Acta biochimica Polonica最新文献

Plant transcriptomes are complex entities shaped spatially and temporally by a multitude of stressors. The aim of this review was to summarize the most relevant transcriptomic responses to selected abiotic (UV radiation, chemical compounds, drought, suboptimal temperature) and biotic (bacteria, fungi, viruses, viroids) stress conditions in a variety of plant species, including model species, crops, and medicinal plants. Selected basic and applicative studies employing RNA-seq from various sequencing platforms and single-cell RNA-seq were involved. The transcriptomic responsiveness of various plant species and the diversity of affected gene families were discussed. Under stress acclimation, plant transcriptomes respond particularly dynamically. Stress response involved both distinct, but also similar gene families, depending on the species, tissue, and the quality and dosage of the stressor. We also noted the over-representation of transcriptomic data for some plant organs. Studies on plant transcriptomes allow for a better understanding of response strategies to environmental conditions. Functional analyses reveal the multitude of stress-affected genes as well as acclimatory mechanisms and suggest metabolome diversity, particularly among medicinal species. Extensive characterization of transcriptomic responses to stress would result in the development of new cultivars that would cope with stress more efficiently. These actions would include modern methodological tools, including advanced genetic engineering, as well as gene editing, especially for the expression of selected stress proteins in planta and for metabolic modifications that allow more efficient synthesis of secondary metabolites.

Context: Oxidative stress is an important factor for vitreomacular interface disease development in a theoretical model.

Purpose: The aim of the study was to evaluate the correlation between oxidative stress in the human epiretinal membrane (ERM) and retinal morphological changes.

Material and methods: The study included patients scheduled for vitrectomy with epiretinal membrane removal. LogMAR best corrected visual acuity was assessed and optical coherence tomography was performed. Patients were divided into three groups: Type 1 - epiretinal membrane with premacular fibrosis; type 2 - epiretinal membrane with co-existing layer hole; and type 3 - ERM with co-existing full-thickness macular hole. During vitrectomy, epiretinal membranes were collected. Total oxidant status was determined by an automated colorimetric method in homogenates of epiretinal membrane.

Statistical analysis: The Mann-Whitney U test, Kruskal-Wallis test and Spearman linear correlation analysis were used. Statistical significance was set with a level of α = 0.05.

Results: Twenty-one Caucasian women (60%) and 14 men (40%) were included in the study. The average age of participants was 74.7 years (95% CI: 71.13-75.45). The mean best corrected visual acuity LogMAR value in the group was 0.8 (95% CI: 0.9-0.7). The mean ratio of total oxidant status to protein level in the collected samples was 0.161 (95% CI: 0.08-0.23) µmol/mg of protein. No correlation was found between total oxidant status and the degree of morphological retinal changes.

Conclusion: The study found no significant correlation between the level of oxidative stress in epiretinal membrane and retinal morphological changes.

[This retracts the article DOI: 10.18388/abp.2023_6398.].

Objective: The aim of our study was to compare the total 25(OH)D fraction, the bioavailable vitamin fraction, and the free vitamin D fraction in spring and fall in a group of healthy individuals. Methods: In our study, we collected blood samples from healthy participants at the end of both summer and winter, and measured serum levels of albumin, DBP, and 25(OH)D. Utilizing these data, we calculated the percentage of free and bioavailable vitamin D. Our cohort comprised 87 participants, with a male-to-female ratio of 14:73, aged 35.95 ± 12.55 years, ranging from 19 to 70 years. We employed the chemiluminescence method to determine the vitamin 25(OH)D levels, the ELISA method was utilized to determine DBP levels, the albumin BCP Assay was performed using the ADVIA biochemical analyzer (Siemens) and an online calculator was used to determine the free and bioavailable 25(OH)D levels. Results: Our findings indicate significantly lower 25(OH)D levels in winter (44.13 ± 17.82 nmol/L) compared to summer (74.97 ± 22.75 nmol/L; p < 0.001). For vitamin D binding protein there was no significant difference from summer (236.2 ± 164.39 mg/L) to winter (239.86 ± 141.9 mg/L; p = 0.77), albumin levels were significantly higher in summer (49.37 ± 4.15 g/L vs. 47.97 ± 3.91 g/L, p = 0.01), but the magnitude of the change may not be large enough to be solely responsible for the stability of vitamin D levels throughout the year. In the winter season a significantly lower calculated bioavailable 25(OH)D vitamin (7.45 ± 5.66 nmol/L against 13.11 ± 8.27 nmol/L; p < 0.001) was observed, and the free fraction also showed a significant decrease (17.3 ± 12.9 pmol/L versus 29.7 ± 19.1 pmol/L; p < 0.0001). We observed a moderately positive correlation between 25(OH)D and bioavailable percentage in winter (r = 0.680; p < 0.001), in contrast with a lower positive association in summer (r = 0.343; p < 0.001). Conclusion: Our data suggest a positive correlation between total and bioavailable 25(OH)D levels. In addition to the statistically significant variation in 25(OH)D between the two observation periods, there was an additional variation in the free vitamin D percentage. The summertime synthesis of vitamin D in the skin could contribute directly to the free fraction of vitamin D. Standardizing the measurement of free 25(OH)D and clinical studies is necessary to establish reference values before these methods can be implemented in clinical practice.

