Expression Of Sodium-hydrogen Exchanger Research Articles

Alleviating sweetpotato salt tolerance through exogenous glutathione and melatonin: A profound mechanism for active oxygen detoxification and preservation of photosynthetic organs

Salt stress profoundly impacts sweetpotato production. Exogenous glutathione (GSH) and melatonin (MT) promoted plant growth under stress, but their specific roles and mechanisms in sweetpotato salt tolerance need exploration. This study investigated GSH and MT’s regulatory mechanisms in sweetpotato under salt stress. Salt stress significantly reduces both growth and biomass by hindering photosynthesis, root traits, K+ content, and K+/Na+ balance, leading to oxidative stress and excessive hydrogen peroxide (H2O2), superoxide ion (O2•−), and malondialdehyde (MDA) production and Na+ accumulation. Nevertheless, GSH (2 mM) and MT (25 μM) pre-treatments effectively mitigated salt-induced oxidative damage and protected the plasma membrane. They reduced osmotic pressure by enhancing K+ uptake, K+/Na+ regulation, osmolyte accumulation, and reducing Na+ accumulation. Improved stomatal traits, chloroplast and grana lamella preservation, and maintenance of mesophyll cells, cell wall, and mitochondrial structure were observed with GSH and MT pre-treatments under salt stress, therefore boosting the photosynthetic system and enhancing plant growth and biomass. Moreover, the findings also indicate that the positive outcomes of GSH and MT pre-treatments result from elevated antioxidant levels, enhanced enzymatic activity, and upregulated expression of sodium hydrogen exchanger 2 (NHX2), K+transporter 1 (AKT1), and cation/H+exchanger (CHX), CBL-interacting protein kinase 1 (CIPK1), and antioxidant enzyme genes. These mechanisms enhance structural stability in photosynthesis and reduce salt stress. Evidently, MT pre-treatment exhibited superior effects compared to GSH. These findings provide a firm theoretical basis for employing GSH and MT to enhance salt tolerance in sweetpotato cultivation.

Amorphous Selenium Nanoparticles Improve Vascular Function in Rats With Chronic Isocarbophos Poisoning via Inhibiting the Apoptosis of Vascular Endothelial Cells.

AimThis study aimed to investigate the preventive effect and possible mechanism of amorphous selenium nanoparticles (A-SeQDs) on isocarbophos induced vascular dysfunction.MethodsA-SeQDs was made by auto redox decomposition of selenosulfate precursor. Male rats were given isocarbophos (0.5 mg/kg/2 days) by intragastric administration for 16 weeks to induce vascular dysfunction. During the course, A-SeQDs (50 mg/kg/day) was added to the water from week 5. Then, the rats were killed to observe and test the influence of A-SeQDs on the vascular dysfunction induced by isocarbophos. Finally, human umbilical vein endothelial cells (HUVECs) were treated with 10% DMEM of isocarbophos (100 μM) for 5 days to detect the related indexes. Before the use of isocarbophos treatment, different drugs were given.ResultsA-SeQDs could reduce total carbon dioxide, MDA, VCAM-1, ICAM-1, IL-1, and IL-6 while increasing oxygen saturation, NO content, and SOD activity in rats. A-SeQDs also resulted in relatively normal vascular morphology, and the expression of sodium hydrogen exchanger 1 (NHE1) and caspase-3 decreased in rats. Furthermore, in HUVECs treated with isocarbophos, A-SeQDs maintained mitochondrial membrane potential, inhibited the cleaved caspase-3 expression, and released cytochrome c from mitochondria to cytosol.ConclusionA-SeQDs can inhibit the apoptosis of HUVECs through the mitochondrial pathway, and effectively treat the impairment of vascular endothelial function caused by isocarbophos, which is NHE1-dependent.

Enhanced expression of sodium hydrogen exchanger (NHE)-1, 2 and 4 in the uteri of rat model for post-menopause under phytoestrogen genistein influence

Maintaining near normal uterine fluid pH is important for restoring uterine function after menopause. We hypothesized that genistein could restore uterine fluid pH via its effect on NHE expression. This study therefore investigated changes in uterine NHE-1, 2 and 4 expression under genistein influence. Ovariectomized female rats received genistein (25, 50 or 100mg/kg/day) for seven consecutive days. Uteri were harvested and NHE-1, 2 and 4 mRNA expression were analyzed by Real-time PCR while distribution of these transporters’ protein was observed by immunohistochemistry. Expression of NHE-1, 2 and 4 mRNA increased with increasing doses of genistein which was antagonized by ICI 182780. Under genistein influence, NHE-1, 2 and 4 proteins were found to be distributed at apical membrane of endometrial luminal epithelia. Enhanced expression of NHE-1, 2 and 4 in ovariectomised rat uteri by genistein might help to restore pH of uterine fluid which could be useful for women after menopause.

Enhanced Expression of Sodium Hydrogen Exchanger (NHE)-1, 2 and 4 in the Cervix of Ovariectomised Rats by Phytoestrogen Genistein.

