RETAMAL LUCERO, MAURICIO ANTONIO

Preferred name

Main Affiliation

Facultad de Medicina Clínica Alemana Universidad del Desarrollo

mretamal@udd.cl

ORCID

0000-0003-2562-6686

Scopus Author ID

8502472600

Goggle Scholar

https://scholar.google.com/citations?user=DSQ3d6YAAAAJ&hl=es&oi=ao

Now showing 1 - 10 of 76

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Astroglial gliotransmitters released via Cx43 hemichannels regulate NMDAR‐dependent transmission and short‐term fear memory in the basolateral amygdala
(2022)
Sergio Linsambarth
;
Francisco J. Carvajal
;
Rodrigo Moraga‐Amaro
;
Luis Mendez
;
Giovanni Tamburini
2Scopus© Citations 36
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Preface
(2024-01-01)
Mammano, Fabio
;
RETAMAL LUCERO, MAURICIO ANTONIO
1
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Molecular Interplay Between Non-Coding RNAs and Connexins and Its Possible Role in Cancer
(MDPI AG, 2025-03-12)
Pablo Pérez-Moreno
;
Juan P. Muñoz
;
RETAMAL LUCERO, MAURICIO ANTONIO
Non-coding RNAs (ncRNAs) are sequences that do not encode for proteins and play key roles in different cellular processes, including cell proliferation and differentiation. On the other hand, connexins (Cxs) are transmembrane proteins that principally allow intercellular communication. In pathological conditions such as cancer, there is a deregulation in the expression and/or function of ncRNAs and Cxs, which in turn leads to an enhancement in the aggressive phenotype, such as a greater proliferative and invasive capacity. This suggests a plausible interplay between ncRNAs and Cxs. Based on that, this review aims to summarize the current knowledge regarding this relationship and to analyze how it may influence the development of aggressive traits in cancer cells and the clinicopathological features of cancer patients. Finally, we discuss the potential of ncRNAs and Cxs as promising clinical biomarkers for cancer diagnosis, prognosis, and therapeutic targeting.
1
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Extracellular Cysteine in Connexins: Role as Redox Sensors
(2016)
RETAMAL LUCERO, MAURICIO ANTONIO
;
Isaac E. García
;
Bernardo I. Pinto
;
Amaury Pupo
;
David Báez
1Scopus© Citations 30
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Carbon Monoxide (CO) Is a Novel Inhibitor of Connexin Hemichannels
(2014)
Carmen G. León-Paravic
;
Vania A. Figueroa
;
Diego J. Guzmán
;
Carlos F. Valderrama
;
Antonio A. Vallejos
Scopus© Citations 30 1
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Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons
(2022)
Claudia M. Lucero
;
Juan Prieto-Villalobos
;
Lucas Marambio-Ruiz
;
Javiera Balmazabal
;
Tanhia F. Alvear
<jats:p>Hypertension is one of the most common risk factors for developing chronic cardiovascular diseases, including hypertensive nephropathy. Within the glomerulus, hypertension causes damage and activation of mesangial cells (MCs), eliciting the production of large amounts of vasoactive and proinflammatory agents. Accordingly, the activation of AT1 receptors by the vasoactive molecule angiotensin II (AngII) contributes to the pathogenesis of renal damage, which is mediated mostly by the dysfunction of intracellular Ca2+ ([Ca2+]i) signaling. Similarly, inflammation entails complex processes, where [Ca2+]i also play crucial roles. Deregulation of this second messenger increases cell damage and promotes fibrosis, reduces renal blood flow, and impairs the glomerular filtration barrier. In vertebrates, [Ca2+]i signaling depends, in part, on the activity of two families of large-pore channels: hemichannels and pannexons. Interestingly, the opening of these channels depends on [Ca2+]i signaling. In this review, we propose that the opening of channels formed by connexins and/or pannexins mediated by AngII induces the ATP release to the extracellular media, with the subsequent activation of purinergic receptors. This process could elicit Ca2+ overload and constitute a feed-forward mechanism, leading to kidney damage.</jats:p>
5Scopus© Citations 23
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Platinum analogs from a chemical and biological point of view
(2022-10-06)
CAMPODONICO GALDAMES, PAOLA ROSSANA
