Cláudia Cavadas

University of Coimbra

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Ana Rita Álvaro

University of Coimbra

Luís Pereira de Almeida

University of Coimbra

Joana Rosmaninho‐Salgado

University of Coimbra

Célia A. Aveleira

University of Coimbra

Eric Grouzmann

University of Lausanne

Magda M. Santana

University of Coimbra

António Francisco Ambrósio

University of Coimbra

Laetitia S. Gaspar

University of Coimbra

Sara Carmo‐Silva

Polytechnic Institute of Coimbra

Marisa Ferreira‐Marques

University of Coimbra

Cooperative Institutions

University of Coimbra

210

Inserm

162

Centre National de la Recherche Scientifique

148

Harvard University

129

University of Michigan–Ann Arbor

126

Chinese Academy of Sciences

Istituti di Ricovero e Cura a Carattere Scientifico

National Institutes of Health

Consejo Superior de Investigaciones Científicas

Instituto de Salud Carlos III

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Neuropeptide Y 1 and Y 5 receptors activation stimulate autophagic flux in mouse hypothalamic neurons

Neuropeptides (2016)

Mariana Botelho Célia A. Aveleira Sara Carmo‐Silva Jorge F. Pascoal Marisa Ferreira‐Marques

10.1016/j.npep.2015.11.035

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Citations (0)

Regulation of catecholamine release and tyrosine hydroxylase in human adrenal chromaffin cells by interleukin‐1β: role of neuropeptide Y and nitric oxide

Journal of Neurochemistry (2009)

Joana Rosmaninho‐Salgado Inês M. Araújo Ana Rita Álvaro A.F. Mendes Lígia Sousa-Ferreira

J. Neurochem . (2009) 109 , 911–922. Abstract Adrenal chromaffin cells synthesize and secrete catecholamines and neuropeptides that may regulate hormonal and paracrine signaling in stress and also during inflammation. The aim of our work was to study the role of the cytokine interleukin‐1β (IL‐1β) on catecholamine release and synthesis from primary cell cultures of human adrenal chromaffin cells. The effect of IL‐1β on neuropeptide Y (NPY) release and the intracellular pathways involved in catecholamine release evoked by IL‐1β and NPY were also investigated. We observed that IL‐1β increases the release of NPY, norepinephrine (NE), and epinephrine (EP) from human chromaffin cells. Moreover, the immunoneutralization of released NPY inhibits catecholamine release evoked by IL‐1β. Moreover, IL‐1β regulates catecholamine synthesis as the inhibition of tyrosine hydroxylase decreases IL‐1β‐evoked catecholamine release and the cytokine induces tyrosine hydroxylase Ser40 phosphorylation. Moreover, IL‐1β induces catecholamine release by a mitogen‐activated protein kinase (MAPK)‐dependent mechanism, and by nitric oxide synthase activation. Furthermore, MAPK, protein kinase C (PKC), protein kinase A (PKA), and nitric oxide (NO) production are involved in catecholamine release evoked by NPY. Using human chromaffin cells, our data suggest that IL‐1β, NPY, and nitric oxide (NO) may contribute to a regulatory loop between the immune and the adrenal systems, and this is relevant in pathological conditions such as infection, trauma, stress, or in hypertension.

Chromaffin cell

10.1111/j.1471-4159.2009.06023.x

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Citations (35)

Unraveling the impact of obstructive sleep apnea on senescent associate secretory phenotype

Branca Maria de Oliveira Santos Laetitia S. Gaspar Catarina Carvalhas-Almeida Ana Teresa Barros-Viegas Sara Carmo‐Silva

