Altered mitochondrial function, calcium signaling, and catecholamine release in chromaffin cells of diabetic and SHR rats

Musial, Diego Castro; Bomfim, Guilherme Henrique Souza; Arranz-Tagarro, Juan Alberto; Méndez-López, Iago; Miranda-Ferreira, Regiane; Jurkiewicz, Aron; Jurkiewicz, Neide Hyppolito; Garcı́a, Antonio G.; Padín, Juan Fernando

doi:10.1016/j.ejphar.2017.09.045

Cited by 11 publications

(4 citation statements)

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“…The mitochondria are the main production organelles and targets of ROS which mediate oxidative stress and apoptosis [34]. Ca 2+ is closely related to the regulation of the mitochondrial function [35]. Its uptake into the mitochondria is involved in buffering and influencing cytosolic Ca 2+ , energy metabolism, and even initiating cell apoptosis [36, 37].…”

Section: Discussionmentioning

confidence: 99%

High Glucose Enhances Bupivacaine-Induced Neurotoxicity via MCU-Mediated Oxidative Stress in SH-SY5Y Cells

Liu

Zhao

Lei

et al. 2019

Oxidative Medicine and Cellular Longevity

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Bupivacaine, a typical local anesthetic, induces neurotoxicity via reactive oxygen species regulation of apoptosis. High glucose could enhance bupivacaine-induced neurotoxicity through regulating oxidative stress, but the mechanism of it is not clear. Mitochondrial calcium uniporter (MCU), a key channel for regulating the mitochondrial Ca2+ (mCa2+) influx, is closely related to oxidative stress via disruption of mCa2+ homeostasis. Whether MCU is involved in high glucose-sensitized bupivacaine-induced neurotoxicity remains unknown. In this study, human neuroblastoma (SH-SY5Y) cells were cultured with high glucose and/or bupivacaine, and the data showed that high glucose enhanced bupivacaine-induced MCU expression elevation, mCa2+ accumulation, and oxidative damage. Next, Ru360, an inhibitor of MCU, was employed to pretreated SH-SY5Y cells, and the results showed that it could decrease high glucose and bupivacaine-induced mCa2+ accumulation, oxidative stress, and apoptosis. Further, with the knockdown of MCU with a specific small interfering RNA (siRNA) in SH-SY5Y cells, we found that it also could inhibit high glucose and bupivacaine-induced mCa2+ accumulation, oxidative stress, and apoptosis. We propose that downregulation expression or activity inhibition of the MCU channel might be useful for restoring the mitochondrial function and combating high glucose and bupivacaine-induced neurotoxicity. In conclusion, our study demonstrated the crucial role of MCU in high glucose-mediated enhancement of bupivacaine-induced neurotoxicity, suggesting the possible use of this channel as a target for curing bupivacaine-induced neurotoxicity in diabetic patients.

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Section: Discussionmentioning

confidence: 99%

High Glucose Enhances Bupivacaine-Induced Neurotoxicity via MCU-Mediated Oxidative Stress in SH-SY5Y Cells

Liu

Zhao

Lei

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…In Hamburg, a collaborator of Arturo, Óscar J. Parada-Parra, presented new experiments concerning the ability of the endoplasmic reticulum (ER) to behave as a “Ca 2+ source” and the higher secretion of catecholamines in SHR rats, compared to respect to normotensive Wistar-Kyoto rats. Altered secretion has also been reported in diabetic rats [ 134 ] and during hypoxia that, curiously, augments the expression of Cav3.2 T-type channels that trigger “low-threshold” exocytosis in adult rat CCs [ 27 ].…”

Section: Frontier Advances Reported At the Isccb-21 Meeting In Hamburgmentioning

confidence: 99%

Forty years of the adrenal chromaffin cell through ISCCB meetings around the world

