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

Varicocele is commonly associated with male infertility because it impairs normal sperm morphology and activity. Polyunsaturated fatty acids (PUFA) are important determinants of sperm cell structure and function, but their relationship with varicocele remains unclear. The aim of the present study was to investigate the PUFA composition in spermatozoa of infertile men with varicocele and to evaluate the potential relationship between PUFA and varicocele. This case control study recruited 92 infertile men with varicocele, 99 infertile men without varicocele and 95 fertile male control subjects. Semen morphology and activity parameters were assessed and seminal plasma 8-hydroxy-2-deoxyguanosine (8-OHdG) content was determined by ELISA. Sperm concentrations of omega-3 and omega-6 fatty acids were measured by gas chromatography. Infertile men with varicocele had lower concentrations of omega-3 PUFA, higher omega-6 : omega-3 PUFA ratios and greater oxidative DNA damage in spermatozoa compared with infertile men without varicocele and normal subjects. The degree of varicocele and DNA damage was associated with decreased omega-3 PUFA concentrations and semen quality in infertile men with varicocele. The findings suggest that omega-3 PUFA deficiency could be implicated in varicocele-associated infertility, and highlight the need for intervention trials to test the usefulness of omega-3 supplementation in reducing sperm abnormalities in infertile men with varicocele.

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

Experimental Biology and Medicine ◽

10.1177/1535370216688568 ◽

2017 ◽

Vol 242 (6) ◽

pp. 645-656 ◽

Cited By ~ 4

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.

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REDUCED RISK OF PROSTATE CANCER IN INFERTILE MEN COMPARED TO MEN WITH PROVEN FERTILITY: A NESTED CASE- CONTROL STUDY

European Urology Supplements ◽

10.1016/s1569-9056(08)60504-7 ◽

2008 ◽

Vol 7 (3) ◽

pp. 197

Author(s):

Y. Ruhayel ◽

A. Giwercman ◽

P.A. Abrahamsson ◽

L. Rylander ◽

J. Manjer ◽

...

Keyword(s):

Prostate Cancer ◽

Case Control Study ◽

Case Control ◽

Infertile Men ◽

Nested Case Control ◽

Control Study ◽

Reduced Risk

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Impact of oxidative stress on semen parameters in normozoospermic infertile men: a case–control study

African Journal of Urology ◽

10.1186/s12301-020-00061-6 ◽

2020 ◽

Vol 26 (1) ◽

Author(s):

Ayad Palani ◽

Ahmed Alahmar

Keyword(s):

Oxidative Stress ◽

Uric Acid ◽

Male Infertility ◽

Seminal Plasma ◽

Case Control Study ◽

Case Control ◽

Semen Parameters ◽

Infertile Men ◽

Total Antioxidant ◽

Control Study

Abstract Background Oxidative stress has been implicated in male infertility through decrease in sperm quality. However, men with normal semen parameters (normozoospermia) may be unable to fertilize their partners even when they have normal sperm function. Thus, they would be considered infertile. The purpose of this study was to investigate the role of oxidative stress in the pathogenesis of unexplained male infertility. Methods In this case–control study, infertile men with normozoospermia (n = 46) and fertile control group (n = 21) underwent seminal fluid analyses according to WHO 2010 criteria. Serum and seminal plasma levels of total antioxidant capacity (TAC), glutathione, malondialdehyde, uric acid and albumin were also measured using colorimetric methods. Results The level of total antioxidant capacity in both serum and seminal plasma was significantly lower in normozoospermic infertile men in comparison with fertile group (p < 0.0001). However, no significant differences were observed in serum and seminal plasma levels of glutathione, uric acid, albumin and malondialdehyde between infertile and fertile groups. Conclusion Low TAC level induces oxidative stress and consequently causes sperm dysfunction and male infertility. Estimation of TAC can be a useful tool in the diagnosis of male infertility. Antioxidant supplementation should be considered in the treatment of oxidative stress-induced male infertility.

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Underexpression of hsa-miR-449 family and their promoter hypermethylation in infertile men: A case-control study

International Journal of Reproductive BioMedicine ◽

10.18502/ijrm.v19i1.8177 ◽

2021 ◽

Author(s):

Reza Najafipour ◽

Abdolmabood Momeni ◽

Farideh Yousefipour ◽

Shaghayegh Mousavi ◽

Sahar Moghbelinejad

Keyword(s):

Case Control Study ◽

Promoter Hypermethylation ◽

Case Control ◽

Methylation Pattern ◽

Specific Pcr ◽

Infertile Men ◽

Pcr Method ◽

Defective Spermatogenesis ◽

Control Study ◽

Control Samples

Background: Post-transcriptional microRNAs (miRNAs) have an important pattern in the spermatogenesis process. Objective: Study of the expression and methylation of hsa-miR-449 family in sperm samples of infertile men. Materials and Methods: In this case-control study, we recruited 74 infertile men (with asthenozoospermia, teratozoospermia, asthenoteratozoospermia, and oligoasthenoteratozoospermia) and 30 control samples. Methylation-specific PCR (MSP) method was used for methylation evaluation of hsa-miR-449 a, b, c promoter. By Real time PCR (qRT-PCR) method,we showed downregulation of hsa-miR-449 a, b, c in the sperm samples of infertile men and compared it to their fertile counterparts. Results: There was significant underexperssion, in hsa-miR-449-b in oligoasthenoteratospermic samples (p = 0.0001, F = 2.9). About the methylation pattern, infertile men showed high frequency of methylation in the promoter of hsa-miR-449 a, b, c in comparison to controls (60.8% vs 23.3%), the highest amount of methylation was observed in oligoasthenoteratospermia samples (81.2%). Conclusion: In this study, low expression and high methylation of hsa-miR-449-b were observed in infertile men in compared to control samples, which can be one of the causes of defective spermatogenesis. Key words: Spermatogenesis, miR-449, Expression, Epigenetic.

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Two four-marker haplotypes on 7q36.1 region indicate that the potassium channel gene HERG1 (KCNH2, Kv11.1) is related to schizophrenia: a case control study

Behavioral and Brain Functions ◽

10.1186/1744-9081-6-27 ◽

2010 ◽

Vol 6 (1) ◽

pp. 27 ◽

Cited By ~ 16

Author(s):

Fatmahan Atalar ◽

Tufan Acuner ◽

Naci Cine ◽

Fatih Oncu ◽

Dogan Yesilbursa ◽

...

Keyword(s):

Potassium Channel ◽

Case Control Study ◽

Case Control ◽

Channel Gene ◽

Potassium Channel Gene ◽

Control Study

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889 Micro-Inflammation and Overexpression of CaV3.2 Ion Channel in the Colonic Mucosa of IBS Patients: A Case-Control Study

Gastroenterology ◽

10.1016/s0016-5085(14)60556-4 ◽

2014 ◽

Vol 146 (5) ◽

pp. S-156

Author(s):

Julien Scanzi ◽

Alison Accarie ◽

Emilie Muller ◽

Frederic A. Carvalho ◽

Bruno Pereira ◽

...

Keyword(s):

Ion Channel ◽

Colonic Mucosa ◽

Case Control Study ◽

Case Control ◽

Control Study

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

10.21203/rs.3.rs-393358/v1 ◽

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.

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