Endogenous electric fields (EFs) serve as a crucial signal to guide cell movement in processes such as wound healing, embryonic development, and cancer metastasis. However, the mechanism underlying cell electrotaxis remains poorly understood. A plausible hypothesis suggests that electrophoretic or electroosmotic forces may rearrange charged components of the cell membrane, including receptors for chemoattractants which induce asymmetric signaling and directional motility. This study aimed to explore the role of Transforming Growth Factor Beta (TGFβ) signaling in the electrotactic reaction of 3T3 fibroblasts. Our findings indicate that inhibiting canonical and several non-canonical signaling pathways originating from the activated TGF-β receptor does not hinder the directed migration of 3T3 cells to the cathode. Furthermore, suppression of TGF-β receptor expression does not eliminate the directional migration effect of 3T3 cells in the electric field. Additionally, there is no observed redistribution of the TGF-β receptor in the electric field. However, our studies affirm the significant involvement of Phosphoinositide 3-Kinase (PI3K) in electrotaxis, suggesting that in our model, its activation is likely associated with factors independent of TGFβ action.

Mitochondrial investigations have extended beyond their traditional functions, covering areas such as ATP synthesis and metabolism. Mitochondria are now implicated in new functional areas such as cytoprotection, cellular senescence, tumor function and inflammation. The basis of these new areas still relies on fundamental biochemical/biophysical mitochondrial functions such as synthesis of reactive oxygen species, mitochondrial membrane potential, and the integrity of the inner mitochondrial membrane i.e., the passage of various molecules through the mitochondrial membranes. In this view transport of potassium cations, known as the potassium cycle, plays an important role. It is believed that K⁺ influx is mediated by various potassium channels present in the inner mitochondrial membrane. In this article, we present an overview of the key findings and characteristics of mitochondrial potassium channels derived from research of many groups conducted over the past 33 years. We propose a list of six fundamental observations and most important ideas dealing with mitochondrial potassium channels. We also discuss the contemporary challenges and future prospects associated with research on mitochondrial potassium channels.

Depression is a common psychiatric disorder. Due to the disadvantages of current clinical drugs, including poor efficacy and unnecessary side effects, research has shifted to novel natural products with minimal or no adverse effects as therapeutic alternatives. The ocean is a vast ecological home, with a wide variety of organisms that can produce a large number of natural products with unique structures, some of which have neuroprotective effects and are a valuable source for the development of new drugs for depression. In this review, we analyzed preclinical and clinical studies of natural products derived from marine organisms with antidepressant potential, including the effects on the pathophysiology of depression, and the underlying mechanisms of these effects. It is expected to provide a reference for the development of new antidepressant drugs.

Human chemokine receptor 8 (CCR8) is a promising drug target for immunotherapy of cancer and autoimmune diseases. Monoclonal antibody-based CCR8 targeted treatment shows significant inhibition in tumor growth. The inhibition of CCR8 results in the improvement of antitumor immunity and patient survival rates by regulating tumor-resident regulatory T cells. Recently monoclonal antibody drug development targeting CCR8 has become a research hotspot, which also promotes the advancement of antibody evaluation methods. Therefore, we constructed a novel engineered customized cell line HEK293-cAMP-biosensor-CCR8 combined with CCR8 and a cAMP-biosensor reporter. It can be used for the detection of anti-CCR8 antibody functions like specificity and biological activity, in addition to the detection of antibody-dependent cell-mediated cytotoxicity and antibody-dependent-cellular-phagocytosis. We obtained a new CCR8 mAb 22H9 and successfully verified its biological activities with HEK293-cAMP-biosensor-CCR8. Our reporter cell line has high sensitivity and specificity, and also offers a rapid kinetic detection platform for evaluating anti-CCR8 antibody functions.

Metformin has shown great promise in the treatment of HCC. Radiofrequency ablation (RFA) deficiency results in recurrence and metastasis of remaining HCC tumors. Here, we aimed to investigate the role and mechanism of metformin in HCC after RFA deficiency. HCC cell line Hep-G2 was selected to simulate RFA deficiency and named HepG2-H cells. After treating cells with different concentrations of metformin (2.5, 5, 10 μM) or transfecting related plasmids, cell proliferation, migration, invasion, apoptosis and angiogenesis were detected, in vitro permeability test was performed, and an angiogenesis-related protein VEGFA was analyzed. The residual HCC model after RFA deficiency was established in mice. Metformin was administered by gavage to detect changes in tumor volume and weight, and CD31 staining was used to observe microvessels. The targeting relationship between miR-302b-3p and TXNIP was demonstrated by the bioinformatics website, dual-luciferase reporter assay, and RNA pull-down assay. The results found that metformin inhibited RFA deficiency-induced growth and angiogenesis of HCC cells in vitro. miR-302b-3p counteracted the therapeutic effect of metformin on RFA deficiency. miR-302b-3p targeted regulation of TXNIP. The up-regulation of TXNIP reversed the effects of overexpression of miR-302b-3p on RFA-deficient HCC cells. Metformin inhibited RFA-deficiency-induced HCC growth and tumor vascular abnormalities in vivo. Overall, metformin promotes the normalization of abnormal blood vessels after RFA deficiency in HCC by miR-302b-3p targeting TXNIP, which can be used to prevent the progression of HCC after RFA.