beta cell line that is functionally equivalent to primary normal or neoplastic beta cells because of difficulties in obtaining and culturing them for long periods of time [1,2]. Therefore, animal insulinoma cell lines are widely used to study both physiological and pathophysiological mechanisms involved in glucose metabolism and to establish in vitro models for the beta cell damage occurring in type 1 diabetes [3-8]. Nevertheless, recent studies comparing sequences that lie upstream of, or flank the transcription start site of the insulin gene among different species, led to the conclusion that the rodent promoters are markedly different from the human one, urging caution in extrapolating data from rodent promoter studies to the etiology and therapy of diabetes [9].Insulinomas are the most common pancreatic islet cell tumors, arising from the beta cells within the islets of Langerhans. Most of them are sporadic [10] and small, displaying a benign behaviour, but still cause substantial morbidity since they produce excessive amounts of hormones. In fact, their key hallmark is uncontrolled insulin secretion, despite hypoglycemia. Compared with norma
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