Percorrer por autor "Almeida, Joana"
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- Adipocyte proteome and secretome influence inflammatory and hormone pathways in gliomaPublication . Almeida, Joana; Costa, J.; Coelho, Pedro; Cea, V.; Galesio, M.; Noronha, J. P.; Diniz, M. S.; Prudêncio, Cristina; Soares, R.; Sala, C.; Fernandes, RúbenGliomas represent the most common primary malignant brain tumors in adults, with an extremely poor prognosis. Among several risk factors, lifestyle was also recently identified as a major risk factor for the development of primary glioma. In the present study, we explore the relationship between obesity and glioma in a cellular model. Thus, we have study the influence of adipocytes secretome on glioma cell line GL261. Using the 3T3-L1 adipocyte cell line, and its conditioned medium (adipokines-enriched medium), we showed that adipocyte-released factors relate with glioma angiogenic, growth, hormones and metabolic behavior by MALDI-TOF-MS and proteomic array analysis. In a first view, STI1, hnRNPs and PGK1 are under expressed on CGl. Similarly, both carbonic anhydrase and aldose reductase are even suppressed in glioma cells that grown under adipokines-enriched environment. Contrariwise, RFC1, KIF5C, ANXA2, N-RAP and RACK1 are overexpressed in GL261 cell the in the presence of the adipokines-enriched medium. We further identified the factors that are released by adipocyte cells, and revealed that several pro-inflammatory and angiogenic factors, such as IL-6, IL-11, LIF, PAI-1, TNF-α, endocan, HGF, VEGF IGF-I, were secreted to the medium into a high extent, whereas TIMP-1 and SerpinE1 were under expressed on CGl. This study discloses an interesting in vitro model for the study of glioma biology under a "obesity" environment, that can be explored for the understanding of cancer cells biology, for the search of biomarkers, prognostic markers and therapeutic approaches.
- Adipocyte-released factors enhance melanocyte’s proliferation and motilityPublication . Fernandes, Rúben; Coelho, Pedro; Almeida, Joana; Prudêncio, Cristina; Soares, RaquelObesity, favored by the modern lifestyle, acquired epidemic proportions nowadays. Obesity has been associated with various major causes of death and morbidity including malignant neoplasms. Cutaneous melanoma incidence rates have also been increasing uring the last four decades in several countries. Obesity involvement in melanoma etiology has been recognized, but the implicated mechanisms remain unclear. We propose to address the above relationship and investigate the mechanism interplaying between obesity and an increased risk of melanoma onset.
- Biomolecules in the relationship of cancer and obesityPublication . Almeida, Joana; Coelho, Pedro; Prudêncio, Cristina; Vieira, Mónica; Fernandes, Rúben; Fonseca, Magda; Soares, Raquel; Silva, Liliana; Faria, Isabel; Monteiro, Armanda; Pinto, Gabriela; Cea, V.; Galesio, M.; Noronha, J. P.; Diniz, M. S.; Sala, C.Obesity has been associated with various major causes of death and morbidity including malignant neoplasms. This increased prevalence has been accompanied by a worldwide increase in cutaneous melanoma incidence rates during the last decades, as well as gliomas, the most common primary malignant brain tumors in adults (Almeida et al., 2019). Although obesity aetiology is established, the implicated mechanisms remain unclear (Coelho et al., 2016). Melanoma is refractory to conventional therapies, and radiotherapy usage as an adjuvant therapy in cutaneous melanoma patients is ineffective, so it is extremely important to understand the antioxidant modulation of melanoma under an environment of obesity (Coelho et al., 2017; Oliveira et al., 2016). Moreover, the metastatic potential of some types of cancer is reduced or inhibited by obesity, which drives major concerns on the prognosis of metastasized patients (Fonseca et al., 2021). All of the studies disclose interesting models for the study of these tumors’ biology under an obese environment, that can be explored for the search of biomarkers, prognostic markers and therapeutic approaches.
- Biotechnology and biochemistry laboratorial education through the SARS-CoV2 pandemic: challenges, truths and takeawaysPublication . Almeida, Joana; Pereira, Cassilda; Coelho, Pedro; Teixeira, Dulce; Louçano, Marta; Bento, C.; Cerqueira, Maria João; Prudêncio, Cristina; Ferraz, Ricardo; Vieira, MónicaIn early 2020, the COVID-19 pandemic forced the higher education institutions to adapt to a new form of teaching and learning, from presential to full remote, blended and hybrid environment.
