Role of KCa3.1 Channels in Proliferation and Migration of Vascular Smooth Muscle Cells by Diabetic Rat Serum

Su, Xingli; Zhao, Hong; Yu, Wei; Wang, Shuang; Zhu, Weijun

doi:10.4077/cjp.2013.bab104

Cited by 5 publications

(1 citation statement)

References 34 publications

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“…The KCa 3.1 channel is expressed by VSMCs and it regulates their cell cycle and proliferation [ 113 , 114 ]. In conditions such as DM, this channel is upregulated and stimulates VSMC proliferation and migration [ 113 , 115 ], causing the onset and growth of atherosclerotic lesions [ 113 , 116 , 117 ]. The same channel KCa 3.1 is expressed also by macrophages, lymphocytes, and platelets [ 113 ].…”

Section: Role Of Ion Channels In the Pathophysiological Continuum mentioning

confidence: 99%

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%

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

Severino

D’Amato

Netti

et al. 2018

IJMS

101

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Modafinil improves monocrotaline-induced pulmonary hypertension rat model

et al. 2016

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Background: Pulmonary arterial hypertension (PAH) progressively leads to increases in pulmonary vasoconstriction. Modafinil plays a role in vasorelaxation and blocking KCa3.1 channel with a result of elevating intracellular cyclic adenosine monophosphate (cAMP) levels. The purpose of this study is to evaluate the effects on modafinil in monocrotaline (MCT)-induced PAH rat. Methods: The rats were separated into three groups: the control group, the monocrotaline (M) group (MCT 60 mg/kg), and the modafinil (MD) group (MCT 60 mg/kg + modafinil). results: Reduced right ventricular pressure (RVP) was observed in the MD group. Right ventricular hypertrophy was improved in the MD group. Reduced number of intra-acinar pulmonary arteries and medial wall thickness were noted in the MD group. After the administration of modafinil, protein expressions of endothelin-1 (ET-1), endothelin receptor A (ERA) and KCa3.1 channel were significantly reduced. Modafinil suppressed pulmonary artery smooth muscle cell (PASMC) proliferation via cAMP and KCa3.1 channel. Additionally, we confirmed protein expressions such as Bcl-2-associated X, vascular endothelial growth factor, tumor necrosis factor-α, and interleukin-6 were reduced in the MD group. conclusion: Modafinil improved PAH by vasorelaxation and a decrease in medial thickening via ET-1, ERA, and KCa3.1 down regulation. This is a meaningful study of a modafinil in PAH model.

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Crocin Improves Endothelial Mitochondrial Dysfunction via GPx1/ROS/KCa3.1 Signal Axis in Diabetes

Cao

et al. 2021

Front. Cell Dev. Biol.

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Mitochondrial dysfunction contributes to excessive reactive oxygen species (ROS) generation, which is a dramatic cause to promote endothelial dysfunction in diabetes. It was previously demonstrated that crocin protected the endothelium based on its diverse medicinal properties, but its effect on the mitochondrion and the potential mechanism are not fully understood. In this study, mitochondrial function was analyzed during the process of excessive ROS generation in high glucose (HG)-cultured human umbilical vein endothelial cells (HUVECs). The role played by KCa3.1 was further investigated by the inhibition and/or gene silence of KCa3.1 in this process. In addition, nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase 2 (NOX2), superoxide dismutase 1 (SOD1), and glutathione peroxidase 1 (GPx1) were also detected in this study. Our data showed that crocin improved mitochondrial dysfunction and maintained normal mitochondrial morphology by enhancing the mitochondrial membrane potential (MMP), mitochondrial mass, and mitochondrial fusion. Furthermore, KCa3.1 was confirmed to be located in the mitochondrion, and the blockade and/or silencing of KCa3.1 improved mitochondrial dysfunction and reduced excessive ROS generation but did not affect NOX2 and/or the SOD1 system. Intriguingly, it was confirmed that KCa3.1 expression was elevated by ROS overproduction in the endothelium under HG and/or diabetes conditions, while crocin significantly suppressed this elevation by promoting GPx1 and subsequently eliminating ROS generation. In addition, crocin enhanced CD31, thrombomodulin (TM), and p-/t-endothelial nitric oxide synthase (eNOS) expressions as well as NO generation and decreased vascular tone. Hence, crocin improved mitochondrial dysfunction through inhibiting ROS-induced KCa3.1 overexpression in the endothelium, which in turn reduced more ROS generation and final endothelial dysfunction in diabetes.

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Role of KCa3.1 Channels in Proliferation and Migration of Vascular Smooth Muscle Cells by Diabetic Rat Serum

Cited by 5 publications

References 34 publications

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

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

Modafinil improves monocrotaline-induced pulmonary hypertension rat model

Crocin Improves Endothelial Mitochondrial Dysfunction via GPx1/ROS/KCa3.1 Signal Axis in Diabetes

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