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Cited by 135Mitochondrial Function and PathologyCircadian rhythm and melatoninAutophagy in Disease and Therapy

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Melatonin reshapes the mitochondrial network and promotes intercellular mitochondrial transfer via tunneling nanotubes after ischemic‐like injury in hippocampal HT22 cells

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Nasoni, Maria Gemma, Carloni, Silvia, Canonico, Barbara, Burattini, Sabrina, Cesarini, Erica, Papa, Stefano, Pagliarini, Marica, Ambrogini, Patrizia, Balduini, Walter, Luchetti, Francesca·2021·Journal of Pineal Research
DOI 10.1111/jpi.12747PMC PMC8365755
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Abstract

Mitochondrial dysfunction is considered one of the hallmarks of ischemia/reperfusion injury. Mitochondria are plastic organelles that undergo continuous biogenesis, fusion, and fission. They can be transferred between cells through tunneling nanotubes (TNTs), dynamic structures that allow the exchange of proteins, soluble molecules, and organelles. Maintaining mitochondrial dynamics is crucial to cell function and survival. The present study aimed to assess the effects of melatonin on mitochondrial dynamics, TNT formation, and mitochondria transfer in HT22 cells exposed to oxygen/glucose deprivation followed by reoxygenation (OGD/R). The results showed that melatonin treatment during the reoxygenation phase reduced mitochondrial reactive oxygen species (ROS) production, improved cell viability, and increased the expression of PGC1α and SIRT3. Melatonin also preserved the expression of the membrane translocase proteins TOM20 and TIM23, and of the matrix protein HSP60, which are involved in mitochondrial biogenesis. Moreover, it promoted mitochondrial fusion and enhanced the expression of MFN2 and OPA1. Remarkably, melatonin also fostered mitochondrial transfer between injured HT22 cells through TNT connections. These results provide new insights into the effect of melatonin on mitochondrial network reshaping and cell survival. Fostering TNTs formation represents a novel mechanism mediating the protective effect of melatonin in ischemia/reperfusion injury.

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Metadata

Authors
Nasoni, M. G., Carloni, S., Canonico, B., Burattini, S., Cesarini, E., Papa, S., Pagliarini, M., Ambrogini, P., Balduini, W., & Luchetti, F.
Affiliations
University of Urbino (IT)
Corresponding author
  • Balduini, Walter
  • Luchetti, Francesca
ORCID
Venue
Journal of Pineal Research
Publisher
Wiley
Published
2021-06-14
Volume
71
Issue
1
Pages
e12747-e12747
ISSN
  • 0742-3098 (ISSN-L)
  • 1600-079X
DOI
10.1111/jpi.12747
PMC
PMC8365755
OpenAlex
W3165578448
Cited by
135
References
2
Citations by year
2026: 21 · 2025: 30 · 2024: 34 · 2023: 29 · 2022: 18 · 2021: 3
FWCI
6.59
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Pineal Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • CINECA IRIS Institutional Research information system (University of Urbino) (submittedVersion, cc-by)
Funders
Università degli Studi di Urbino Carlo Bo
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords
melatonin, tunneling nanotubes, intercellular mitochondrial transfer, mitochondrial dynamics, mitochondrial fusion, mitochondrial fission, ischemia-reperfusion injury, oxygen-glucose deprivation, HT22 cells, PGC-1α, SIRT3, Tom20, Tim23, HSP60, mitofusin 2, OPA1, reactive oxygen species, neuroprotection
MeSH terms
Animals, Cell Line, Brain Ischemia, Hippocampus, Melatonin, Mitochondria, Neurons, Reperfusion Injury, Cell Membrane Structures, Nanotubes, Mice

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