Maneu

Borges

Gandı́a

et al. 2023

Pflugers Arch - Eur J Physiol

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This historical review focuses on the evolution of the knowledge accumulated during the last two centuries on the biology of the adrenal medulla gland and its chromaffin cells (CCs). The review emerged in the context of a series of meetings that started on the Spanish island of Ibiza in 1982 with the name of the International Symposium on Chromaffin Cell Biology (ISCCB). Hence, the review is divided into two periods namely, before 1982 and from this year to 2022, when the 21st ISCCB meeting was just held in Hamburg, Germany. The first historical period extends back to 1852 when Albert Kölliker first described the fine structure and function of the adrenal medulla. Subsequently, the adrenal staining with chromate salts identified the CCs; this was followed by the establishment of the embryological origin of the adrenal medulla, and the identification of adrenaline-storing vesicles. By the end of the nineteenth century, the basic morphology, histochemistry, and embryology of the adrenal gland were known. The twentieth century began with breakthrough findings namely, the experiment of Elliott suggesting that adrenaline was the sympathetic neurotransmitter, the isolation of pure adrenaline, and the deciphering of its molecular structure and chemical synthesis in the laboratory. In the 1950s, Blaschko isolated the catecholamine-storing vesicles from adrenal medullary extracts. This switched the interest in CCs as models of sympathetic neurons with an explosion of studies concerning their functions, i.e., uptake of catecholamines by chromaffin vesicles through a specific coupled transport system; the identification of several vesicle components in addition to catecholamines including chromogranins, ATP, opioids, and other neuropeptides; the calcium-dependence of the release of catecholamines; the underlying mechanism of exocytosis of this release, as indicated by the co-release of proteins; the cross-talk between the adrenal cortex and the medulla; and the emission of neurite-like processes by CCs in culture, among other numerous findings. The 1980s began with the introduction of new high-resolution techniques such as patch-clamp, calcium probes, marine toxins-targeting ion channels and receptors, confocal microscopy, or amperometry. In this frame of technological advances at the Ibiza ISCCB meeting in 1982, 11 senior researchers in the field predicted a notable increase in our knowledge in the field of CCs and the adrenal medulla; this cumulative knowledge that occurred in the last 40 years of history of the CC is succinctly described in the second part of this historical review. It deals with cell excitability, ion channel currents, the exocytotic fusion pore, the handling of calcium ions by CCs, the kinetics of exocytosis and endocytosis, the exocytotic machinery, and the life cycle of secretory vesicles. These concepts together with studies on the dynamics of membrane fusion with super-resolution imaging techniques at the single-protein level were extensively reviewed by top scientists in the field at the 21st ISCCB meeting in Hamburg in the summer of 2022; this frontier topic is also briefly reviewed here. Many of the concepts arising from those studies contributed to our present understanding of synaptic transmission. This has been studied in physiological or pathophysiological conditions, in CCs from animal disease models. In conclusion, the lessons we have learned from CC biology as a peripheral model for brain and brain disease pertain more than ever to cutting-edge research in neurobiology. In the 22nd ISCCB meeting in Israel in 2024 that Uri Asheri is organizing, we will have the opportunity of seeing the progress of the questions posed in Ibiza, and on other questions that undoubtedly will arise.

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“…Merecen destacarse la disminución de las corrientes a través de los canales ca v y K v , lo que unido a una mayor acumulación y liberación de ca 2+ inducida por ca 2+ desde el retículo endoplásmico favorecería elevaciones de la concentración intracelular de ca 2+ de mayor amplitud y duración, con la consiguiente potenciación de la respuesta secretora (81, 90, 91, 92) (Figura 1). Es de destacar que estas alteraciones se producirían también en otros modelos experimentales de HtA como los que consisten en la administración de alcohol, de deoxicorticosterona y sal o de estreptozotocina (induce también diabetes), lo que reforzaría el vínculo entre la médula adrenal y la HtA (83,92,93). Además, el hecho de que en ratas SHR prehipertensas se observen también algunas de estas alteraciones, apoyaría una relación causal con la HtA (84).…”

Section: Hipertensión Arterialunclassified

“…La estimulación colinérgica (nicotínica y muscarínica) y la despolarización directa de la membrana celular con una solución extracelular de alto K + inducen una mayor respuesta secretora de catecolaminas en las ratas SHR que en las WKY (78; ver, no obstante, 79). El incremento de la respuesta secretora sería debido a la exocitosis de un número mayor de gránulos cromafines con, además, un mayor contenido de catecolaminas (80,81), lo que a nivel estructural se ha relacionado con una mayor densidad de gránulos cromafines en la vecindad de la membrana plasmática (82,83,84). Los resultados obtenidos sobre las enzimas de la ruta biosintética de las catecolaminas son contradictorios, habiéndose descrito tanto el aumento como la disminución del ARNm y de la proteína de la tH y la PNMt (85,86,87,88,89).…”

Section: Hiperalgesia Y Dolor Neuropáticounclassified

Adaptation of the adrenal medulla to stress: Pathophysiological implications

Olivos-Oré

Arribas-Blázquez

Gomariz

et al. 2022

an.ranf

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There is no life without stress and without adaptation to stress there is no life. Adaptation to stress requires the intervention of the nervous system for proper coordination and adjustment of the intensity of the response to stressful stimuli (stressors). The sympathetic nervous system is primarily responsible for rapid adaptive responses to stress, of which the classic example is the “fight or flight” response. This response is mediated by adrenaline secreted from the adrenal medulla and noradrenaline released both from the adrenal medulla and postganglionic sympathetic neurons. However, inadequate sympathetic activation, both in duration and intensity, may be at the origin of several “stress-related” diseases (hypertension, heart failure, pain, etc.). Although the sympathetic nervous system has traditionally been viewed as a one functional unit, the idea of a differentiated contribution to the stress response between the adrenal medulla and the sympathetic neurons, also with differentiated pathophysiological implications, is gradually gaining ground. Keywords: stress; sympathetic nervous system; adrenal medulla; chromaffin cell; stress-related diseases

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Altered mitochondrial function, calcium signaling, and catecholamine release in chromaffin cells of diabetic and SHR rats

Cited by 11 publications

References 53 publications

High Glucose Enhances Bupivacaine-Induced Neurotoxicity via MCU-Mediated Oxidative Stress in SH-SY5Y Cells

High Glucose Enhances Bupivacaine-Induced Neurotoxicity via MCU-Mediated Oxidative Stress in SH-SY5Y Cells

Forty years of the adrenal chromaffin cell through ISCCB meetings around the world

Adaptation of the adrenal medulla to stress: Pathophysiological implications

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