Introduction: Obstructive Sleep Apnea (OSA), one of the most common sleep disorders worldwide has been suggested to promote aging by inducing cellular and molecular aging mechanisms (Gaspar, et al. 2017). Understanding OSA putative effect on aging might contribute to understand new strategies to improve OSA diagnosis and treatment but also to counteract aging. Aim: To investigate cellular senescence and senescent associate secretory phenotype (SASP), a hallmark of aging, in OSA patients and the impact of OSA treatment. Methods: A cohort of 9 adult male patients diagnosed with severe OSA was followed from the moment of diagnosis with polysomnography (PSG), up to 4 months and 24 months of treatment with continuous pressure positive mask (CPAP). SASP biomarkers were evaluated in OSA patients in comparison to age-matched controls and younger controls, both validated by PSG. Results: OSA patients show a deregulation of pro- and anti-inflammatory cytokine levels, in comparison with age-matched and young controls, an effect that is no longer observed after treatment. In addition, OSA patients show alterations in extracellular vesicles release that are not fully re-established upon CPAP treatment. Conclusion: These results suggest that OSA might induce SASP. CPAP treatment might partially re-stablish some alterations. Hence, OSA early diagnosis and specific treatment may constitute a new strategy to delay ageing.

Extracellular Vesicles

Senescence

10.1183/23120541.sleepandbreathing-2021.82

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SIRT1 activation and its circadian clock control: a promising approach against (frailty in) neurodegenerative disorders

Aging Clinical and Experimental Research (2022)

Rodrigo F.N. Ribeiro Dina Pereira Luís Pereira de Almeida Maria Manuel Silva Cláudia Cavadas

SIRT2

10.1007/s40520-022-02257-y

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Citations (16)

Assessment of circadian rhythm markers and clock genes expression in patients with Chronic Insomnia

Sleep Medicine (2024)

Catarina Carvalhas-Almeida Branca Maria de Oliveira Santos L. Gaspar Maria João Ferreira Joana Serra

Chronic Insomnia

10.1016/j.sleep.2023.11.461

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Nuclear aging in polyglutamine-induced neurodegeneration

bioRxiv (Cold Spring Harbor Laboratory) (2023)

Dina Pereira Janete Cunha‐Santos Ana Vasconcelos‐Ferreira Joana Duarte‐Neves Isabel Onofre

Abstract Machado-Joseph disease (MJD) is an autosomal dominantly-inherited neurodegenerative disorder characterized by an over-repetition of the CAG trinucleotide of the ATXN3 gene, conferring a toxic gain-of-function to the resulting ataxin-3 protein. Despite the significant advances produced over the last years, the molecular mechanisms involved in MJD are still unclear and no treatment able to modify the disease progression is available. Aging is the major risk factor for neurodegenerative disorders, being associated with the occurrence and progression of several diseases, such as Alzheimer’s, Huntington’s, among others. The nuclear membrane proteins - lamins - and lamin-processing related proteins, such as ZMPSTE24, have been shown to be altered, not only during normal aging, but also in neurodegenerative disorders, such as Alzheimer’s disease. Taking this into account, we aimed at investigating the role of aging in MJD by evaluating the presence of age-related markers in human and animal MJD models. Decreased levels of lamins B and C, together with decreased ZMPSTE24 levels were identified in the different MJD models. Accordingly, abnormalities in nuclear circularity, a hallmark of aging, were also observed in a N2a MJD cellular model, supporting an age-related phenotype. Furthermore, overexpressing progerin, the abnormal lamin A, generated in Hutchinson Guilford Progeria Syndrome patients that present premature and accelerated aging, in a relevant brain area of a lentiviral MJD mouse model, induced an aggravation of MJD-associated neuropathology. Our results suggest that aging is a key player in the context of MJD pathogenesis, unveiling new pathways for the development of future therapies for the disease.

