Publications by authors named "Donato D'Angelo"

Mitochondria regulate several physiological functions through mitochondrial Ca2+ dynamics. However, role of mitochondrial Ca2+ signaling in melanosome biology remains unknown. Here, we show that pigmentation requires mitochondrial Ca2+ uptake.

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Intimate partner violence (IPV) is a significant public health concern whose neurological/behavioral sequelae remain to be mechanistically explained. Using a mouse model recapitulating an IPV scenario, we evaluated the female brain neuroendocrine alterations produced by a reiterated male-to-female violent interaction (RMFVI). RMFVI prompted anxiety-like behavior in female mice whose hippocampus displayed a marked neuronal loss and hampered neurogenesis, namely reduced BrdU-DCX-positive nuclei and diminished dendritic arborization in the dentate gyrus (DG): effects paralleled by a substantial downregulation of the estrogen receptor β (ERβ).

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Ca ions serve as pleiotropic second messengers in the cell, regulating several cellular processes. Mitochondria play a fundamental role in Ca homeostasis since mitochondrial Ca (mitCa) is a key regulator of oxidative metabolism and cell death. MitCa uptake is mediated by the mitochondrial Ca uniporter complex (MCUc) localized in the inner mitochondrial membrane (IMM).

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Calcium (Ca) ions act as a second messenger, regulating several cell functions. Mitochondria are critical organelles for the regulation of intracellular Ca. Mitochondrial calcium (mtCa) uptake is ensured by the presence in the inner mitochondrial membrane (IMM) of the mitochondrial calcium uniporter (MCU) complex, a macromolecular structure composed of pore-forming and regulatory subunits.

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Article Synopsis
  • - Mitochondrial calcium (mitCa) uptake is vital for maintaining both mitochondrial functions and regulating calcium levels in the cytosol, impacting processes like ATP production and cellular signaling.
  • - Increased mitCa levels activate key enzymes in the TCA cycle, producing energy while also generating reactive oxygen species (ROS) as byproducts.
  • - Under stress, excess mitCa can lead to mitochondrial dysfunction by opening the mitochondrial permeability transition pore (mPTP), initiating apoptosis, with the uptake process governed by the mitochondrial Ca uniporter (MCU) and its regulatory complex, as revealed by advanced imaging techniques.
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Article Synopsis
  • Skeletal muscle is unique in its ability to fully regenerate after injuries caused by various factors like trauma, unlike other tissues that do not regenerate well.
  • The protocol outlined focuses on using a cardiotoxin (CTX) to induce a muscle injury model in mice, specifically targeting the tibialis anterior muscles.
  • This method is less invasive and more reproducible than other techniques, minimizing animal pain and stress, while effectively allowing researchers to study the regeneration process at different recovery stages.
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This paper presents the main surgical techniques applied in the treatment of anterior recurrent shoulder dislocation, aiming the achievement of the normality of articulate movements. This was obtained by combining distinct surgical procedures, which allowed the recovery of a complete functional capacity of the shoulder, without jeopardizing the normality of movement, something that has not been recorded in the case of the tense sutures of the surgical procedures of Putti-Platt, Bankart, Latarjet, Dickson-O'Dell and others. The careful review of the methods applied supports the conclusion that recurrent shoulder dislocation can be cured, since cure has been obtained in 97% of the treated cases.

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