Connexin43 in cardiomyocyte mitochondria contributes to mitochondrial potassium uptake

Miró-Casas, Elisabet; Ruiz‐Meana, Marisol; Agulló, Esperanza; Stahlhofen, Sabine; Rodríguez‐Sinovas, Antonio; Cabestrero, Alberto; Jorge, Inmaculada; Torre, Iratxe; Vázquez, Jesús; Boengler, Kerstin; Schulz, Rainer; Heusch, Gerd; Garcı́a-Dorado, David

doi:10.1093/cvr/cvp157

Cited by 128 publications

(146 citation statements)

References 42 publications

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“…6A). As previously described in cardiomyocytes (24), application of 25 mM K ϩ caused an increase in mitochondrial PBFI-derived BI 340 / BI 380 ratio values (Fig. 6B).…”

Section: Measurement Of Mitochondrial Ksupporting

confidence: 83%

“…Measurement of Mitochondrial K ϩ -Measurements of mitochondrial K ϩ were performed using a PBFI loading protocol that favors mitochondrial dye localization (24,32,33). In brief, astrocytes were placed for 1 h at 37°C in standard HEPESbuffered medium containing 10 M PBFI and 0.05% pluronic F-127.…”

Section: Measurement Of Mitochondrial Kmentioning

confidence: 99%

“…The Contribution of Cx43 to Mitochondrial K ϩ Sequestration-Cx43 is highly expressed in astrocytes (56), is permeable to K ϩ (57), has been shown using a variety of techniques (including electron microscopy) to be present in mitochondria (58,59), and has been shown to be important in K ϩ uptake into isolated mitochondria (24). Therefore, we examined whether Cx43 plays a role in the temporary sequestration of K ϩ by astrocyte mitochondria.…”

Section: Measurement Of Mitochondrial Kmentioning

confidence: 99%

“…22 and 23) we assessed mitochondrial K ϩ uptake in intact astrocytes. We determined that mitochondrial K ATP channels (mito-K ATP ) and potentially mitochondrial connexin43 (Cx43), a protein that is abundantly expressed in astrocytes and has recently been found to contribute to K ϩ uptake in isolated cardiac mitochondria (24), play a role in the temporary sequestration of K ϩ by astrocyte mitochondria.…”

mentioning

confidence: 99%

“…The Role of Connexin43 in Mitochondrial K ϩ Uptake-Given the abundance of gap junction proteins in astrocytes (56), their permeability to K ϩ ions (57), the reported presence of Cx43 on mitochondria (24,(57)(58)(59)(60)71), and their contribution to K ϩ uptake in isolated mitochondria (24), we employed pharmacological and genetic approaches to examine the potential role of Cx43 in mitochondrial K ϩ sequestration in situ. The combination of approaches was designed to overcome the limitations of each method.…”

mentioning

confidence: 99%

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Temporary Sequestration of Potassium by Mitochondria in Astrocytes

Kozoriz¹,

Church

Ozog

et al. 2010

Journal of Biological Chemistry

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“…6A). As previously described in cardiomyocytes (24), application of 25 mM K ϩ caused an increase in mitochondrial PBFI-derived BI 340 / BI 380 ratio values (Fig. 6B).…”

Section: Measurement Of Mitochondrial Ksupporting

confidence: 83%

Section: Measurement Of Mitochondrial Kmentioning

confidence: 99%

Section: Measurement Of Mitochondrial Kmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Temporary Sequestration of Potassium by Mitochondria in Astrocytes

Kozoriz¹,

Church

Ozog

et al. 2010

Journal of Biological Chemistry

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Pharmaceutical Manipulation of Mitochondrial F0F1‐ATP Synthase Enables Imaging and Protection of Myocardial Ischemia/Reperfusion Injury Through Stress‐induced Selective Enrichment

Chen,

Tan,

Jin

et al. 2023

Advanced Science

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To rescue ischemic myocardium from progressing to myocardial infarction, timely identification of the infarct size and reperfusion is crucial. However, fast and accurate identification, as well as the targeted protection of injured cardiomyocytes following ischemia/reperfusion (I/R) injury, remain significantly challenging. Here, a near infrared heptamethine dye IR‐780 is shown that has the potential to quickly monitor the area at risk following I/R injury by selectively entering the cardiomyocytes of the at‐risk heart tissues. Preconditioning with IR‐780 or timely IR‐780 administration before reperfusion significantly protects the heart from ischemia and oxidative stress‐induced cell death, myocardial remodeling, and heart failure in both rat and pig models. Furthermore, IR‐780 can directly bind to F0F1‐ATP synthase of cardiomyocytes, rapidly decrease the mitochondrial membrane potential, and subsequently slow down the mitochondrial energy metabolism, which induces the mitochondria into a “quiescent state” and results in mitochondrial permeability transition pore inhibition by preventing mitochondrial calcium overload. Collectively, the findings show the feasibility of IR‐780‐based imaging and protection strategy for I/R injury in a preclinical context and indicate that moderate mitochondrial function depression is a mode of action that can be targeted in the development of cardioprotective reagents.

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Gap Junctions

Nielsen,

Nygaard Axelsen,

Sorgen

et al. 2012

Comprehensive Physiology

352

347

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Gap junctions are essential to the function of multicellular animals, which require a high degree of coordination between cells. In vertebrates, gap junctions comprise connexins and currently 21 connexins are known in humans. The functions of gap junctions are highly diverse and include exchange of metabolites and electrical signals between cells, as well as functions, which are apparently unrelated to intercellular communication. Given the diversity of gap junction physiology, regulation of gap junction activity is complex. The structure of the various connexins is known to some extent; and structural rearrangements and intramolecular interactions are important for regulation of channel function. Intercellular coupling is further regulated by the number and activity of channels present in gap junctional plaques. The number of connexins in cell‐cell channels is regulated by controlling transcription, translation, trafficking, and degradation; and all of these processes are under strict control. Once in the membrane, channel activity is determined by the conductive properties of the connexin involved, which can be regulated by voltage and chemical gating, as well as a large number of posttranslational modifications. The aim of the present article is to review our current knowledge on the structure, regulation, function, and pharmacology of gap junctions. This will be supported by examples of how different connexins and their regulation act in concert to achieve appropriate physiological control, and how disturbances of connexin function can lead to disease. © 2012 American Physiological Society. Compr Physiol 2:1981‐2035, 2012.

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Connexin43 in cardiomyocyte mitochondria contributes to mitochondrial potassium uptake

Abstract: These results indicate that mCx43 contributes to mitochondrial K(+) flux in cardiomyocytes, potentially by forming hemichannel-like structures.

Cited by 128 publications

References 42 publications

Temporary Sequestration of Potassium by Mitochondria in Astrocytes

Temporary Sequestration of Potassium by Mitochondria in Astrocytes

Pharmaceutical Manipulation of Mitochondrial F0F1‐ATP Synthase Enables Imaging and Protection of Myocardial Ischemia/Reperfusion Injury Through Stress‐induced Selective Enrichment

Gap Junctions

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