scholarly journals Inhibition of β-catenin Protects Mouse Hearts From Ventricular Arrhythmias After Myocardial Infarction Independent of Ion Channel Gene Changes

2021 ◽  
Author(s):  
Jerry Wang ◽  
Ying Xia ◽  
Aizhu Lu ◽  
Hongwei Wang ◽  
Darryl R. Davis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ion Channel ◽  
Chronic Phase ◽  
Gene Expressions ◽  
Structural Remodeling ◽  
Channel Gene ◽  
Signaling Activation ◽  
Ventricular Tachycardias ◽  
Ion Channel Gene ◽  
Gene Alterations

Abstract The Wnt/β-catenin signaling regulates ion channel gene expressions in cardiomyocytes. Because Wnt/β-catenin signaling is activated in myocardial infarction (MI), this study aims to investigate if β-catenin inhibition affects post-MI ion channel gene alterations and ventricular tachycardias (VT). MI was induced by permanent ligation of left anterior descending artery in wild-type (WT) and cardiomyocyte-specific β-catenin knockout (KO) mice. KO mice showed reduced susceptibility to VT (18% vs. 77% in WT) at week-8 after MI, associated with attenuated structural remodeling (reduced scar size and attenuated left ventricle dilation) as compared to WT. However, at the subacute phase (week-1) and chronic phase (week-8) after MI, Wnt/β-catenin signaling activation was found in non-cardiomyocytes, but not in cardiomyocytes. Downregulations of Scn5a (encoding Nav1.5) and Gja1 (encoding Cx43) were found at week-1 but not at week-8, while downregulations of K+ channel genes were present at both week-1 and -8. Consistent with no activation of Wnt/β-catenin pathway in cardiomyocytes at week-1 and -8, these alterations in ion channel/transporter genes were not different between KO and WT mice. This study demonstrated that mice with cardiomyocyte-specific β-catenin deletion have reduced VT susceptibility after MI which is caused by attenuated structural remodeling, instead of alterations in ion channel gene expressions.

scholarly journals Cardiomyocyte-specific deletion of β-catenin protects mouse hearts from ventricular arrhythmias after myocardial infarction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jerry Wang ◽  
Ying Xia ◽  
Aizhu Lu ◽  
Hongwei Wang ◽  
Darryl R. Davis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ion Channel ◽  
Chronic Phase ◽  
Channel Gene ◽  
Cardiac Sodium Channel ◽  
Wnt Ligands ◽  
Ventricular Tachycardias ◽  
Specific Deletion ◽  
Ion Channel Gene ◽  
Gene Alterations

AbstractWnt/β-catenin signaling is activated in the heart after myocardial infarction (MI). This study aims to investigate if β-catenin deletion affects post-MI ion channel gene alterations and ventricular tachycardias (VT). MI was induced by permanent ligation of left anterior descending artery in wild-type (WT) and cardiomyocyte-specific β-catenin knockout (KO) mice. KO mice showed reduced susceptibility to VT (18% vs. 77% in WT) at 8 weeks after MI, associated with reduced scar size and attenuated chamber dilation. qPCR analyses of both myocardial tissues and purified cardiomyocytes demonstrated upregulation of Wnt pathway genes in border and infarct regions after MI, including Wnt ligands (such as Wnt4) and receptors (such as Fzd1 and Fzd2). At 1 week after MI, cardiac sodium channel gene (Scn5a) transcript was reduced in WT but not in KO hearts, consistent with previous studies showing Scn5a inhibition by Wnt/β-catenin signaling. At 8 weeks after MI when Wnt genes have declined, Scn5a returned to near sham levels and K+ channel gene downregulations were not different between WT and KO mice. This study demonstrated that VT susceptibility in the chronic phase after MI is reduced in mice with cardiomyocyte-specific β-catenin deletion primarily through attenuated structural remodeling, but not ion channel gene alterations.

scholarly journals Inhibition of β-catenin Protects Mouse Hearts From Ventricular Arrhythmias After Myocardial Infarction Independent of Ion Channel Gene Changes

