Acetylation mediates Cx43 reduction caused by electrical stimulation

Meraviglia, Viviana; Azzimato, Valerio; Colussi, Claudia; Florio, Maria Cristina; Binda, Anna; Panariti, Alice; Qanud, Khaled; Suffredini, Silvia; Gennaccaro, Laura; Miragoli, Michele; Barbuti, Andrea; Lampe, Paul D.; Gaetano, Carlo; Pramstaller, Peter P.; Capogrossi, Maurizio C.; Recchia, Fabio A.; Pompilio, Giulio; Rivolta, Ilaria; Rossini, Alessandra

doi:10.1016/j.yjmcc.2015.08.001

Cited by 17 publications

(14 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cx43 is the main constituent of gap junctions, and participates in cell-to-cell signaling ( 10 , 11 ). Studies have found that the expression and distribution of Cx43 would be changed after myocardial infarction ( 12 , 13 ).…”

Section: Discussionmentioning

confidence: 99%

Metoprolol protects cardiomyocytes in rabbit model of heart failure by regulating Cx43

2017

View full text Add to dashboard Cite

This study investigated the protective effect of metoprolol on cardiomyocytes in rabbits with heart failure and its possible mechanism. Sixty New Zealand white rabbits were randomly divided into infarction group and non-infarction group, 30 in each group. Myocardial infarction was constructed by ligation of anterior descending branch of coronary artery. Coronary artery threading without ligation after thoracotomy was performed for rabbits in non-infarction group. After model construction, rabbits in each group were further divided into control group (n=15) and metoprolol group (n=15), and fed with normal diet and normal diet + metoprolol. Animals were sacrificed 8 weeks later, and ventricular tissue around infarction area was collected. Expression of connexin 43 (Cx43) in myocardium was detected by immunohistochemistry. Expression of Cx43 protein and mRNA in each group was detected by western blot and reverse transcription PCR. The Cx43 protein was positively expressed in non-infarction group and was evenly distributed in intercellular space. Compared with non-infarction group, expression of Cx43 in infarction group was significantly decreased or even disappeared, while the decrease in expression level of Cx43 and the degree of dispersion were lower in metoprolol group than in control group. There was no significant difference in expression of level of Cx43 protein and mRNA between the subgroups of non-infarction group (P>0.05). In infarction group, expression level of Cx43 protein and mRNA in the metoprolol group were significantly higher than those in control group (P<0.05). The results showed that metoprolol can protect cardiomyocytes after myocardial infarction, and the possible mechanism is related to the regulation of Cx43 expression in cardiomyocytes.

show abstract

Section: Discussionmentioning

confidence: 99%

Metoprolol protects cardiomyocytes in rabbit model of heart failure by regulating Cx43

2017

View full text Add to dashboard Cite

show abstract

“…PES also affects epigenetics through acetylation, histone modifications, alteration of the structural organization of chromatin, demethylation, as well as affecting RNA. PES downregulates histone deacetylase activities in HL-1 cells, with a significant reduction in Cx43 expression and cellcell communication (Meraviglia et al, 2015). PES can also reversibly downregulate the activity of histone 1 kinase in pig oocytes (Leal and Liu, 1998).…”

Section: Intracellular Components and Organellesmentioning

confidence: 98%

Diverse effects of pulsed electrical stimulation on cells - with a focus on chondrocytes and cartilage regeneration

