Kv1.3 potassium channel mediates macrophage migration in atherosclerosis by regulating ERK activity

Kan, Xiao-Hong; Gao, Haiqing; Ma, Zhiyong; Liu, Lin; Ling, Mingying; Wang, Yuan‐Yuan

doi:10.1016/j.abb.2015.12.013

Cited by 30 publications

(24 citation statements)

References 20 publications

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“…The Kv1.3 channel is expressed both by vascular smooth muscle cells, where it stimulates their proliferation and migration [ 121 , 122 ], and by lymphocytes, where it promotes proliferation and cytokine production [ 122 , 123 , 124 , 125 ]. Kan et al studied the role of the Kv1.3 channel in macrophages and in the pathogenesis of atherosclerosis [ 122 ]. They showed high expression of the Kv1.3 channel in macrophages of patients with acute coronary syndrome, hypothesizing a role of this channel in the initiation and progression of atherosclerosis and in the instability of the plaques [ 122 ].…”

Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

“…Kan et al studied the role of the Kv1.3 channel in macrophages and in the pathogenesis of atherosclerosis [ 122 ]. They showed high expression of the Kv1.3 channel in macrophages of patients with acute coronary syndrome, hypothesizing a role of this channel in the initiation and progression of atherosclerosis and in the instability of the plaques [ 122 ]. The upregulation of Kv1.3 channel expression and function may stimulate greater activation of extracellular signal-regulated kinase (ERK) through its phosphorylation [ 122 ].…”

Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

“…They showed high expression of the Kv1.3 channel in macrophages of patients with acute coronary syndrome, hypothesizing a role of this channel in the initiation and progression of atherosclerosis and in the instability of the plaques [ 122 ]. The upregulation of Kv1.3 channel expression and function may stimulate greater activation of extracellular signal-regulated kinase (ERK) through its phosphorylation [ 122 ]. ERK belongs to the mitogen-activated protein kinase (MAPK) family and mainly promotes macrophage recruitment into the arterial intima [ 122 ].…”

Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

“…The upregulation of Kv1.3 channel expression and function may stimulate greater activation of extracellular signal-regulated kinase (ERK) through its phosphorylation [ 122 ]. ERK belongs to the mitogen-activated protein kinase (MAPK) family and mainly promotes macrophage recruitment into the arterial intima [ 122 ].…”

Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

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Diabetes Mellitus and Ischemic Heart Disease: The Role of Ion Channels

Severino

D’Amato

Netti

et al. 2018

IJMS

101

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Diabetes mellitus is one the strongest risk factors for cardiovascular disease and, in particular, for ischemic heart disease (IHD). The pathophysiology of myocardial ischemia in diabetic patients is complex and not fully understood: some diabetic patients have mainly coronary stenosis obstructing blood flow to the myocardium; others present with coronary microvascular disease with an absence of plaques in the epicardial vessels. Ion channels acting in the cross-talk between the myocardial energy state and coronary blood flow may play a role in the pathophysiology of IHD in diabetic patients. In particular, some genetic variants for ATP-dependent potassium channels seem to be involved in the determinism of IHD.

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Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

See 2 more Smart Citations

Diabetes Mellitus and Ischemic Heart Disease: The Role of Ion Channels

Severino

D’Amato

Netti

et al. 2018

IJMS

101

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“…; Kan et al. ). In other studies, K V channels have been shown to regulate proliferation in multiple tumor cell lines, with strong evidence specifically indicating K V 10.1 and K V 11.1 (EAG and hEAG) channels (Bianchi et al.…”

Section: Discussionmentioning

confidence: 98%

Sine-wave electrical stimulation initiates a voltage-gated potassium channel-dependent soft tissue response characterized by induction of hemocyte recruitment and collagen deposition

2016

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Soft tissue repair is a complex process that requires specific communication between multiple cell types to orchestrate effective restoration of physiological functions. Macrophages play a critical role in this wound healing process beginning at the onset of tissue injury. Understanding the signaling mechanisms involved in macrophage recruitment to the wound site is an essential step for developing more effective clinical therapies. Macrophages are known to respond to electrical fields, but the underlying cellular mechanisms mediating this response is unknown. This study demonstrated that low‐amplitude sine‐wave electrical stimulation (ES) initiates a soft tissue response in the absence of injury in Procambarus clarkii. This cellular response was characterized by recruitment of macrophage‐like hemocytes to the stimulation site indicated by increased hemocyte density at the site. ES also increased tissue collagen deposition compared to sham treatment (P < 0.05). Voltage‐gated potassium (KV) channel inhibition with either 4‐aminopyridine or astemizole decreased both hemocyte recruitment and collagen deposition compared to saline infusion (P < 0.05), whereas inhibition of calcium‐permeable channels with ruthenium red did not affect either response to ES. Thus, macrophage‐like hemocytes in P. clarkii elicit a wound‐like response to exogenous ES and this is accompanied by collagen deposition. This response is mediated by KV channels but independent of Ca2+ channels. We propose a significant role for KV channels that extends beyond facilitating Ca2+ transport via regulation of cellular membrane potentials during ES of soft tissue.

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