Rodrigo Atique

Universidade de São Paulo

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Maria Rita Passos‐Bueno

Universidade de São Paulo

Felipe Augusto André Ishiy

Almac (United Kingdom)

Roberto D. Fanganiello

Université Laval

Nivaldo Alonso

Universidade de São Paulo

Erika Yeh

University of California, San Francisco

Hamilton Matushita

Universidade de São Paulo

Kátia M. Rocha

Universidade de São Paulo

Eduardo Calpena

University of Oxford

Andrew T. Timberlake

NYU Langone Health

Carla Rosenberg

Universidade de São Paulo

Cooperative Institutions

Universidade de São Paulo

Instituto Biológico

University of Oxford

John Radcliffe Hospital

MRC Weatherall Institute of Molecular Medicine

Universidade Federal do Espírito Santo

Boston Children's Hospital

Escola Superior de Ciências da Santa Casa de Misericórdia de Vitória

Universidade Brasil

Yale University

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Dissecting Major Signaling Pathways throughout the Development of Prostate Cancer

Prostate Cancer (2013)

Henrique B. da Silva Eduardo P. Amaral Eduardo Lima Nolasco Nathália Cruz de Victo Rodrigo Atique

Prostate cancer (PCa) is one of the most common malignancies found in males. The development of PCa involves several mutations in prostate epithelial cells, usually linked to developmental changes, such as enhanced resistance to apoptotic death, constitutive proliferation, and, in some cases, to differentiation into an androgen deprivation-resistant phenotype, leading to the appearance of castration-resistant PCa (CRPCa), which leads to a poor prognosis in patients. In this review, we summarize recent findings concerning the main deregulations into signaling pathways that will lead to the development of PCa and/or CRPCa. Key mutations in some pathway molecules are often linked to a higher prevalence of PCa, by directly affecting the respective cascade and, in some cases, by deregulating a cross-talk node or junction along the pathways. We also discuss the possible environmental and nonenvironmental inducers for these mutations, as well as the potential therapeutic strategies targeting these signaling pathways. A better understanding of how some risk factors induce deregulation of these signaling pathways, as well as how these deregulated pathways affect the development of PCa and CRPCa, will further help in the development of new treatments and prevention strategies for this disease.

10.1155/2013/920612

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Citations (65)

Optimization of Parameters for a More Efficient Use of Adipose-Derived Stem Cells in Regenerative Medicine Therapies

Stem Cells International (2012)

Meire Aguena Roberto D. Fanganiello Luiz Alexandre Lorico Tissiani Felipe Augusto André Ishiy Rodrigo Atique

Adipose tissue-derived stem cells (ASCs) association to fat in autologous lipotransfer is promising for a more effective soft tissue reconstruction, and optimization of protocols to isolate ASCs from lipoaspirate fat is much needed. We demonstrated that an increase in adipocyte differentiation is dependent on the number of ASCs. In a sample of 10 donors, we found a higher concentration of nucleated cells in the lower abdomen compared to flank (P=0.015). In a sample of 6 donors we did not find differences in the cell yield obtained by manual or pump-assisted aspiration (P=0.56). We suggest that the increase in the number of ASCs in the reinjected fat may enhance the efficiency of newly formed adipose tissue and that the anatomical region from which to harvest fat tissue needs to be considered to optimize the number of ASCs in the harvested tissue. Finally, pump-assisted aspiration can be used without any significant harm to the viability of cells.

Regenerative Medicine

10.1155/2012/303610

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Citations (56)

FGFR2 Mutation Confers a Less Drastic Gain of Function in Mesenchymal Stem Cells Than in Fibroblasts

Stem Cell Reviews and Reports (2011)

Erika Yeh Rodrigo Atique Felipe Augusto André Ishiy Roberto D. Fanganiello Nivaldo Alonso

Gain-of-function mutations in FGFR2 cause Apert syndrome (AS), a disease characterized by craniosynostosis and limb bone defects both due to abnormalities in bone differentiation and remodeling. Although the periosteum is an important cell source for bone remodeling, its role in craniosynostosis remains poorly characterized. We hypothesized that periosteal mesenchymal stem cells (MSCs) and fibroblasts from AS patients have abnormal cell phenotypes that contribute to the recurrent fusion of the coronal sutures. MSCs and fibroblasts were obtained from the periostea of 3 AS patients (S252W) and 3 control individuals (WT). We evaluated the proliferation, migration, and osteogenic differentiation of these cells. Interestingly, S252W mutation had opposite effects on different cell types: S252W MSCs proliferated less than WT MSCs, while S252W fibroblasts proliferated more than WT fibroblasts. Under restrictive media conditions, only S252W fibroblasts showed enhanced migration. The presence of S252W mutation increased in vitro and in vivo osteogenic differentiation in both studied cell types, though the difference compared to WT cells was more pronounced in S252W fibroblasts. This osteogenic differentiation was reversed through inhibition of JNK. We demonstrated that S252W fibroblasts can induce osteogenic differentiation in periosteal MSCs but not in MSCs from another tissue. MSCs and fibroblasts responded differently to the pathogenic effects of the FGFR2(S252W) mutation. We propose that cells from the periosteum have a more important role in the premature fusion of cranial sutures than previously thought and that molecules in JNK pathway are strong candidates for the treatment of AS patients.