Tong¹,

Zhang²,

Heng³

et al. 2019

eCM

View full text Add to dashboard Cite

Biological effects of pulsed electrical stimulation (PES) on cells and tissues have been intensively studied with the aim of advancing their biomedical applications. These effects vary significantly depending on PES parameters, cell and tissue types, which can be attributed to the diverse variety of signaling pathways, ion channels, and epigenetic mechanisms involved. The development of new technology platforms, such as nanosecond pulsed electric fields (nsPEFs) with finely tuned parameters, have added further complexity. The present review systematically examines current research progress in various aspects of PES, from physical models to biological effects on cells and tissues, including voltage-sensing domains of voltage-gated channels, pore formation, intracellular components/organelles, and signaling pathways. Emphasis is placed on the complexity of PES parameters and inconsistency of induced biological effects, with the aim of exploring the underlying physical and cellular mechanisms of the physiological effects of electrical stimulation on cells. With chondrogenic differentiation of stem cells and cartilage regeneration as examples, the underlying mechanisms involved were reviewed and analyzed, hoping to move forward towards potential biomedical applications. Hopefully, the present review will inspire more interest in the wider clinical applications of PES and lay the basis for further comprehensive studies in this field. F i g . 4 . P o s s i b l e signalling pathways i n d u c e d b y P E S during chondrogenic d i f f e r e n t i a t i o n o f MSCs. Parameters: field strength could range from mV/cm to kV/cm. Duration could range from ns to ms.

show abstract

“…Electrical stimulation causes rat muscle dysfunction by altering miRNA-related signaling pathways 30 . Also, electrical stimulation modulates the gap junction-mediated cardiac cell-cell communication by regulating histone acetylase and deacetylase activities 16 . Chromatin structures were changed in BlCa cells exposed to ROS, and high levels of ROS increased H3K9me3 expression in human BlCa tissues 31 .…”

Section: Figure 1 Effects Of Electrofusion On Rabbit Scnt Embryos (A)mentioning

confidence: 99%

“…Also, abnormal epigenetic reprogramming occurs in a large proportion of cloned embryos, and this impedes improvement in SCNT efficiency 1,9 . Electrostimulation also regulates the epigenetic state in somatic cells; however, there are few reports on the effect of electrostimulation on the epigenetic state of embryos 16,17 . In this study, we optimized the electrofusion procedure, and studied its effects on SCNT embryos, oxidative stress, epigenetic state and ER stress.…”

mentioning

confidence: 99%

Melatonin Protects Rabbit Somatic Cell Nuclear Transfer (SCNT) Embryos from Electrofusion Damage

Shen

et al. 2020

Sci Rep

View full text Add to dashboard Cite

The study's objectives were to examine the effects of electrofusion on rabbit somatic cell nuclear transfer (SCNT) embryos, and to test melatonin as a protective agent against electrofusion damage to SCNT embryos. The levels of reactive oxygen species (ROS), the epigenetic state (H3K9me3), and the content of endoplasmic reticulum (ER) stress-associated transcripts (IRE-1 and CHOP) were measured. Melatonin was added during the preimplantation development period. The total blastocyst cell numbers were counted, and the fragmentation rate and apoptotic index were determined and used to assess embryonic development. Electrofusion increased (1) ROS levels at the 1-, 2-, 4-, and 8-cell stages; (2) H3K9me3 levels at the 2-, 4-, and 8-cell stage; and (3) the expression of IRE-1 and CHOP at the 8-cell, 16-cell, morula, and blastocyst stages. The treatment of SCNT embryos with melatonin significantly reduced the level of ROS and H3K9me3, and the expression levels of IRE-1 and CHOP. This treatment also significantly reduced the fragmentation rate and apoptotic index of blastocysts and increased their total cell number. In conclusion, the electrofusion of rabbit SCNT embryos induced oxidative stress, disturbed the epigenetic state, and caused ER stress, while melatonin reduced this damage. Our findings are of signal importance for improving the efficiency of SCNT and for optimizing the application of electrical stimulation in other biomedical areas. open Scientific RepoRtS | (2020) 10:2186 | https://doi.

show abstract

Acetylation mediates Cx43 reduction caused by electrical stimulation

Cited by 17 publications

References 52 publications

Metoprolol protects cardiomyocytes in rabbit model of heart failure by regulating Cx43

Metoprolol protects cardiomyocytes in rabbit model of heart failure by regulating Cx43

Diverse effects of pulsed electrical stimulation on cells - with a focus on chondrocytes and cartilage regeneration

Melatonin Protects Rabbit Somatic Cell Nuclear Transfer (SCNT) Embryos from Electrofusion Damage

Contact Info

Product

Resources

About