Spatial alterations of Kv channels expression and K+ currents in post-MI remodeled rat heart

Huang, Biao; Qin, DAYl; El‐Sherif, Nabil

doi:10.1016/s0008-6363(01)00378-9

Cited by 36 publications

(31 citation statements)

References 23 publications

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“…This reduction was greater in epicardial than in endocardial myocytes (226). Furthermore, this decrease in I to precedes the onset of hypertrophy, supporting the argument that I to reduction contributes to hypertrophy and remains reduced up to 16 wk (88,163). The changes in I to,f correlated with decreased mRNA and protein levels of Kv4.2 and Kv4.3 (87,88).…”

Section: Cardiac Pathologymentioning

confidence: 53%

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Structure and Function of Kv4-Family Transient Potassium Channels

Birnbaum

Varga

et al. 2004

Physiological Reviews

319

360

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Shal-type (Kv4.x) K+ channels are expressed in a variety of tissue, with particularly high levels in the brain and heart. These channels are the primary subunits that contribute to transient, voltage-dependent K+ currents in the nervous system (A currents) and the heart (transient outward current). Recent studies have revealed an enormous degree of complexity in the regulation of these channels. In this review, we describe the surprisingly large number of ancillary subunits and scaffolding proteins that can interact with the primary subunits, resulting in alterations in channel trafficking and kinetic properties. Furthermore, we discuss posttranslational modification of Kv4.x channel function with an emphasis on the role of kinase modulation of these channels in regulating membrane properties. This concept is especially intriguing as Kv4.2 channels may integrate a variety of intracellular signaling cascades into a coordinated output that dynamically modulates membrane excitability. Finally, the pathophysiology that may arise from dysregulation of these channels is also reviewed.

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Section: Cardiac Pathologymentioning

confidence: 53%

“…Left ventricle myocytes show a decrease in I to following MI in rodent models (87,88,157,226). This reduction was greater in epicardial than in endocardial myocytes (226).…”

Section: Cardiac Pathologymentioning

confidence: 98%

Structure and Function of Kv4-Family Transient Potassium Channels

Birnbaum

Varga

et al. 2004

Physiological Reviews

319

360

View full text Add to dashboard Cite

show abstract

“…A range of apparent molecular weights have been detected for Kv2.1 α-subunits in different tissues. Kv2.1 α-subunits have been described either as M r 130 000 in the rat brain [123], as M r 132 000 in PC12 cells [124], as M r 125 000 in rat aortic myocytes [125], and as M r 130 000 in rat atrial and ventricular myocytes [126,127], while rat mesenteric artery smooth muscle cells express what seems to be an unphosphorylated M r 95 000 Kv2.1 subunit [128]. Insulin secreting cells express a Kv2.1 α-subunit that is approximately M r 108 000 [3,55,66].…”

Section: Post-translational Phosphorylationmentioning

confidence: 99%

Voltage-dependent K + channels in pancreatic beta cells: Role, regulation and potential as therapeutic targets

2003

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Insulin secretion from pancreatic islet beta cells is acutely regulated by a complex interplay of metabolic and electrogenic events. The electrogenic mechanism regulating insulin secretion from beta cells is commonly referred to as the ATP-sensitive K + (K ATP ) channel dependent pathway. Briefly, an increase in ATP and, perhaps more importantly, a decrease in ADP stimulated by glucose metabolism depolarises the beta cell by closing K ATP channels. Membrane depolarisation results in the opening of voltage-dependent Ca 2+ channels, and influx of Ca 2+ is the main trigger for insulin secretion. Repolarisation of pancreatic beta cell action potential is mediated by the activation of voltage-dependent K + (Kv) channels. Various Kv channel homologues have been detected in insulin secreting cells, and recent studies have shown a role for specific Kv channels as modulators of insulin secretion. Here we review the evidence supporting a role for Kv channels in the regulation of insulin secretion and discuss the potential and the limitations for beta-cell Kv channels as therapeutic targets. Furthermore, we review recent investigations of mechanisms regulating Kv channels in beta cells, which suggest that Kv channels are active participants in the regulation of beta-cell electrical activity and insulin secretion. [Diabetologia (2003[Diabetologia ( ) 46:1046[Diabetologia ( -1062

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“…There may be compensatory upregulation of Kv1.4 subunits (Kaprielian et al, 2002), although downregulation of Kv1.4 has also been reported (Gidh-Jain et al, 1996). Decreases in rat I K correlate with downregulation of the putative -subunit Kv2.1 (Huang et al, 2001b). The effects of postinfarction remodeling on spatial dispersion of electrophysiological properties in noninfarcted tissues are controversial, with one study showing increases in dispersion (Huang et al, 2001b) and another decreased spatial heterogeneity (Kaprielian et al, 2002).…”

Section: Changes In Kmentioning

confidence: 99%

Mechanisms of Postinfarction Electrophysiological Abnormality: Sympathetic Neural Remodeling, Electrical Remodeling and Gap Junction Remodeling

Zhong¹,

Li²,

Ke³

et al. 2012

Advances in Electrocardiograms - Clinical Applications

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Spatial alterations of Kv channels expression and K+ currents in post-MI remodeled rat heart

Abstract: Our results suggest that regional downregulation of Kv channels expression and density of K(+) currents can be a significant determinant of increased spatial electrophysiological heterogeneity and contribute to increased electrical instability of the post-MI heart.

Cited by 36 publications

References 23 publications

Structure and Function of Kv4-Family Transient Potassium Channels

Structure and Function of Kv4-Family Transient Potassium Channels

Voltage-dependent K + channels in pancreatic beta cells: Role, regulation and potential as therapeutic targets

Mechanisms of Postinfarction Electrophysiological Abnormality: Sympathetic Neural Remodeling, Electrical Remodeling and Gap Junction Remodeling

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