Percorrer por autor "Rodrigues, Joana"
A mostrar 1 - 4 de 4
Resultados por página
Opções de ordenação
- Ioxynil and diethylstilbestrol increase the risks of cardiovascular and thyroid dysfunction in zebrafishPublication . Li, Yi-Feng; Rodrigues, Joana; Campinho, Marco AntónioEndocrine disruption results from exposure to chemicals that alter the function of the endocrine system in animals. Chronic 60 days of exposure to a low dose (0.1 mu M) of ioxynil (IOX) or diethylstilbestrol (DES) via food was used to determine the effects of these chemicals on the physiology of the heart and thyroid follicles in juvenile zebrafish. Immunofluorescence analysis and subsequent 3D morphometric analysis of the zebrafish heart revealed that chronic exposure to IOX induced ventricle deformation and significant volume increase (p < 0.001). DES exposure caused a change in ventricle morphology, but volume was unaffected. Alongside, it was found that DES exposure upregulated endothelial related genes (angptl1b, mhc1lia, mybpc2a, ptgir, notch1b and vwf) involved in vascular homeostasis. Both IOX and DES exposure caused a change in thyroid follicle morphology. Notably, in IOX exposed juveniles, thyroid fol-licle hypertrophy was observed; and in DES-exposed fish, an enlarged thyroid field was present. In summary, chronic exposure of juvenile zebrafish to IOX and DES affected the heart and the thyroid. Given that both chemicals are able to change the morphology of the thyroid it indicates that they behave as endocrine disruptive chemicals (EDCs). Heart function dynamically changes thyroid morphology, and function and hence it is likely that the observed cardiac effects of IOX and DES are the source of altered thyroid status in these fish.
- Maternal thyroid hormone is required to develop the hindbrain vasculature in zebrafishPublication . Trindade, Marlene; Silva, Nádia; Rodrigues, Joana; Kawakami, Koichi; Campinho, Marco AntónioThyroid hormone (TH) signaling is important and necessary for proper neurodevelopment. Inadequate levels of maternally derived THs (MTH) supply affect target gene expression profiles, which are fundamental for the brain’s normal growth, maturation, and function. The monocarboxylate transporter 8 (SLC16A2, MCT8) is the main TH transporter present in the brain during embryonic development, and mutations in this transporter lead to a rare and debilitating human condition known as the Allan-Herndon-Dudley Syndrome (AHDS). This mutation affects the capacity for intracellular transport of the hormone, leading to impaired brain development that constitutes the main pathophysiological basis of AHDS. Like humans, zebrafish embryos express slc16a2 that transports exclusively T3 at zebrafish physiological temperature. Studies in zebrafish Mct8 knockdown (KD) models found impaired hindbrain vasculature development. Here, using zebrafish Mct8 KD and knockout (KO) models, we shed light on the maternal T3 (MT3)-dependent developmental mechanism behind hindbrain vasculature development. We first demonstrate that MT3-regulates hindbrain vegfaa expression. We provide evidence that hindbrain neurons are not the source of vegfaa, instead, restricted pax6a+ neuroprogenitor cells (NPCs) instruct central arteries (CtAs) ingression into the hindbrain. Therefore, MT3 acts as an integrator, providing the regulatory cues necessary for the timely ingression of the CtAs into the hindbrain.
- Unraveling the potential of gasotransmitters as neurogenic and neuroprotective molecules: focus on Alzheimer's and Parkinson's diseases.Publication . Simao, Sonia; Filipa Santos, Daniela; Teixeira, Mariana; Agostinho, Rafaela R.; Rodrigues, Joana; Vitorino, Marta; Araújo, Inês M.Alzheimer's disease and Parkinson's disease are the two most prevalent neurodegenerative disorders worldwide, both characterized by progressive neuronal loss. Despite distinct pathophysiological features, they share cellular dysfunctions such as abnormal protein aggregation, oxidative stress, and neuroinflammation, research into which might be beneficial for developing novel therapeutic strategies that could tackle both conditions. This review highlights the emerging role of the gasotransmitters nitric oxide, carbon monoxide and hydrogen sulfide as modulators of adult neurogenesis and neuroprotection in Alzheimer's disease and Parkinson's disease. We have gathered recent evidence demonstrating that these endogenous gases exert anti-inflammatory, antioxidant, and anti-apoptotic effects, and, critically, promote neurogenesis - suggesting a dual neuroprotective and neuroregenerative therapeutic potential. The unique physicochemical features of these gasotransmitters, including their ability to cross the blood-brain barrier and diffuse rapidly throughout the neural tissue, further support their suitability as candidates for innovative neuroregenerative treatments. While clinical translation remains challenging, harnessing the neurogenic and neuroprotective actions of these gasotransmitters may offer transformative avenues for addressing the increasing burden of Alzheimer's disease and Parkinson's disease.
- Unraveling the potential of gasotransmitters as neurogenic and neuroprotective molecules: focus on Alzheimer's and Parkinson's diseases.Publication . Simao, Sonia; Filipa Santos, Daniela; Teixeira, Mariana; Ribeiro Agostinho, Rafaela; Rodrigues, Joana; Vitorino, Marta; Pombinho de Araújo, Inês MariaAlzheimer's disease and Parkinson's disease are the two most prevalent neurodegenerative disorders worldwide, both characterized by progressive neuronal loss. Despite distinct pathophysiological features, they share cellular dysfunctions such as abnormal protein aggregation, oxidative stress, and neuroinflammation, research into which might be beneficial for developing novel therapeutic strategies that could tackle both conditions. This review highlights the emerging role of the gasotransmitters nitric oxide, carbon monoxide and hydrogen sulfide as modulators of adult neurogenesis and neuroprotection in Alzheimer's disease and Parkinson's disease. We have gathered recent evidence demonstrating that these endogenous gases exert anti-inflammatory, antioxidant, and anti-apoptotic effects, and, critically, promote neurogenesis - suggesting a dual neuroprotective and neuroregenerative therapeutic potential. The unique physicochemical features of these gasotransmitters, including their ability to cross the blood-brain barrier and diffuse rapidly throughout the neural tissue, further support their suitability as candidates for innovative neuroregenerative treatments. While clinical translation remains challenging, harnessing the neurogenic and neuroprotective actions of these gasotransmitters may offer transformative avenues for addressing the increasing burden of Alzheimer's disease and Parkinson's disease.