c-Jun N-terminal kinase activation contributes to reduced connexin43 and development of atrial arrhythmias

Yan, Jiajie; Kong, Wei; Zhang, Qiang; Beyer, Eric C.; Walcott, Gregory P.; Fast, Vladimir G.; Ai, Xun

doi:10.1093/cvr/cvs366

Cited by 67 publications

(109 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In HL-1 cell cultures, JNK activation by anisomycin treatment led to reduction of connexin 43, which impaired cell-cell communication between atrial myocytes and ultimately prompted the development of atrial arrhythmias. These effects were prevented by the specific JNK inhibitor, SP600125 13 . An in vivo study in rabbits showed that treatment with anisomycin reduced connexin 43 by 34% and increased pacing-induced atrial arrhythmias 13 .…”

Section: Cell-cell Junction Formationmentioning

confidence: 99%

“…These effects were prevented by the specific JNK inhibitor, SP600125 13 . An in vivo study in rabbits showed that treatment with anisomycin reduced connexin 43 by 34% and increased pacing-induced atrial arrhythmias 13 . Collectively, these studies suggest that there is an intracellular link between stress-induced JNK signaling pathway and GJ function, ultimately affecting intercellular communication and cellular behavior 62 …”

Section: Cell-cell Junction Formationmentioning

confidence: 99%

See 1 more Smart Citation

JNK is a novel regulator of intercellular adhesion

You¹,

Lei²,

Andreadis³

2013

Tissue Barriers

View full text Add to dashboard Cite

c-Jun N-terminal Kinase (JNK) is a family of protein kinases, which are activated by stress stimuli such as inflammation, heat stress and osmotic stress, and regulate diverse cellular processes including proliferation, survival and apoptosis. In this review, we focus on a recently discovered function of JNK as a regulator of intercellular adhesion. We summarize the existing knowledge regarding the role of JNK during the formation of cell-cell junctions. The potential mechanisms and implications for processes requiring dynamic formation and dissolution of cell-cell junctions including wound healing, migration, cancer metastasis and stem cell differentiation are also discussed.

show abstract

Section: Cell-cell Junction Formationmentioning

confidence: 99%

Section: Cell-cell Junction Formationmentioning

confidence: 99%

JNK is a novel regulator of intercellular adhesion

You¹,

Lei²,

Andreadis³

2013

Tissue Barriers

View full text Add to dashboard Cite

show abstract

“…3. Calculate action potential or calcium transient conduction velocity (CV) vectors on the AT matrix using the vector field analysis method as previously described with minor modifications 12,18 . 1.…”

Section: Dual Channel Optical Mappingmentioning

confidence: 99%

“…1. Calculate the CV vector of a data channel relative to its surrounding AT data points (5 × 5 neighboring averaged data channels) to simulate a smooth polynomial surface of activation times (AT surface) using a least-square algorithm within the MATLAB program 12,18 . 2.…”

Section: Dual Channel Optical Mappingmentioning

confidence: 99%

“…These cells express cardiac genes and proteins, including important cardiac ion channels (i.e., L-and T-type calcium channels) 9 and mature isoforms of sarcomeric contractile proteins normally found in adult atrial myocytes as others and we have previously reported. [10][11][12][13] In addition, HL-1 cells can be cultured to form a 2-dimensional (2-D) myocyte monolayer. Thus, the advantages of using cultured HL-1 monolayers include: 1) relatively lower cost and easier to maintain a myocyte culture line than isolating and culturing primary neonatal myocytes; 2) a confluent monolayer of cells reduces the structural complexities that result from the 3-D structure of the heart; 3) a cell monolayer can eliminate the interference of interstitial fibrosis that occurs in the intact heart.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Voltage and Calcium Dual Channel Optical Mapping of Cultured HL-1 Atrial Myocyte Monolayer

Yan

Thomson

Zhao

et al. 2015

JoVE

Self Cite

View full text Add to dashboard Cite

Optical mapping has proven to be a valuable technique to detect cardiac electrical activity on both intact ex vivo hearts and in cultured myocyte monolayers. HL-1 cells have been widely used as a 2-Dimensional cellular model for studying diverse aspects of cardiac physiology. However, it has been a great challenge to optically map calcium (Ca) transients and action potentials simultaneously from the same field of view in a cultured HL-1 atrial cell monolayer. This is because special handling and care is required to prepare healthy cells that can be electrically captured and optically mapped. Therefore, we have developed an optimal working protocol for dual channel optical mapping. In this manuscript, we have described in detail how to perform the dual channel optical mapping experiment. This protocol is a useful tool to enhance the understanding of action potential propagation and Ca kinetics in arrhythmia development. Video LinkThe video component of this article can be found at

show abstract

The Stress-Response MAP Kinase Signaling in Cardiac Arrhythmias

Yan

Carrillo

et al. 2016

Reviews of Physiology, Biochemistry and Pharmacology

Self Cite

View full text Add to dashboard Cite

Stress-response kinases, the mitogen-activated protein kinases (MAPKs) are activated in response to the challenge of a myriad of stressors. c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinases (ERKs), and p38 MAPKs are the predominant members of the MAPK family in the heart. Extensive studies have revealed critical roles of activated MAPKs in the processes of cardiac injury and heart failure and many other cardiovascular diseases. Recently, emerging evidence suggests that MAPKs also promote the development of cardiac arrhythmias. Thus, understanding the functional impact of MAPKs in the heart could shed new light on the development of novel therapeutic approaches to improve cardiac function and prevent arrhythmia development in the patients. This review will summarize the recent findings on the role of MAPKs in cardiac remodeling and arrhythmia development and point to the critical need of future studies to further elucidate the fundamental mechanisms of MAPK activation and arrhythmia development in the heart.

show abstract

c-Jun N-terminal kinase activation contributes to reduced connexin43 and development of atrial arrhythmias

Abstract: JNK activation contributes to Cx43 reductions that promote development of AF. Modulation of JNK may be a potential novel therapeutic approach to prevent and treat AF.

Cited by 67 publications

References 31 publications

JNK is a novel regulator of intercellular adhesion

JNK is a novel regulator of intercellular adhesion

Voltage and Calcium Dual Channel Optical Mapping of Cultured HL-1 Atrial Myocyte Monolayer

The Stress-Response MAP Kinase Signaling in Cardiac Arrhythmias

Contact Info

Product

Resources

About