Restoring the pH of cervicovaginal fluid is important for the cervicovaginal health after menopause. Genistein, which is a widely consumed dietary health supplement to overcome the post-menopausal complications could help to restore the cervicovaginal fluid pH. We hypothesized that genistien effect involves changes in expression of NHE-1, 2 and 4 proteins and mRNAs in the cervix. This study investigated effect of genistein on NHE-1, 2 and 4 protein and mRNA expression in the cervix in order to elucidate the mechanisms underlying possible effect of this compound on cervicovaginal fluid pH after menopause. Methods: Ovariectomised adult female rats received 25, 50 and 100 mg/kg/day genistein for seven consecutive days. At the end of the treatment, animals were sacrificed and cervix was harvested. Expression of Nhe-1, 2 and 4 mRNA were analyzed by Real-time PCR while distribution of NHE-1, 2 and 4 protein were observed by immunohistochemistry. Results: Treatment with 50 and 100 mg/kg/day genistein caused marked increase in the levels of expression and distribution of NHE-1, 2 and 4 proteins in the endocervical epithelia. Levels of Nhe-1, 2 and 4 mRNA in the cervix were also increased. Coadministration of ICI 182 780 and genistein reduced the expression levels of NHE-1, 2 and 4 proteins and mRNAs in the cervix. Conclusions: Enhanced expression of NHE-1, 2 and 4 proteins and mRNAs expression in cervix under genistein influence could help to restore the cervicovaginal fluid pH that might help to prevent cervicovaginal complications related to menopause.

Abstract 391: Enhanced Coronary Vasoconstriction in Western Diet-Induced Obesity is Associated with Alterations in NHE1, SERCA2a and 3

Cardiovascular disease (CVD) remains a major risk factor and cause of mortality in type 2 diabetes but, the effect of western diet (WD) on coronary artery vasoconstriction has not been well characterized. Therefore, the purpose of this study was to identify potential calcium (Ca 2+ ) molecular mechanism(s) underlying alterations in coronary constriction in WD-induced obesity. C57Bl/6J mice were fed a WD or control diet for 16wks. Coronary vascular function was assessed with wire myography and human coronary vascular smooth muscle cells (VSMC) were cultured. WD enhanced coronary constriction to the thromboxane analog U46619. This was associated with increased coronary VSMC expression of sodium-hydrogen exchanger 1 (NHE1) and SERCA3 with decreased expression of SERCA2a. Oxidation of SERCA2a cysteine-674, a signal for SERCA2a degradation, was increased in WD coronary VSMC. Exposure of cultured human coronary VSMC to hyperinsulinemic conditions elicited similar changes in SERCA2a, 3 and NHE1. This study suggests that enhanced thromboxane-mediated coronary constriction in WD and insulin resistance/hyperinsulinemia may result from NHE1-dependent changes in intracellular pH and/or impaired Ca 2+ handling at the level of the sarcoplasmic reticulum.

753 Spermidine Upregulates the Function and Expression of Sodium-Hydrogen Exchanger 3 (SLC9A3) in CaCo2 Cells

753 Spermidine Upregulates the Function and Expression of Sodium-Hydrogen Exchanger 3 (SLC9A3) in CaCo2 Cells

Hydrostatic intestinal edema induced signaling pathways: Potential role of mechanical forces

Hydrostatic intestinal edema initiates a signal transduction cascade that results in smooth muscle contractile dysfunction. Given the rapid and concurrent alterations in the mechanical properties of edematous intestine observed with the development of edema, we hypothesize that mechanical forces may serve as a stimulus for the activation of certain signaling cascades. We sought to examine whether isolated similar magnitude mechanical forces induced the same signal transduction cascades associated with edema. The distal intestine from adult male Sprague Dawley rats was stretched longitudinally for 2 h to 123% its original length, which correlates with the interstitial stress found with edema. We compared wet-to-dry ratios, myeloperoxidase activity, nuclear signal transduction and activator of transcription (STAT)-3 and nuclear factor (NF)-kappa B DNA binding, STAT-3 phosphorylation, myosin light chain phosphorylation, baseline and maximally stimulated intestinal contractile strength, and inducible nitric oxide synthase (iNOS) and sodium hydrogen exchanger 1-3 messenger RNA (mRNA) in stretched and adjacent control segments of intestine. Mechanical stretch did not induce intestinal edema or an increase in myeloperoxidase activity. Nuclear STAT-3 DNA binding, STAT-3 phosphorylation, and nuclear NF-kappa B DNA binding were significantly increased in stretched seromuscular samples. Increased expression of sodium hydrogen exchanger 1 was found but not an increase in iNOS expression. Myosin light chain phosphorylation was significantly decreased in stretched intestine as was baseline and maximally stimulated intestinal contractile strength. Intestinal stretch, in the absence of edema/inflammatory/ischemic changes, leads to the activation of signaling pathways known to be altered in intestinal edema. Edema may initiate a mechanotransductive cascade that is responsible for the subsequent activation of various signaling cascades known to induce contractile dysfunction.