- Book of abstracts 4th Meeting on Medicinal Biotechnology (4EBtM)Publication . Costa, Ana Rita; Dias, Ana Rita; Prudêncio, Cristina; Borges, Cristina; Teixeira, Dulce; Almeida, Joana; Vieira, Mónica; Coelho, Pedro; Ferraz, Ricardo; Cunha, SofiaThese meetings have been held once a year since 2015 and have played an important role as a point of contact among several professionals and students in Medicinal Biotechnology. Like the Medicinal Biotechnology field itself, these meetings have also been expanding, not only in the number of participants, but also in their geographical origin. Therefore, it is our goal to act as an interface between students and biotechnology companies/researchers, as well as to increasingly promote networking, projects and collaborations within this field for the upcoming years.
- Book of Abstracts of 5th Meeting of Medicinal Biotechnology (5MBtM) and 2nd Iberian Congress on Medicinal BiotechnologyPublication . Sieiro, Carmen; Pereira, Cassilda; Prudêncio, Cristina; Oliveira, Daniela; Teixeira, Dulce; Barros, Eduarda; Almeida, Joana; Cerqueira, Maria João; Louçano, Marta; Vieira, Mónica; Coelho, Pedro; Ferraz, Ricardo
- Book of abstracts of the III Encontro de Biotecnologia Medicinal/ I Iberian Congress on Medicinal BiotechnologyPublication . Costa, Ana Rita; Prudêncio, Cristina; Teixeira, Dulce; Almeida, Joana; Vieira, Mónica; Coelho, Pedro; Ferraz, Ricardo; Cunha, Sofia; Dias, Ana RitaEstes encontros de Biotecnologia Medicinal iniciaram-se em 2015 e sentimos que estamos a crescer, tal como a Biotecnologia Medicinal. Esta área da Biotecnologia tem ganho relevância, quer em empresas, quer a nível académico, criando interfaces entre a biologia molecular, a microbiologia e a química medicinal.
- Effect of Adipocyte Secretome in Melanoma Progression and Vasculogenic MimicryPublication . Coelho, Pedro; Almeida, Joana; Prudêncio, Cristina; Fernandes, Rúben; Soares, RaquelObesity, favored by the modern lifestyle, acquired epidemic proportions nowadays. Obesity has been associated with various major causes of death and morbidity including malignant neoplasms. This increased prevalence has been accompanied by a worldwide increase in cutaneous melanoma incidence rates during the last decades. Obesity involvement in melanoma aetiology has been recognized, but the implicated mechanisms remain unclear. In the present study, we address this relationship and investigate the influence of adipocytes secretome on B16-F10 and MeWo melanoma cell lines. Using the 3T3-L1 adipocyte cell line, as well as ex vivo subcutaneous (SAT) and visceral (VAT) adipose tissue conditioned medium, we were able to show that adipocyte-released factors play a dual role in increasing melanoma cell overall survival, both by enhancing proliferation and decreasing apoptosis. B16-F10 cell migration and cell-cell and cell-matrix adhesion capacity were predominantly enhanced in the presence of SAT and VAT released factors. Melanocytes morphology and melanin content were also altered by exposure to adipocyte conditioned medium disclosing a more dedifferentiated phenotype of melanocytes. In addition, exposure to adipocyte-secreted molecules induced melanocytes to rearrange, on 3D cultures, into vessel-like structures, and generate characteristic vasculogenic mimicry patterns. These findings are corroborated by the released factors profile of 3T3-L1, SAT, and VAT assessed by microarrays, and led us to highlight the mechanisms by which adipose secretome from sub-cutaneous or visceral depots promote melanoma progression.
