http://sedici.unlp.edu.ar:80/handle/10915/125295 Fri, 30 Oct 2026 03:54:41 GMT 2026-10-30T03:54:41Z http://sedici.unlp.edu.ar:80/handle/10915/131291 Articulo Physiological Mini Reviews (PMR); vol. 6, no. 7 Autophagy plays an important role in human pathologies, such as miopathies and neurodegenerative diseases. Moreover, metabolic disease processes such as diabetes and pancreatitis, as well as tumor cells and cancer chemotherapy, activate autophagy. Furthermore, a selective type of autophagy of pancreatic zymogen granules has been discovered and characterized as a protective cellular process triggered by acute pancreatitis. In this review we describe the physiological bases and molecular mechanisms in the autophagic process and the possible role of autophagy in human disease. Understanding the events and molecular mechanisms of this complex cellular process will help in the design of new strategies for more effective diagnosis and treatment. Tue, 01 Jan 2013 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/131291 2013-01-01T00:00:00Z Autophagy plays an important role in human pathologies, such as miopathies and neurodegenerative diseases. Moreover, metabolic disease processes such as diabetes and pancreatitis, as well as tumor cells and cancer chemotherapy, activate autophagy. Furthermore, a selective type of autophagy of pancreatic zymogen granules has been discovered and characterized as a protective cellular process triggered by acute pancreatitis. In this review we describe the physiological bases and molecular mechanisms in the autophagic process and the possible role of autophagy in human disease. Understanding the events and molecular mechanisms of this complex cellular process will help in the design of new strategies for more effective diagnosis and treatment. http://sedici.unlp.edu.ar:80/handle/10915/131290 Articulo Physiological Mini Reviews (PMR); vol. 6, no. 6 In mammals, the sense of hearing relies on the normal function of two types of specialized cells: inner hair cells (IHC) and outer hair cells (OHC). They both possess the capacity to detect and convert mechanical movements within the cochlea, associated with sounds, into electrical potentials. A set of stereocilias in their apical end is where the mechano-electrical transduction actually occurs. IHC and OHC have very different functions within the complex process of hearing. IHC are responsible for transmitting the electrical information to the brain, for which they possess a specialized glutamatergic synapse with very unique properties. Neurotransmitter is released without pause and with high temporal precision, taking advantage of a synaptic organelle called the ribbon. OHC are exquisite piezoelectric devices, as changes in their membrane potential produce measurable changes in length. This capacity of OHC provides refined frequency selectivity and extra sensitivity to low intensity sounds. Interestingly, OHC function is regulated by an inhibitory innervation that descends from the brainstem and is mediated by acetylcholine. A very special type of nicotinic receptor, α9α10, participates in this synapse. Recent advances have shed light on the importance of this efferent control on acoustic trauma and higher hearing capabilities. Tue, 01 Jan 2013 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/131290 2013-01-01T00:00:00Z In mammals, the sense of hearing relies on the normal function of two types of specialized cells: inner hair cells (IHC) and outer hair cells (OHC). They both possess the capacity to detect and convert mechanical movements within the cochlea, associated with sounds, into electrical potentials. A set of stereocilias in their apical end is where the mechano-electrical transduction actually occurs. IHC and OHC have very different functions within the complex process of hearing. IHC are responsible for transmitting the electrical information to the brain, for which they possess a specialized glutamatergic synapse with very unique properties. Neurotransmitter is released without pause and with high temporal precision, taking advantage of a synaptic organelle called the ribbon. OHC are exquisite piezoelectric devices, as changes in their membrane potential produce measurable changes in length. This capacity of OHC provides refined frequency selectivity and extra sensitivity to low intensity sounds. Interestingly, OHC function is regulated by an inhibitory innervation that descends from the brainstem and is mediated by acetylcholine. A very special type of nicotinic receptor, α9α10, participates in this synapse. Recent advances have shed light on the importance of this efferent control on acoustic trauma and higher hearing capabilities. http://sedici.unlp.edu.ar:80/handle/10915/131287 Articulo Physiological Mini Reviews (PMR); vol. 6, no. 5 The coordinated release and reuptake of calcium into the sarcoplasmic reticulum (SR) is critical to maintain an adequate heart function. Reactive oxygen species (ROS) and reactive nitrogen species (RNS), generated in the heart under normal basal condition, modulate the function of different proteins via the reversible oxidation of critical cysteine residues. Excess ROS/RNS generation has been shown to impair heart function, but extensive evidence indicates that the controlled production of these molecules increases cardiac contractility by targeting SR calcium proteins. Ryanodine receptors (RyR2) are endogenously S-nitrosylated and S-glutathionylated and both redox modifications increase the activity of these channels in vitro. Moreover, exercise