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RETAMAL LUCERO, MAURICIO ANTONIO
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Cortés Fuentes, Ignacio
;
Gormaz, Juan G.
1
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Dataset - The role of astrocytes in depression, its prevention, and treatment by targeting astroglial gliotransmitter release
(GitHub, 2024)
RETAMAL LUCERO, MAURICIO ANTONIO
;
ALARCÓN, RODRIGO
2
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Cardiac remodeling and arrhythmogenesis are ameliorated by administration of Cx43 mimetic peptide Gap27 in heart failure rats
(2020)
Claudia M. Lucero
;
David C. Andrade
;
Camilo Toledo
;
Hugo S. Díaz
;
Katherin V. Pereyra
<jats:title>Abstract</jats:title><jats:p>Alterations in connexins and specifically in 43 isoform (Cx43) in the heart have been associated with a high incidence of arrhythmogenesis and sudden death in several cardiac diseases. We propose to determine salutary effect of Cx43 mimetic peptide Gap27 in the progression of heart failure. High-output heart failure was induced by volume overload using the arterio-venous fistula model (AV-Shunt) in adult male rats. Four weeks after AV-Shunt surgery, the Cx43 mimetic peptide Gap27 or scrambled peptide, were administered via osmotic minipumps (AV-Shunt<jats:sub>Gap27</jats:sub> or AV-Shunt<jats:sub>Scr</jats:sub>) for 4 weeks. Cardiac volumes, arrhythmias, function and remodeling were determined at 8 weeks after AV-Shunt surgeries. At 8<jats:sup>th</jats:sup> week, AV-Shunt<jats:sub>Gap27</jats:sub> showed a marked decrease in the progression of cardiac deterioration and showed a significant improvement in cardiac functions measured by intraventricular pressure-volume loops. Furthermore, AV-Shunt<jats:sub>Gap27</jats:sub> showed less cardiac arrhythmogenesis and cardiac hypertrophy index compared to AV-Shunt<jats:sub>Scr</jats:sub>. Gap27 treatment results in no change Cx43 expression in the heart of AV-Shunt rats. Our results strongly suggest that Cx43 play a pivotal role in the progression of cardiac dysfunction and arrhythmogenesis in high-output heart failure; furthermore, support the use of Cx43 mimetic peptide Gap27 as an effective therapeutic tool to reduce the progression of cardiac dysfunction in high-output heart failure.</jats:p>
1Scopus© Citations 31
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GABAergic Regulation of Astroglial Gliotransmission through Cx43 Hemichannels
(2022)
Ivanka Jiménez-Dinamarca
;
Rachel Reyes-Lizana
;
Yordan Lemunao-Inostroza
;
Kevin Cárdenas
;
Raimundo Castro-Lazo
<jats:p>Gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain. It is produced by interneurons and recycled by astrocytes. In neurons, GABA activates the influx of Cl- via the GABAA receptor or efflux or K+ via the GABAB receptor, inducing hyperpolarization and synaptic inhibition. In astrocytes, the activation of both GABAA and GABAB receptors induces an increase in intracellular Ca2+ and the release of glutamate and ATP. Connexin 43 (Cx43) hemichannels are among the main Ca2+-dependent cellular mechanisms for the astroglial release of glutamate and ATP. However, no study has evaluated the effect of GABA on astroglial Cx43 hemichannel activity and Cx43 hemichannel-mediated gliotransmission. Here we assessed the effects of GABA on Cx43 hemichannel activity in DI NCT1 rat astrocytes and hippocampal brain slices. We found that GABA induces a Ca2+-dependent increase in Cx43 hemichannel activity in astrocytes mediated by the GABAA receptor, as it was blunted by the GABAA receptor antagonist bicuculline but unaffected by GABAB receptor antagonist CGP55845. Moreover, GABA induced the Cx43 hemichannel-dependent release of glutamate and ATP, which was also prevented by bicuculline, but unaffected by CGP. Gliotransmission in response to GABA was also unaffected by pannexin 1 channel blockade. These results are discussed in terms of the possible role of astroglial Cx43 hemichannel-mediated glutamate and ATP release in regulating the excitatory/inhibitory balance in the brain and their possible contribution to psychiatric disorders.</jats:p>
17Scopus© Citations 16

RETAMAL LUCERO, MAURICIO ANTONIO

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