Progeria

Machado–Joseph disease

LMNA

10.1101/2023.06.09.544056

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Citations (1)

Neuropeptide Y stimulates retinal neural cell proliferation – involvement of nitric oxide

Journal of Neurochemistry (2008)

Ana Rita Álvaro João Martins Inês M. Araújo Joana Rosmaninho‐Salgado António Francisco Ambrósio

Abstract Neuropeptide Y (NPY) is a 36 amino acid peptide widely present in the CNS, including the retina. Previous studies have demonstrated that NPY promotes cell proliferation of rat post‐natal hippocampal and olfactory epithelium precursor cells. The aim of this work was to investigate the role of NPY on cell proliferation of rat retinal neural cells. For this purpose, primary retinal cell cultures expressing NPY, and NPY Y 1 , Y 2 , Y 4 and Y 5 receptors [Álvaro et al. , (2007) Neurochem. Int., 50, 757] were used. NPY (10–1000 nM) stimulated cell proliferation through the activation of NPY Y 1 , Y 2 and Y 5 receptors. NPY also increased the number of proliferating neuronal progenitor cells (BrdU + /nestin + cells). The intracellular mechanisms coupled to NPY receptors activation that mediate the increase in cell proliferation were also investigated. The stimulatory effect of NPY on cell proliferation was reduced by l ‐nitroarginine‐methyl‐esther ( l ‐NAME; 500 μM), a nitric oxide synthase inhibitor, 1H‐[1,2,4]oxadiazolo‐[4, 3‐a]quinoxalin‐1‐one (ODQ; 20 μM), a soluble guanylyl cyclase inhibitor or U0126 (1 μM), an inhibitor of the extracellular signal‐regulated kinase 1/2 (ERK 1/2). In conclusion, NPY stimulates retinal neural cell proliferation, and this effect is mediated through nitric oxide–cyclic GMP and ERK 1/2 pathways.

Soluble guanylyl cyclase

10.1111/j.1471-4159.2008.05334.x

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Citations (52)

In vitro susceptibility of Trypanosoma brucei brucei to selected essential oils and their major components

Experimental Parasitology (2018)

Sonya Costa Cláudia Cavadas Carlos Cavaleiro Lı́gia Salgueiro Maria do Céu Sousa

10.1016/j.exppara.2018.05.002

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Citations (28)

Neuropeptide Y protects ganglion cells against excitotoxicity and modulates microglia activation in the rat retina

Investigative Ophthalmology & Visual Science (2013)

António Francisco Ambrósio Filipe Elvas Maria Madeira Tiago Martins João Martins

Excitotoxicity

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Ataxin-2 in the hypothalamus at the crossroads between metabolism and clock genes

Journal of Molecular Endocrinology (2022)

Sara Carmo‐Silva Marisa Ferreira‐Marques Clévio Nóbrega Mariana Botelho Daniela G. Costa

ATXN2 gene, encoding for ataxin-2, is located in a trait locus for obesity. Atxn2 knockout (KO) mice are obese and insulin resistant; however, the cause for this phenotype is still unknown. Moreover, several findings suggest ataxin-2 as a metabolic regulator, but the role of this protein in the hypothalamus was never studied before. The aim of this work was to understand if ataxin-2 modulation in the hypothalamus could play a role in metabolic regulation. Ataxin-2 was overexpressed/re-established in the hypothalamus of C57Bl6/Atxn2 KO mice fed either a chow or a high-fat diet (HFD). This delivery was achieved through stereotaxic injection of lentiviral vectors encoding for ataxin-2. We show, for the first time, that HFD decreases ataxin-2 levels in mouse hypothalamus and liver. Specific hypothalamic ataxin-2 overexpression prevents HFD-induced obesity and insulin resistance. Ataxin-2 re-establishment in Atxn2 KO mice improved metabolic dysfunction without changing body weight. Furthermore, we observed altered clock gene expression in Atxn2 KO that might be causative of metabolic dysfunction. Interestingly, ataxin-2 hypothalamic re-establishment rescued these circadian alterations. Thus, ataxin-2 in the hypothalamus is a determinant for weight, insulin sensitivity and clock gene expression. Ataxin-2's potential role in the circadian clock, through the regulation of clock genes, might be a relevant mechanism to regulate metabolism. Overall, this work shows hypothalamic ataxin-2 as a new player in metabolism regulation, which might contribute to the development of new strategies for metabolic disorders.

10.1530/jme-21-0272

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Citations (6)