or rapid pacing increases the RyR2 S-glutathionylation, a modification that depends on the activation of NADPH oxidase (NOX2). In isolated cardiomyocytes, this enzyme is rapidly activated by stretch, generating an immediate burst of ROS which increases calcium release by RyR2. Nitroxyl, a particular ROS/RNS, increases cardiac inotropy in vivo, by targeting critical thiols in RyR2, the SR Ca2+-ATPase and phospholamban, allowing the simultaneous increase in calcium release and reuptake, required to produce a sustained increase in the calcium transient. In this minireview we present some of the recent work on the redox regulation of SR calcium cycling proteins. Tue, 01 Jan 2013 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/131287 2013-01-01T00:00:00Z The coordinated release and reuptake of calcium into the sarcoplasmic reticulum (SR) is critical to maintain an adequate heart function. Reactive oxygen species (ROS) and reactive nitrogen species (RNS), generated in the heart under normal basal condition, modulate the function of different proteins via the reversible oxidation of critical cysteine residues. Excess ROS/RNS generation has been shown to impair heart function, but extensive evidence indicates that the controlled production of these molecules increases cardiac contractility by targeting SR calcium proteins. Ryanodine receptors (RyR2) are endogenously S-nitrosylated and S-glutathionylated and both redox modifications increase the activity of these channels in vitro. Moreover, exercise or rapid pacing increases the RyR2 S-glutathionylation, a modification that depends on the activation of NADPH oxidase (NOX2). In isolated cardiomyocytes, this enzyme is rapidly activated by stretch, generating an immediate burst of ROS which increases calcium release by RyR2. Nitroxyl, a particular ROS/RNS, increases cardiac inotropy in vivo, by targeting critical thiols in RyR2, the SR Ca2+-ATPase and phospholamban, allowing the simultaneous increase in calcium release and reuptake, required to produce a sustained increase in the calcium transient. In this minireview we present some of the recent work on the redox regulation of SR calcium cycling proteins. http://sedici.unlp.edu.ar:80/handle/10915/131285 Articulo Physiological Mini Reviews (PMR); vol. 6, no. 3 Sodium is the main extracellular cation, and its osmotic pressure is an important determinant of the extracellular fluid volume. We were interested in the expression and functional characteristics of the epithelial sodium channel (ENaC) that mediates the Na+ entry into the cells from the luminal fluid in many reabsorbing epithelia and in the human placenta. Aldosterone is a key regulator of ENaC channel and stimulates protein methylation on the β-subunit of ENaC. Aldosterone and 8Br-cAMP promoted cellular migration in a wound healing model in trophoblastic BeWo cells. Amiloride blocked this effect. Electrophysiological studies showed an increase in ENaC current in the presence of aldosterone. We suggest that aldosterone positively influences wound healing through methylation of ENaC. On the other hand, we found a diminished expression of the three subunits of the ENaC in the membranes of preeclamptic placentas in comparison with the normal ones and this may have consequences for the cell migration and ion transport involved in the pathophysiology of preeclampsia. Tue, 01 Jan 2013 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/131285 2013-01-01T00:00:00Z Sodium is the main extracellular cation, and its osmotic pressure is an important determinant of the extracellular fluid volume. We were interested in the expression and functional characteristics of the epithelial sodium channel (ENaC) that mediates the Na+ entry into the cells from the luminal fluid in many reabsorbing epithelia and in the human placenta. Aldosterone is a key regulator of ENaC channel and stimulates protein methylation on the β-subunit of ENaC. Aldosterone and 8Br-cAMP promoted cellular migration in a wound healing model in trophoblastic BeWo cells. Amiloride blocked this effect. Electrophysiological studies showed an increase in ENaC current in the presence of aldosterone. We suggest that aldosterone positively influences wound healing through methylation of ENaC. On the other hand, we found a diminished expression of the three subunits of the ENaC in the membranes of preeclamptic placentas in comparison with the normal ones and this may have consequences for the cell migration and ion transport involved in the pathophysiology of preeclampsia. http://sedici.unlp.edu.ar:80/handle/10915/131281 Edicion de revista Physiological Mini Reviews (PMR); vol. 6, no. 2 Contiene el programa y los resúmenes de los trabajos presentados en el Congreso de la Sociedad Argentina de Fisiología, celebrado en la ciudad de Rosario (Santa Fe, Argentina), el 4 y 5 de octubre de 2012. Tue, 01 Jan 2013 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/131281 2013-01-01T00:00:00Z Contiene el programa y los resúmenes de los trabajos presentados en el Congreso de la Sociedad Argentina de Fisiología, celebrado en la ciudad de Rosario (Santa Fe, Argentina), el 4 y 5 de octubre de 2012. http://sedici.unlp.edu.ar:80/handle/10915/131279 Articulo Physiological Mini Reviews (PMR); vol. 6, no. 1 Thymulin is a thymic hormone exclusively produced by the thymic epithelial cells. After its discovery and initial characterization in the ‘70s, it was demonstrated that thymulin production and secretion is strongly influenced by the neuroendocrine system. Conversely, a growing core