2021 ◽  
Author(s):  
Jerry Wang ◽  
Ying Xia ◽  
Aizhu Lu ◽  
Hongwei Wang ◽  
Darryl R. Davis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ion Channel ◽  
Ventricular Arrhythmias ◽  
Chronic Phase ◽  
Channel Gene ◽  
Cardiac Sodium Channel ◽  
Wnt Ligands ◽  
Ventricular Tachycardias ◽  
Ion Channel Gene ◽  
Gene Alterations

Abstract Wnt/β-catenin signaling is activated in the heart after myocardial infarction (MI). This study aims to investigate if β-catenin deletion affects post-MI ion channel gene alterations and ventricular tachycardias (VT). MI was induced by permanent ligation of left anterior descending artery in wild-type (WT) and cardiomyocyte-specific β-catenin knockout (KO) mice. KO mice showed reduced susceptibility to VT (18% vs. 77% in WT) at 8 weeks after MI, associated with reduced scar size and attenuated chamber dilation. qPCR analyses of both myocardial tissues and purified cardiomyocytes demonstrated upregulation of Wnt pathway genes in border and infarct regions after MI, including Wnt ligands (such as Wnt4) and receptors (such as Fzd1 and Fzd2).. At 1 week after MI, cardiac sodium channel gene (Scn5a) transcript was reduced in WT but not in KO hearts, consistent with previous studies showing Scn5a inhibition by Wnt/β-catenin signaling. At 8 weeks after MI when Wnt genes have declined, Scn5a returned to near sham levels and K+ channel gene downregulations were not different between WT and KO mice. This study demonstrated that VT susceptibility in the chronic phase after MI is reduced in mice with cardiomyocyte-specific β-catenin deletion primarily through attenuated structural remodeling, but not ion channel gene alterations.

scholarly journals Impaired redox environment modulates cardiogenic and ion-channel gene expression in cardiac-resident and non-resident mesenchymal stem cells

2017 ◽  
Vol 242 (6) ◽  
pp. 645-656 ◽  
Author(s):  
Baskar Subramani ◽  
Sellamuthu Subbannagounder ◽  
Chithra Ramanathanpullai ◽  
Sekar Palanivel ◽  
Rajesh Ramasamy
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Ascorbic Acid ◽  
Mesenchymal Stem Cells ◽  
Ion Channel ◽  
Oxygen Species ◽  
Gene Expressions ◽  
Redox Imbalance ◽  
Channel Gene ◽  
Ion Channel Gene

Redox homeostasis plays a crucial role in the regulation of self-renewal and differentiation of stem cells. However, the behavioral actions of mesenchymal stem cells in redox imbalance state remain elusive. In the present study, the effect of redox imbalance that was induced by either hydrogen peroxide (H2O2) or ascorbic acid on human cardiac-resident (hC-MSCs) and non-resident (umbilical cord) mesenchymal stem cells (hUC-MSCs) was evaluated. Both cells were sensitive and responsive when exposed to either H2O2 or ascorbic acid at a concentration of 400 µmol/L. Ascorbic acid pre-treated cells remarkably ameliorated the reactive oxygen species level when treated with H2O2. The endogenous antioxidative enzyme gene (Sod1, Sod2, TRXR1 and Gpx1) expressions were escalated in both MSCs in response to reactive oxygen species elevation. In contrast, ascorbic acid pre-treated hUC-MSCs attenuated considerable anti-oxidative gene (TRXR1 and Gpx1) expressions, but not the hC-MSCs. Similarly, the cardiogenic gene (Nkx 2.5, Gata4, Mlc2a and β-MHC) and ion-channel gene ( IKDR, IKCa, Ito and INa.TTX) expressions were significantly increased in both MSCs on the oxidative state. On the contrary, reduced environment could not alter the ion-channel gene expression and negatively regulated the cardiogenic gene expressions except for troponin-1 in both cells. In conclusion, redox imbalance potently alters the cardiac-resident and non-resident MSCs stemness, cardiogenic, and ion-channel gene expressions. In comparison with cardiac-resident MSC, non-resident umbilical cord-MSC has great potential to tolerate the redox imbalance and positively respond to cardiac regeneration. Impact statement Human mesenchymal stem cells (h-MSCs) are highly promising candidates for tissue repair in cardiovascular diseases. However, the retention of cells in the infarcted area has been a major challenge due to its poor viability and/or low survival rate after transplantation. The regenerative potential of mesenchymal stem cells (MSCs) repudiate and enter into premature senescence via oxidative stress. Thus, various strategies have been attempted to improve the MSC survival in ‘toxic’ conditions. Similarly, we investigated the response of cardiac resident MSC (hC-MSCs) and non-resident MSCs against the oxidative stress induced by H2O2. Supplementation of ascorbic acid (AA) into MSCs culture profoundly rescued the stem cells from oxidative stress induced by H2O2. Our data showed that the pre-treatment of AA is able to inhibit the cell death and thus preserving the viability and differentiation potential of MSCs.

