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Calcium signaling around Mitochondria Associated Membranes (MAMs).

Patergnani S, Suski JM, Agnoletto C, Bononi A, Bonora M, De Marchi E, Giorgi C, Marchi S, Missiroli S, Poletti F, Rimessi A, Duszynski J, Wieckowski MR, Pinton P - Cell Commun. Signal (2011)

Bottom Line: Mitochondria are also major components of calcium signalling, capable of modulating both the amplitude and the spatio-temporal patterns of Ca2+ signals.In this review, we summarize the most up-to-date findings on the modulation of intracellular Ca2+ release and Ca2+ uptake mechanisms.We also explore the tight interplay between ER- and mitochondria-mediated Ca2+ signalling, covering the structural and molecular properties of the zones of close contact between these two networks.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Experimental and Diagnostic Medicine, Section of General Pathology, Interdisciplinary Center for the Study of Inflammation (ICSI), Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy. paolo.pinton@unife.it.

ABSTRACT
Calcium (Ca2+) homeostasis is fundamental for cell metabolism, proliferation, differentiation, and cell death. Elevation in intracellular Ca2+ concentration is dependent either on Ca2+ influx from the extracellular space through the plasma membrane, or on Ca2+ release from intracellular Ca2+ stores, such as the endoplasmic/sarcoplasmic reticulum (ER/SR). Mitochondria are also major components of calcium signalling, capable of modulating both the amplitude and the spatio-temporal patterns of Ca2+ signals. Recent studies revealed zones of close contact between the ER and mitochondria called MAMs (Mitochondria Associated Membranes) crucial for a correct communication between the two organelles, including the selective transmission of physiological and pathological Ca2+ signals from the ER to mitochondria. In this review, we summarize the most up-to-date findings on the modulation of intracellular Ca2+ release and Ca2+ uptake mechanisms. We also explore the tight interplay between ER- and mitochondria-mediated Ca2+ signalling, covering the structural and molecular properties of the zones of close contact between these two networks.

No MeSH data available.


Related in: MedlinePlus

PML and p66Shc regulates cell span at the MAMs level. The tumor suppressor PML in resting conditions resides in a specific multi-protein complex with IP3R, PP2a and AKT, essential for a normal Ca2+ flux from ER to mitochondria and, consequently, for correct apoptosis levels (upper panel). Aging and ROS determine phosphorylation and accumulation of p66Shc in the MAMs fraction. The presence of phospho-p66Shc at the mitochondrial level determines alterations in mitochondrial homeostasis, including Ca2+ signalling, and ultimately increases apoptotic and senescence responses (lower panel).
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Figure 2: PML and p66Shc regulates cell span at the MAMs level. The tumor suppressor PML in resting conditions resides in a specific multi-protein complex with IP3R, PP2a and AKT, essential for a normal Ca2+ flux from ER to mitochondria and, consequently, for correct apoptosis levels (upper panel). Aging and ROS determine phosphorylation and accumulation of p66Shc in the MAMs fraction. The presence of phospho-p66Shc at the mitochondrial level determines alterations in mitochondrial homeostasis, including Ca2+ signalling, and ultimately increases apoptotic and senescence responses (lower panel).

Mentions: PML is another protein recently identified in the MAM fraction. There, it is believed to regulate the ER machinery responsible for Ca2+ release. The lack of PML results in a decreased Ca2+ release from the ER and a subsequent lower Ca2+ influx into mitochondria. Detailed studies on the role of PML protein in the MAM fraction contributed to the formation of the hypothesis that this protein regulates cell survival through the ER-cytosol/mitochondria calcium signalling [70] (Figure 2).


Calcium signaling around Mitochondria Associated Membranes (MAMs).

Patergnani S, Suski JM, Agnoletto C, Bononi A, Bonora M, De Marchi E, Giorgi C, Marchi S, Missiroli S, Poletti F, Rimessi A, Duszynski J, Wieckowski MR, Pinton P - Cell Commun. Signal (2011)

PML and p66Shc regulates cell span at the MAMs level. The tumor suppressor PML in resting conditions resides in a specific multi-protein complex with IP3R, PP2a and AKT, essential for a normal Ca2+ flux from ER to mitochondria and, consequently, for correct apoptosis levels (upper panel). Aging and ROS determine phosphorylation and accumulation of p66Shc in the MAMs fraction. The presence of phospho-p66Shc at the mitochondrial level determines alterations in mitochondrial homeostasis, including Ca2+ signalling, and ultimately increases apoptotic and senescence responses (lower panel).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3198985&req=5

Figure 2: PML and p66Shc regulates cell span at the MAMs level. The tumor suppressor PML in resting conditions resides in a specific multi-protein complex with IP3R, PP2a and AKT, essential for a normal Ca2+ flux from ER to mitochondria and, consequently, for correct apoptosis levels (upper panel). Aging and ROS determine phosphorylation and accumulation of p66Shc in the MAMs fraction. The presence of phospho-p66Shc at the mitochondrial level determines alterations in mitochondrial homeostasis, including Ca2+ signalling, and ultimately increases apoptotic and senescence responses (lower panel).
Mentions: PML is another protein recently identified in the MAM fraction. There, it is believed to regulate the ER machinery responsible for Ca2+ release. The lack of PML results in a decreased Ca2+ release from the ER and a subsequent lower Ca2+ influx into mitochondria. Detailed studies on the role of PML protein in the MAM fraction contributed to the formation of the hypothesis that this protein regulates cell survival through the ER-cytosol/mitochondria calcium signalling [70] (Figure 2).

Bottom Line: Mitochondria are also major components of calcium signalling, capable of modulating both the amplitude and the spatio-temporal patterns of Ca2+ signals.In this review, we summarize the most up-to-date findings on the modulation of intracellular Ca2+ release and Ca2+ uptake mechanisms.We also explore the tight interplay between ER- and mitochondria-mediated Ca2+ signalling, covering the structural and molecular properties of the zones of close contact between these two networks.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Experimental and Diagnostic Medicine, Section of General Pathology, Interdisciplinary Center for the Study of Inflammation (ICSI), Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy. paolo.pinton@unife.it.

ABSTRACT
Calcium (Ca2+) homeostasis is fundamental for cell metabolism, proliferation, differentiation, and cell death. Elevation in intracellular Ca2+ concentration is dependent either on Ca2+ influx from the extracellular space through the plasma membrane, or on Ca2+ release from intracellular Ca2+ stores, such as the endoplasmic/sarcoplasmic reticulum (ER/SR). Mitochondria are also major components of calcium signalling, capable of modulating both the amplitude and the spatio-temporal patterns of Ca2+ signals. Recent studies revealed zones of close contact between the ER and mitochondria called MAMs (Mitochondria Associated Membranes) crucial for a correct communication between the two organelles, including the selective transmission of physiological and pathological Ca2+ signals from the ER to mitochondria. In this review, we summarize the most up-to-date findings on the modulation of intracellular Ca2+ release and Ca2+ uptake mechanisms. We also explore the tight interplay between ER- and mitochondria-mediated Ca2+ signalling, covering the structural and molecular properties of the zones of close contact between these two networks.

No MeSH data available.


Related in: MedlinePlus