of information, to be reviewed here, points to thymulin as a hypophysiotropic peptide. Additionally, the substantial body of evidence pointing to thymulin and some synthetic analogs as anti-inflammatory and analgesic molecules in the brain and other organs will be also reviewed. In recent years, a synthetic DNA sequence coding for a biologically active analog of thymulin, metFTS, was constructed and cloned in different adenoviral vectors. A number of recent studies suggest that thymulin gene therapy may be a suitable therapeutic strategy to prevent some of the endocrine and reproductive alterations that typically appear in congenitally athymic (nude) mice, used as a suitable model of neuroendocrine and reproductive aging. Summing up, the present article briefly reviews the literature on the physiology of the thymulin-neuroendocrine axis and the anti-inflammatory properties of the molecule and its analogs. The availability of novel biotechnological tools should boost basic studies on the molecular biology of thymulin and should also allow an assessment of the potential of gene therapy to restore circulating thymulin levels in thymodeficient animal models and eventually, in humans. Sun, 01 Jan 2012 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/131279 2012-01-01T00:00:00Z Thymulin is a thymic hormone exclusively produced by the thymic epithelial cells. After its discovery and initial characterization in the ‘70s, it was demonstrated that thymulin production and secretion is strongly influenced by the neuroendocrine system. Conversely, a growing core of information, to be reviewed here, points to thymulin as a hypophysiotropic peptide. Additionally, the substantial body of evidence pointing to thymulin and some synthetic analogs as anti-inflammatory and analgesic molecules in the brain and other organs will be also reviewed. In recent years, a synthetic DNA sequence coding for a biologically active analog of thymulin, metFTS, was constructed and cloned in different adenoviral vectors. A number of recent studies suggest that thymulin gene therapy may be a suitable therapeutic strategy to prevent some of the endocrine and reproductive alterations that typically appear in congenitally athymic (nude) mice, used as a suitable model of neuroendocrine and reproductive aging. Summing up, the present article briefly reviews the literature on the physiology of the thymulin-neuroendocrine axis and the anti-inflammatory properties of the molecule and its analogs. The availability of novel biotechnological tools should boost basic studies on the molecular biology of thymulin and should also allow an assessment of the potential of gene therapy to restore circulating thymulin levels in thymodeficient animal models and eventually, in humans. http://sedici.unlp.edu.ar:80/handle/10915/104654 Articulo Physiological Mini Reviews; vol. 6, no. 4 To allow the control of their intracellular pH (pHi) and bicarbonate (HCO3 - ) levels, cells express HCO3 - transport proteins (NBC) that rapidly and selectively move HCO3 - across the plasma membrane. In the heart electroneutral NBCn1 and electrogenic NBCe1 Na+ /HCO3 - cotransporters facilitate the transmembrane movement of HCO3 - ions into cardiomyocytes, as a response to acid loading. NBCe1 associates with carbonic anhydrases (CA), the enzymes that catalyze the reversible conversion of CO2 to HCO3 - , to form a transport metabolon, a weakly associated complex of sequential metabolic enzymes. NBCe1 physically/functionally interact with the isoforms II, IV, and IX of CA, to increase the HCO3 - flux through cell membranes. NBCe1 and CAs interaction occurs in different cellular compartments in the heart muscle. Physiologically, the NBCe1/CA complex could contribute to the removal of H+ ions accumulated as the result of the contractile activity of the cardiac muscle cell, and this process may occur at the surface sarcolemma (CAII-NBCe1-CAIV complex) or at the ttubule (CAII-NBCe1-CAIX complex) of the cardiomyocyte. Pathologically, upregulation of the NBCe1/CA metabolon system upon ischemic/hypoxic conditions of the heart would favor the hypertrophic growth of the cardiac cells. Sun, 01 Jan 2012 00:00:00 GMT http://sedici.unlp.edu.ar:80/handle/10915/104654 2012-01-01T00:00:00Z To allow the control of their intracellular pH (pHi) and bicarbonate (HCO3 - ) levels, cells express HCO3 - transport proteins (NBC) that rapidly and selectively move HCO3 - across the plasma membrane. In the heart electroneutral NBCn1 and electrogenic NBCe1 Na+ /HCO3 - cotransporters facilitate the transmembrane movement of HCO3 - ions into cardiomyocytes, as a response to acid loading. NBCe1 associates with carbonic anhydrases (CA), the enzymes that catalyze the reversible conversion of CO2 to HCO3 - , to form a transport metabolon, a weakly associated complex of sequential metabolic enzymes. NBCe1 physically/functionally interact with the isoforms II, IV, and IX of CA, to increase the HCO3 - flux through cell membranes. NBCe1 and CAs interaction occurs in different cellular compartments in the heart muscle. Physiologically, the NBCe1/CA complex could contribute to the removal of H+ ions accumulated as the result of the contractile activity of the cardiac muscle cell, and this process may occur at the surface sarcolemma (CAII-NBCe1-CAIV complex) or at the ttubule (CAII-NBCe1-CAIX complex) of the cardiomyocyte. Pathologically, upregulation of the NBCe1/CA metabolon system upon ischemic/hypoxic conditions of the heart would favor the hypertrophic growth of the cardiac cells.