Gain of function

10.1007/s12015-011-9327-6

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Citations (16)

Erratum to: FGFR2 Mutation Confers a Less Drastic Gain of Function in Mesenchymal Stem Cells than in Fibroblasts

Stem Cell Reviews and Reports (2013)

Erika Yeh Rodrigo Atique Felipe Augusto André Ishiy Roberto D. Fanganiello Nivaldo Alonso

Gain of function

10.1007/s12015-013-9470-3

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Cell Type-Dependent Nonspecific Fibroblast Growth Factor Signaling in Apert Syndrome

Stem Cells and Development (2016)

Erika Yeh Rodrigo Atique Roberto D. Fanganiello Daniele Yumi Sunaga Felipe Augusto André Ishiy

Apert Syndrome (AS) is one of the most severe forms of craniosynostosis. It is caused by gain-of-function mutations in the receptor fibroblast growth factor receptor 2 (FGFR2), which leads to ligand-receptor promiscuity. Here, we aimed to better understand the behavior of mesenchymal stem cells (MSCs) and of fibroblastoid cells, cellular populations that are part of the suture complex, when stimulated with different fibroblast growth factors (FGFs). We also aimed to verify whether FGFR2 specificity loss due to AS mutations would change their signaling behavior. We tested this hypothesis through cell proliferation and differentiation assays and through gene expression profiling. We found that FGF19 and FGF10 increase proliferation of fibroblastoid cells harboring the FGFR2 p.S252W mutation, but not of mutant MSCs. FGF19 and FGF10 were associated with different expression profiles in p.S252W cells. Further, in accordance to our gene expression microarray data, FGF19 decreases bone differentiation rate of mutant fibroblastoid cells and increases bone differentiation rate of MSCs. This effect in osteogenesis appears to be mediated by BMP signaling. The present data indicate that non-natural FGFR2 ligands, such as FGF10 and FGF19, are important factors in the pathophysiology of AS. Further research is needed to determine the role of modulation of MSC proliferation or use of FGF19 or anti-BMP2 as inhibitors of osteogenesis in AS subjects' cells, and whether these findings can be used in the clinical management of AS.

Apert syndrome

10.1089/scd.2016.0018

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Citations (5)

Craniosynostosis in 10q26 deletion patients: A consequence of brain underdevelopment or altered suture biology?

American Journal of Medical Genetics Part A (2015)

Ágatha Cristhina Oliveira Faria Eliete Rabbi‐Bortolini Maria R. G. O. Rebouças Andréia L. A. de S. Thiago Pereira Milena G. Tonini Frasson

Approximately a hundred patients with terminal 10q deletions have been described. They present with a wide range of clinical features always accompanied by delayed development, intellectual disability and craniofacial dysmorphisms. Here, we report a girl and a boy with craniosynostosis, developmental delay and other congenital anomalies. Karyotyping and molecular analysis including Multiplex Ligation dependent probe amplification (MLPA) and Array Comparative Genomic Hybridization (aCGH) were performed in both patients. We detected a 13.1 Mb pure deletion at 10q26.12-q26.3 in the girl and a 10.9 Mb pure deletion at 10q26.13-q26.3 in the boy, both encompassing about 100 genes. The clinical and molecular findings in these patients reinforce the importance of the DOCK1 smallest region of overlap I (SRO I), previously suggested to explain the clinical signs, and together with a review of the literature suggest a second 3.5 Mb region important for the phenotype (SRO II). Genotype-phenotype correlations and literature data suggest that the craniosynostosis is not directly related to dysregulated signaling in suture development, but may be secondary to alterations in brain development instead. Further, genes at 10q26 may be involved in the molecular crosstalk between brain and cranial vault.

Comparative genomic hybridization

Cranial vault

Craniosynostoses

Craniofacial abnormality

10.1002/ajmg.a.37448

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Citations (14)

Unexpected role of SIX1 variants in craniosynostosis: expanding the phenotype of SIX1-related disorders

Journal of Medical Genetics (2021)

Eduardo Calpena Maud Wurmser Simon J. McGowan Rodrigo Atique Débora Romeo Bertola

Pathogenic heterozygous

Craniosynostoses

10.1136/jmedgenet-2020-107459

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Citations (8)