scholarly journals Mitochondrial and ion channel gene alterations in autism

2012 ◽  
Vol 1817 (10) ◽  
pp. 1796-1802 ◽  
Author(s):  
Moyra Smith ◽  
Pamela L. Flodman ◽  
John J. Gargus ◽  
Mariella T. Simon ◽  
Kimberley Verrell ◽  
...  
Keyword(s):  
Ion Channel ◽  
Channel Gene ◽  
Ion Channel Gene ◽  
Gene Alterations

scholarly journals Ion channel gene expressions in infertile men: A case-control study

2017 ◽  
Vol 15 (12) ◽  
pp. 749-756 ◽  
Author(s):  
Serkan Carkci ◽  
Ebru Onalan Etem ◽  
Seda Ozaydin ◽  
Ahmet Karakeci ◽  
Ahmet Tektemur ◽  
...  
Keyword(s):  
Ion Channel ◽  
Case Control Study ◽  
Case Control ◽  
Gene Expressions ◽  
Channel Gene ◽  
Infertile Men ◽  
Control Study ◽  
Ion Channel Gene

scholarly journals Ion Channel Gene Expression in Lung Adenocarcinoma: Potential Role in Prognosis and Diagnosis

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e86569 ◽  
Author(s):  
Jae-Hong Ko ◽  
Wanjun Gu ◽  
Inja Lim ◽  
Hyoweon Bang ◽  
Eun A. Ko ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Adenocarcinoma ◽  
Ion Channel ◽  
Potential Role ◽  
Channel Gene ◽  
Ion Channel Gene

scholarly journals Crispri Ion Channel Gene Modulation in Human iPSC-Cardiomyocytes

2020 ◽  
Vol 118 (3) ◽  
pp. 569a
Author(s):  
Julie L. Han ◽  
Emilia Entcheva
Keyword(s):  
Ion Channel ◽  
Gene Modulation ◽  
Channel Gene ◽  
Human Ipsc ◽  
Ion Channel Gene

scholarly journals A microbial TRP-like polycystic-kidney-disease-related ion channel gene

2005 ◽  
Vol 387 (1) ◽  
pp. 211-219 ◽  
Author(s):  
Christopher P. PALMER ◽  
Ebru AYDAR ◽  
Mustafa B. A. DJAMGOZ
Keyword(s):  
Cell Wall ◽  
Kidney Disease ◽  
Ion Channel ◽  
Polycystic Kidney Disease ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Cell Wall Synthesis ◽  
Polycystic Kidney ◽  
Channel Gene ◽  
Ion Channel Gene

Ion channel genes have been discovered in many microbial organisms. We have investigated a microbial TRP (transient receptor potential) ion channel gene which has most similarity to polycystic-kidney-disease-related ion channel genes. We have shown that this gene (pkd2) is essential for cellular viability, and is involved in cell growth and cell wall synthesis. Expression of this gene increases following damage to the cell wall. This fission yeast pkd2 gene, orthologues of which are found in all eukaryotic cells, appears to be a key signalling component in the regulation of cell shape and cell wall synthesis in yeast through an interaction with a Rho1-GTPase. A model for the mode of action of this Schizosaccharomyces pombe protein in a Ca2+ signalling pathway is hypothesized.

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