Search

Fe deficiency is a widespread nutritional disorder in plants. The basic helix-loop-helix ( bHLH) transcription factors ( TFs), especially Ib subgroup bHLH TFs which are involved in iron uptake, have been identified. In this study, an IVc subgroup bHLH TF Mdb HLH104 was identified and characterized as a key component in the response to Fe deficiency in apple. The overexpression of the Mdb HLH104 gene noticeably increased the H+- ATPase activity under iron limitation conditions and the tolerance to Fe deficiency in transgenic apple plants and calli. Further investigation showed that Mdb HLH104 proteins bonded directly to the promoter of the Md AHA8 gene, thereby positively regulating its expression, the plasma membrane ( PM) H+- ATPase activity and Fe uptake. Similarly, Mdb HLH104 directly modulated the expression of three Fe-responsive bHLH genes, Mdb HLH38, Mdb HLH39 and Md PYE. In addition, Mdb HLH104 interacted with 5 other IVc subgroup bHLH proteins to coregulate the expression of the Md AHA8 gene, the activity of PM H+- ATPase and the content of Fe in apple calli. Therefore, Mdb HLH104 acts together with other apple bHLH TFs to regulate Fe uptake by modulating the expression of the Md AHA8 gene and the activity of PM H+- ATPase in apple. [ABSTRACT FROM AUTHOR]

Differential expression of microRNA (miR)‑335‑5p, a key tumor suppressor, has been detected in pre‑eclampsia (PE) placentas. However, the role of miR‑335‑5p in the pathogenesis of PE and the factor modulating its aberrant expression remain unknown. The present study used JEG‑3 cells in vitro to investigate these mechanisms. The role of miR‑335‑5p in proliferation, apoptosis and migration of JEG‑3 cells was investigated using MTT, Annexin V‑FITC/PI, Transwell migration and wound healing assays, respectively. miR‑335‑5p expression levels were analyzed using reverse transcription‑quantitative PCR. The expression levels of E‑cadherin, N‑cadherin, Snail, specificity protein 1 (Sp1) and p53 were assessed using western blot analysis. Cell viability analysis was performed using the Cell Counting Kit‑8 assay. The intracellular reactive oxygen species (ROS) levels were detected using a 2,7‑dichlorodihydrofluorescein diacetate assay. The present results suggested that miR‑335‑5p did not affect the proliferation or apoptotic rate of JEG‑3 cells. Overexpression of miR‑335‑5p significantly inhibited the migration of JEG‑3 cells, decreased the expression levels of Sp1, N‑cadherin and Snail, and increased E‑cadherin expression. Sp1 silencing produced similar results in JEG‑3 cells. H2O2 significantly increased the intracellular ROS levels and miR‑335‑5p expression, whereas N‑acetyl‑cysteine pretreatment prior to H2O2 treatment reversed the increases in miR‑335‑5p expression. Knockdown of p53 significantly decreased the expression levels of miR‑335‑5p in JEG‑3 cells and in H2O2‑treated cells. The present results suggested that miR‑335‑5p expression levels in trophoblast cells could be increased by ROS in a p53‑dependent manner, leading to the downregulation of Sp1 and subsequent inhibition of epithelial to mesenchymal transition and cell migration. The present results may provide novel evidence on the etiology of PE.

Abnormal human coronary artery smooth muscle cells (hCASMCs) proliferation and migration are key factors in coronary artery restenosis after percutaneous coronary intervention. Platelets release 5-hydroxytryptamine (5-HT), which is a strong mitogen for pulmonary artery smooth muscle cells proliferation and migration. Here, we investigated the effects of 5-HT and role of 5-HT transporter (5-HTT) on hCASMCs proliferation and migration. The 5-HT (10(-6)-10(-5) mol/l) significantly increased hCASMCs proliferation and migration, and these effects were inhibited by fluoxetine (10(-5) mol/l) and citalopram (10(-6) mol/l), two 5-HTT blocker. Overexpression in hCASMCs enhanced 5-HT induced cells proliferation and migration. The 5-HTT and interleukin-1 beta (IL-1β) expression were increased in rat balloon injury carotid arteries. Treatment with IL-1β (10 ng/ml, 3d) upregulates 5-HTT expression in hCASMCs and increased 5-HT induced currents in Human Embryonic Kidney 293-5-HTT cells.