Quantification of Mitochondrial Network Characteristics in Health and Disease

Valente, Andrew; Fonseca, João; Moradi, Fereshteh; Foran, Gregory; Necakov, Alexander; Stuart, Jeffrey A.

doi:10.1007/978-981-13-8367-0_10

Cited by 13 publications

(16 citation statements)

References 64 publications

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“…The reasons for that are not clear, one of possible explanation is different composition of culture media, including different glucose concentration, which is known to strongly affect mitochondrial network morphology of the cultured cells. 35 The results from our analysis of the mitochondrial size distribution are in line with those reported by Perez et al 20 We detected a higher percentage of the smallest mitochondria and fewer individual mitochondria per cell in AD fibroblasts. Thus, when looking only at the size of the elements separated from the network, one may assume enhanced mitochondrial fission.…”

Section: Discussionsupporting

confidence: 92%

“…The importance of mitochondrial network morphology, which translates into their functionality, is increasingly explored. 35 However, its research is often based only F I G U R E 4 Mitochondrial dynamics in control and sAD fibroblasts. A, Representative images showing the alterations in the mitochondrial size and quantity of separate fragments of mitochondrial network observed during the analysis.…”

Section: Discussionmentioning

confidence: 99%

“…This does not follow the general view of increased mitochondrial fragmentation in AD and other neurodegenerative diseases. 35 However, when it comes to AD, there is a considerable variety concerning mitochondrial network morphology observed in different study models, which include animal models, patient-derived cells and tissues, as well as Aβ treated cell cultures. Many reports have shown the mitochondrial network fragmentation in cultured cells upon Aβ treatment [37][38][39] and in mouse models related to pathological Aβ deposition.…”

Section: Discussionmentioning

confidence: 99%

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Adaptation of mitochondrial network dynamics and velocity of mitochondrial movement to chronic stress present in fibroblasts derived from patients with sporadic form of Alzheimer’s disease

et al. 2021

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Alzheimer's disease (AD) is one of the most common neurodegenerative disorders, but its etiology remains unknown. Only a fraction of all cases (~10%) of AD are suspected to be associated with known genetic mutations in amyloid precursor protein (APP), presenilin 1 (PSEN1) or PSEN2 1,2 (familial form of AD), whereas 90% of cases are sporadic form of AD, which occurs in the absence of an obvious family history.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Adaptation of mitochondrial network dynamics and velocity of mitochondrial movement to chronic stress present in fibroblasts derived from patients with sporadic form of Alzheimer’s disease

et al. 2021

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“…In cells, mitochondria can exist as either punctate, individual mitochondria or branched, highly connected architectures (Bleck et al, 2018;Valente et al, 2019) termed the mitochondrial network or reticulum (Figure 3). For example, mitochondria in vascular smooth muscles are ovoid or rod-shaped (Nixon et al, 1994;McCarron et al, 2013).…”

Section: Mitochondrial Network Structurementioning

confidence: 99%

The Functional Impact of Mitochondrial Structure Across Subcellular Scales

et al. 2020

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Mitochondria are key determinants of cellular health. However, the functional role of mitochondria varies from cell to cell depending on the relative demands for energy distribution, metabolite biosynthesis, and/or signaling. In order to support the specific needs of different cell types, mitochondrial functional capacity can be optimized in part by modulating mitochondrial structure across several different spatial scales. Here we discuss the functional implications of altering mitochondrial structure with an emphasis on the physiological trade-offs associated with different mitochondrial configurations. Within a mitochondrion, increasing the amount of cristae in the inner membrane improves capacity for energy conversion and free radical-mediated signaling but may come at the expense of matrix space where enzymes critical for metabolite biosynthesis and signaling reside. Electrically isolating individual cristae could provide a protective mechanism to limit the spread of dysfunction within a mitochondrion but may also slow the response time to an increase in cellular energy demand. For individual mitochondria, those with relatively greater surface areas can facilitate interactions with the cytosol or other organelles but may be more costly to remove through mitophagy due to the need for larger phagophore membranes. At the network scale, a large, stable mitochondrial reticulum can provide a structural pathway for energy distribution and communication across long distances yet also enable rapid spreading of localized dysfunction. Highly dynamic mitochondrial networks allow for frequent content mixing and communication but require constant cellular remodeling to accommodate the movement of mitochondria. The formation of contact sites between mitochondria and several other organelles provides a mechanism for specialized communication and direct content transfer between organelles. However, increasing the number of contact sites between mitochondria and any given organelle reduces the mitochondrial surface area available for contact sites with other organelles as well as for metabolite exchange with cytosol. Though the precise mechanisms guiding the coordinated multi-scale mitochondrial configurations observed in different cell types have yet to be elucidated, it is clear that mitochondrial structure is tailored at every level to optimize mitochondrial function to meet specific cellular demands.

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“…However, Morton et al also demonstrated a significantly higher maximal respiration capacity of lymphocytes from healthy individuals compared with lymphocytes from acute pancreatitis patients with a simultaneously unchanged basal oxygen consumption [36]. We suggest TGF-ß1 activates a program that increases the maximal respiratory potential of mitochondria, possibly due to mitochondrial mass or architecture, improved fission and fusion, and/or altered reactive oxygen species concentrations [37].…”

Section: Discussionmentioning

confidence: 61%

TGF-ß1 Induces Changes in the Energy Metabolism of White Adipose Tissue-Derived Human Adult Mesenchymal Stem/Stromal Cells In Vitro

et al. 2020

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Adipose tissue plays an active role in the regulation of the body’s energy balance. Mesenchymal stem/stromal cells from adipose tissue (adMSC) are the precursor cells for repair and adipogenesis. Since the balance of the differentiation state of adipose tissue-resident cells is associated with the development of various diseases, the examination of the regulation of proliferation and differentiation of adMSC might provide new therapeutic targets. Transforming growth factor-β1 (TGF-ß1) is synthetized by many cell types and is involved in various biological processes. Here, we investigated the effects of different concentrations of TGF-ß1 (1–10 ng/mL) on adMSC proliferation, metabolic activity, and analyzed the gene expression data obtained from DNA microarrays by bioinformatics. TGF-ß1 induced the concentration- and time-dependent increase in the cell number of adMSC with simultaneously unchanged cell cycle distributions. The basal oxygen consumption rates did not change significantly after TGF-ß1 exposure. However, glycolytic activity was significantly increased. The gene expression analysis identified 3275 differentially expressed genes upon exposure to TGF-ß1. According to the pathway enrichment analyses, they also included genes associated with energy metabolism. Thus, it was shown that TGF-ß1 induces changes in the energy metabolism of adMSC. Whether these effects are of relevance in vivo and whether they contribute to pathogenesis should be addressed in further examinations.

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Quantification of Mitochondrial Network Characteristics in Health and Disease

Cited by 13 publications

References 64 publications

Adaptation of mitochondrial network dynamics and velocity of mitochondrial movement to chronic stress present in fibroblasts derived from patients with sporadic form of Alzheimer’s disease

Adaptation of mitochondrial network dynamics and velocity of mitochondrial movement to chronic stress present in fibroblasts derived from patients with sporadic form of Alzheimer’s disease

The Functional Impact of Mitochondrial Structure Across Subcellular Scales

TGF-ß1 Induces Changes in the Energy Metabolism of White Adipose Tissue-Derived Human Adult Mesenchymal Stem/Stromal Cells In Vitro

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