miR-383-5p, miR-181a-5p, and miR-181b-5p as Predictors of Response to First-Generation Somatostatin Receptor Ligands in Acromegaly.

Acromegaly is a chronic systemic disease caused in the vast majority of cases by growth hormone (GH)-secreting adenoma, with surgery being the first-line treatment. When a cure is not attained with surgery, first-generation somatostatin receptor ligands (fg-SRLs) are the most common medication prescribed. Predictors of response to fg-SRLs have been studied; however, they cannot fully predict the response to fg-SRL.

Adiponectin, the adiponectin paradox, and Alzheimer's Disease: Is this association biologically plausible?

Dementia, especially Alzheimer's Disease (AD) and vascular dementia, is a major public health problem that continues to expand in both economically emerging and hegemonic countries. In 2017, the World Alzheimer Report estimated that over 50 million people were living with dementia globally. Metabolic dysfunctions of brain structures such as the hippocampus and cerebral cortex have been implicated as risk factors for dementia.

Insights Into the Controversial Aspects of Adiponectin in Cardiometabolic Disorders.

In 2016, the World Health Organization estimated that more than 1.9 billion adults were overweight or obese. This impressive number shows that weight excess is pandemic.

GANT-61 Induces Autophagy and Apoptosis in Glioblastoma Cells despite their heterogeneity.

Glioblastoma (GBM) is the most common adult primary tumor of the CNS characterized by rapid growth and diffuse invasiveness into the brain parenchyma. The GBM resistance to chemotherapeutic drugs may be due to the presence of cancer stem cells (CSCs). The CSCs activate the same molecular pathways as healthy stem cells such as WNT, Sonic hedgehog (SHH), and Notch.

Palmitate treated-astrocyte conditioned medium contains increased glutathione and interferes in hypothalamic synaptic network in vitro.

Excessive fat consumption increases the level of fatty acids (FAs) in the blood, which reach the hypothalamus and damage the circuit related to energy balance. In the present study, we used palmitate in a primary culture of purified astrocytes to mimic the fat-rich environment found in obesity. Our results showed increased glial fibrillary acidic protein (GFAP) reactivity in hypothalamic astrocytes compared to cortical astrocytes.

Derivation of Functional Human Astrocytes from Cerebral Organoids.

Astrocytes play a critical role in the development and homeostasis of the central nervous system (CNS). Astrocyte dysfunction results in several neurological and degenerative diseases. However, a major challenge to our understanding of astrocyte physiology and pathology is the restriction of studies to animal models, human post-mortem brain tissues, or samples obtained from invasive surgical procedures.

TGF-β1 promotes cerebral cortex radial glia-astrocyte differentiation in vivo.

The major neural stem cell population in the developing cerebral cortex is composed of the radial glial cells, which generate glial cells and neurons. The mechanisms that modulate the maintenance of the radial glia (RG) stem cell phenotype, or its differentiation, are not yet completely understood. We previously demonstrated that the transforming growth factor-β1 (TGF-β1) promotes RG differentiation into astrocytes in vitro (Glia 2007; 55:1023-33) through activation of multiple canonical and non-canonical signaling pathways (Dev Neurosci 2012; 34:68-81).

LPA-primed astrocytes induce axonal outgrowth of cortical progenitors by activating PKA signaling pathways and modulating extracellular matrix proteins.

Lysophosphatidic acid (LPA) is one of the main membrane-derived lysophospholipids, inducing diverse cellular responses like cell proliferation, cell death inhibition, and cytoskeletal rearrangement, and thus is important in many biological processes. In the central nervous system (CNS), post-mitotic neurons release LPA extracellularly whereas astrocytes do not. Astrocytes play a key role in brain development and pathology, producing various cytokines, chemokines, growth factors, and extracellular matrix (ECM) components that act as molecular coordinators of neuron-glia communication.

Lycopene and beta-carotene induce growth inhibition and proapoptotic effects on ACTH-secreting pituitary adenoma cells.

Pituitary adenomas comprise approximately 10-15% of intracranial tumors and result in morbidity associated with altered hormonal patterns, therapy and compression of adjacent sella turcica structures. The use of functional foods containing carotenoids contributes to reduce the risk of chronic diseases such as cancer and vascular disorders. In this study, we evaluated the influence of different concentrations of beta-carotene and lycopene on cell viability, colony formation, cell cycle, apoptosis, hormone secretion, intercellular communication and expression of connexin 43, Skp2 and p27(kip1) in ACTH-secreting pituitary adenoma cells, the AtT20 cells, incubated for 48 and 96 h with these carotenoids.

Sphingosine 1-phosphate-primed astrocytes enhance differentiation of neuronal progenitor cells.

Sphingosine 1-phosphate (S1P) is a bioactive signaling lysophospholipid. Effects of S1P on proliferation, survival, migration, and differentiation have already been described; however, its role as a mediator of interactions between neurons and glial cells has been poorly explored. Here we describe effects of S1P, via the activation of its receptors in astrocytes, on the differentiation of neural progenitor cells (NPC) derived from either embryonic stem cells or the developing cerebral cortex.

Astrocytes treated by lysophosphatidic acid induce axonal outgrowth of cortical progenitors through extracellular matrix protein and epidermal growth factor signaling pathway.

Lysophosphatidic acid (LPA) plays important roles in many biological processes, such as brain development, oncogenesis and immune functions, via its specific receptors. We previously demonstrated that LPA-primed astrocytes induce neuronal commitment of cerebral cortical progenitors (Spohr et al. 2008).

Effect of thyroid hormone depletion on cultured murine cerebral cortex astrocytes.

Astrocytes play a crucial role in several steps of brain development, such as the proliferation of neural precursors, neuronal migration and differentiation, axonal growth, and synaptogenesis. Astrocyte generation and maturation is dramatically modulated by thyroid hormones (THs). Here, we propose a modified model for studying THs action on astroglial cells, in vitro.