Luis A. Cea
Autonomous University of Chile
Internal medicinePannexinEndocrinologyGap junctionMembrane potentialChemistrySarcolemmaConnexonImmunologyMyocyteMuscle atrophyDenervationMuscular dystrophyDysferlinopathySkeletal muscleConnexinAtrophyExtracellularMembrane permeabilityDysferlinMyogenesisMutationPurinergic receptorIntracellularBiologyCell biology
22Publications
11H-index
388Citations
Publications 22
Newest
#1Luis A. CeaH-Index: 11
Last. Juan C. Sáez (CSIC: Spanish National Research Council)H-Index: 67
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Dysferlinopathies are muscle dystrophies caused by mutations in the gene encoding dysferlin, a relevant protein for membrane repair and trafficking. These diseases are untreatable, possibly due to the poor knowledge of relevant molecular targets. Previously, we have shown that human myofibers from patient biopsies as well as myotubes derived from immortalized human myoblasts carrying a mutated form of dysferlin express connexin proteins, but their relevance in myoblasts fate and function remaine...
2 CitationsSource
#2Guisselle Arias-Bravo (Autonomous University of Chile)H-Index: 1
Last. Luis A. CeaH-Index: 11
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Abstract Dysferlinopathy is a genetic human disease caused by mutations in the gene that encodes the dysferlin protein (DYSF). Dysferlin is believed to play a relevant role in cell membrane repair. However, in dysferlin-deficient (blAJ) mice (a model of dysferlinopathies) the recovery of the membrane resealing function by means of the expression of a mini-dysferlin does not arrest progressive muscular damage, suggesting the participation of other unknown pathogenic mechanisms. Here, we show that...
3 CitationsSource
#1Paz García-Campos (Valpo: Valparaiso University)H-Index: 1
#2Ximena Báez-Matus (Valpo: Valparaiso University)H-Index: 7
Last. Ana M. Cárdenas (Valpo: Valparaiso University)H-Index: 18
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Dysferlinopathy is an autosomal recessive muscular dystrophy resulting from mutations in the dysferlin gene. Absence of dysferlin in the sarcolemma and progressive muscle wasting are hallmarks of this disease. Signs of oxidative stress have been observed in skeletal muscles of dysferlinopathy patients, as well as in dysferlin-deficient mice. However, the contribution of the redox imbalance to this pathology and the efficacy of antioxidant therapy remain unclear. Here, we evaluated the effect of ...
1 CitationsSource
#1Elisa Balboa (UC: Pontifical Catholic University of Chile)H-Index: 9
#2Fujiko Saavedra (UC: Pontifical Catholic University of Chile)H-Index: 1
Last. Juan C. Sáez (CSIC: Spanish National Research Council)H-Index: 67
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Glucocorticoids are frequently used as anti-inflammatory and immunosuppressive agents. However, high doses and/or prolonged use induce undesired secondary effects such as muscular atrophy. Recently, de novo expression of connexin43 and connexin45 hemichannels (Cx43 HCs and Cx45 HCs, respectively) has been proposed to play a critical role in the mechanism underlying myofiber atrophy induced by dexamethasone (Dex: a synthetic glucocorticoid), but their involvement in specific muscle changes promot...
2 CitationsSource
#1Bruno A. Cisterna (University of Talca)H-Index: 12
#2Aníbal A. VargasH-Index: 9
Last. Juan C. Sáez (Valpo: Valparaiso University)H-Index: 6
view all 14 authors...
Denervation of skeletal muscles induces severe muscle atrophy, which is preceded by cellular alterations such as increased plasma membrane permeability, reduced resting membrane potential and accelerated protein catabolism. The factors that induce these changes remain unknown. Conversely, functional recovery following denervation depends on successful reinnervation. Here, we show that activation of nicotinic acetylcholine receptors (nAChRs) by quantal release of acetylcholine (ACh) from motoneur...
10 CitationsSource
#1Luis A. CeaH-Index: 11
#2Elisa Balboa (UC: Pontifical Catholic University of Chile)H-Index: 9
Last. Juan C. Sáez (CSIC: Spanish National Research Council)H-Index: 6
view all 8 authors...
Abstract Endotoxemia caused by bacterial lipopolysaccharides (LPSs) leads to severe skeletal muscular deterioration, starting with higher membrane permeability and decline in resting membrane potential (RMP). However, the molecular mechanism of such changes remains unclear. Here, we evaluated the possible involvement of connexin43- and conneixn45-based hemichannels (Cx43 and Cx45 HCs, respectively) as putative mediators of sarcolemmal dysfunctions induced by LPS in control (Cx43fl/flCx45fl/fl) a...
6 CitationsSource
#1Elisa Balboa (UC: Pontifical Catholic University of Chile)H-Index: 9
#2Fujiko Saavedra-Leiva (UC: Pontifical Catholic University of Chile)H-Index: 2
Last. Tomás RegueiraH-Index: 15
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Fondo Nacional de Ciencia y Tecnologia (FONDECYT) 1141092 1150291 FONDECYT 3160594 11160739 CONICYT/PAI 79140023 ICM-Economia Centro Interdisciplinario de Neurociencias de Valparaiso P09-022-F
7 CitationsSource
#1Aníbal A. Vargas (UC: Pontifical Catholic University of Chile)H-Index: 9
#2Bruno A. Cisterna (Valpo: Valparaiso University)H-Index: 12
Last. Juan C. Sáez (Valpo: Valparaiso University)H-Index: 67
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Although connexins (Cxs) are broadly expressed by cells of mammalian organisms, Cx39 has a very restricted pattern of expression and the biophysical properties of Cx39-based channels (hemichannels: HCs and gap junction channels: GJCs) remain largely unknown. Here, we used HeLa cells transfected with Cx39 (HeLa-Cx39 cells) in which intercellular electrical coupling was not detected, indicating the absence of GJCs. However, functional HCs were found on the surface of cells exposed to conditions kn...
13 CitationsSource
#1Luis A. Cea (University of Chile)H-Index: 11
#2Elisa Balboa (UC: Pontifical Catholic University of Chile)H-Index: 9
Last. Juan C. Sáez (Valpo: Valparaiso University)H-Index: 67
view all 8 authors...
Abstract Long-term treatment with high glucocorticoid doses induces skeletal muscle atrophy. However, the molecular mechanism of such atrophy remains unclear. We evaluated the possible involvement of connexin-based hemichannels (Cx HCs) in muscle atrophy induced by dexamethasone (DEX), a synthetic glucocorticoid, on control (Cx43 fl/fl Cx45 fl/fl ) and Cx43/Cx45 expression-deficient (Cx43 fl/fl Cx45 fl/fl :Myo-Cre) skeletal myofibers. Myofibers of Cx43 fl/fl Cx45 fl/fl mice treated with DEX (5 h...
20 CitationsSource
#1Sanjeev Sivakumar (BCM: Baylor College of Medicine)H-Index: 6
#2Fabio Silvio Taccone (Erasmus Hospital)H-Index: 70
Last. Lc Azevedo (USP: University of São Paulo)H-Index: 6
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Introduction In addition to systemic hemodynamics, the management of neurocritically ill patients is often informed by neuromonitoring. In the absence of high-level evidence clinicians are often guided by personal and local expertise. Little is known about practices as they pertain to the use of such monitoring in patients with acute brain injury (ABI). Objectives To investigate practices in bedside monitoring for ABI patients. Particularly interested in differences among “neurointensivists” (NI...
1 CitationsSource