- Glioma behavior under the influence of Cinnamic Acid: a cellular approachPublication . Moreira, Ana; Almeida, Joana; Ferraz, Ricardo; Ferraz, RicardoCancer is one of the biggest health problems worldwide, characterized by uncontrolled proliferation, rapid growth and the ability to invade other tissues (1). Gliomas are highly challenging tu-mours from a therapeutic perspective, so new and more effective therapeutic strategies have been in-vestigated, with particular focus on the therapeu-tic potential of plant-derived compounds, such as Cinnamic Acid (2,3). Cinnamic Acid, extracted from Cinnamomum cassia, has proved to be a promising therapeutic agent, as it exhibits antitumor properties and low cytotoxicity toward healthy cells (4–6). This phenolic compound has the ability to cross the blood-brain barrier and affect tumour cell survival by reduc-ing their proliferation rate, inducing apoptosis and inhibiting key signalling pathways involved in tumour growth (7–9). This study aims to evaluate the glioma behaviour under the influence of cinnamic acid, using a GL261 cell model. To this end, cells were cultured and treated with different concentrations of cinnamic acid (1x10-3 mol/L to 4x10-3 mol/L), followed by in vi-tro assays to assess its impact on cell viability and cell migration. The MTT assay performed on the GL261 cell line demonstrated that Cinnamic Acid is capable of reducing cell viability at all tested concentrations, with a cytotoxic effect that tends to be dose-dependent. At lower concentrations (1x10-3 mol/L and 2x10-3 mol/L), cell viability was approximately 83% (SD=13,3% and 13,9%, respectively) and the most pronounced reduc-tion in cell viability was detected at the highest tested concentration (4x10-3 mol/L), with a viability of 76% ± 13,9%, corresponding to an approximately 24% re-duction relative to the control (viability of 100%).
- Linfangiogénese no tecido adiposo em modelos de doença inflamatória crónica (asma e obesidade): uma abordagem por imunohistoquímica e lipidómicaPublication . Almeida, Joana; Fernandes, Rúben; Soares, RaquelO tecido adiposo é um órgão endócrino dinâmico, secretando factores importantes na regulação do metabolismo, fluxo vascular sanguíneo e linfático, e função imunológica, entre outros. Em caso de acumulação de tecido adiposo por ingestão de uma dieta gorda, ou por disfunção metabólica, os adipócitos podem desencadear uma reacção inflamatória por falha na drenagem linfática, acumulando-se mediadores inflamatórios, os quais potenciam a propagação da reacção. Assim, questiona-se uma potencial associação entre o aumento de tecido adiposo na obesidade, hipóxia adipocitária e estimulação da linfangiogénese. Além disso, a expressão de adipocinas varia de acordo com a distribuição do tecido adiposo (subcutâneo, TAS e visceral, TAV). Deste modo, pretende-se com este estudo contribuir para o aumento do conhecimento sobre os complexos mecanismos moleculares subjacentes à linfangiogénese. Ensaios com ratinhos da estirpe C57Bl/6J (modelo de obesidade) e BALB/c (modelo de asma e obesidade), divididos em grupos submetidos a dieta normal e dieta rica em gordura. Avaliação semi-quantitativa da expressão tecidular de LYVE-1 (marcador da linfangiogénese) por imunohistoquímica em material embebido em parafina, no TAS e TAV, e cromatografia líquida de ultra-performance acoplada de espectrometria de massa (UPLC-MS) para análise da expressão plasmática de ceramida e esfingosina-1-fosfato (S1P). No modelo de obesidade observou- -se diminuição do número de vasos linfáticos e expressão de LYVE-1 ao longo do tempo no TAV, e aumento de ambos os parâmetros e hipertrofia adipocitária no TAS. As concentrações de ceramida e S1P corroboram a existência de um processo inflamatório nos ratinhos em estudo, ainda que numa fase muito inicial. No modelo de asma e obesidade, após 17 semanas de tratamento, observou-se incremento da linfangiogénese no TAV, mas não no TAS. A resposta inflamatória avaliada através dos diferentes parâmetros permite afirmar que num estadio inicial de obesidade a proliferação linfática poderá estar a ser retardada pela hipertrofia adipocitária. A libertação de adipocinas será observada apenas numa fase posterior, desencadeando todo o processo inflamatório que incrementará a proliferação linfática. Adicionalmente, é possível sugerir que a maior pressão à qual o TAV se encontra sujeito não favorece a proliferação linfática, pelo menos num estadio incial.
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