Molecular Biology Reports最新文献

Bees play a critical role as pollinators in ecosystem services, contributing significantly to the sexual reproduction and diversity of plants. The Caatinga biome in Brazil, home to around 200 bee species, provides an ideal habitat for these species due to its unique climate conditions. However, this biome faces threats from anthropogenic processes, making it urgent to characterise the local bee populations efficiently. Traditional taxonomic surveys for bee identification are complex due to the lack of suitable keys and expertise required. As a result, molecular barcoding has emerged as a valuable tool, using genome regions to compare and identify bee species. However, little is known about Caatinga bees to develop these molecular tools further. This study addresses this gap, providing an updated list of 262 Caatinga bee species across 86 genera and identifying ~ 40 primer sets to aid in barcoding these species. The findings highlight the ongoing work needed to fully characterise the Caatinga biome's bee distribution and species or subspecies to support more effective monitoring and conservation efforts.

Growth hormone (GH) is a key polypeptide hormone secreted by somatotroph cells in the anterior pituitary gland, essential for postnatal growth, metabolism, and systemic homeostasis. Its secretion is regulated by hypothalamic neuropeptides, including GH-releasing hormone and somatostatin. GH exerts effects through direct interaction with the growth hormone receptor and indirect pathways mediated by the GH-IGF-I axis. GHR activation triggers signaling pathways, such as JAK-STAT, PI3K/AKT, and MAPK, promoting cellular proliferation, differentiation, and metabolic balance. The GH-IGF-I axis is critical for bone growth, lipid and carbohydrate metabolism, and organ-specific physiological functions. Dysregulation of GH results in diverse disorders. Congenital deficiencies, like isolated GH deficiency and syndromic conditions (e.g., Turner syndrome), stem from genetic mutations. Acquired deficiencies arise from trauma, tumors, infections, or autoimmune damage, while GH overproduction causes gigantism in children and acromegaly in adults, often due to pituitary adenomas. Idiopathic deficiencies, lacking identifiable causes, complicate management further. Advances in therapy have transformed outcomes for GH disorders. Recombinant human growth hormone provides effective replacement therapy for deficiencies. Somatostatin analogs, dopamine receptor agonists, and GH receptor antagonists are pivotal for managing GH excess. Surgical and radiotherapeutic interventions remain essential for pituitary adenomas. However, GH therapy requires close monitoring to prevent side effects like insulin resistance and metabolic complications. This review provides a comprehensive evaluation of the molecular mechanisms underlying GH action, its physiological roles, GH-related disorders, and therapeutic approaches to optimize patient outcomes.

The cholinergic anti-inflammatory pathway (CAP) is comprised of the vagus nerve, acetylcholine, nicotinic acetylcholine receptors, the spleen, and the splenic nerve. It represents a sophisticated neuroimmune axis that critically regulates the crosstalk between the nervous system and the immune response via the vagus nerve. Here, we provided a nuanced exploration of the CAP's role in curbing inflammatory processes and its broad therapeutic potential across a spectrum of diseases. We meticulously dissect the intricate mechanisms by which the CAP modulates key signaling cascades, including the NF-κB, JAK2/STAT3, MAPK/ERK, PI3K/AKT, COX2/PGE2, and NRF2/HO-1 pathways, which are quintessential in the pathogenesis of various conditions. Additionally, we also summarized the CAP's profound implications in the management of inflammatory diseases, neurodegenerative disorders, metabolic syndromes, and oncological malignancies, elucidating its capacity to mitigate disease severity and progression through sophisticated immune modulation. The modulation of the CAP is suggested as a novel strategy that could potentially transform treatment approaches for a variety of conditions. However, the precise cellular and molecular underpinnings of the CAP's effects, as well as its translatability to clinical settings, remain subjects of ongoing investigation. The review calls for further research to demystify the mechanisms of the CAP and to harness its therapeutic potential fully, with the aim of developing innovative and efficacious treatment modalities that exploit the pathway's unique attributes.

Melatonin released from the pineal gland plays an important role in maintaining the light/dark cycle. Melatonin exerts its effects on various organs through receptor and nonreceptor pathways. Recently, the role of melatonin in various metabolic disorders has been investigated. This review focuses on the molecular pathways associated with melatonin and its role in metabolic disorders. In humans, melatonin acts through two G protein-coupled receptors (MT1 and MT2). Melatonin modulates insulin release, such as elevated insulin levels in the evening compared to morning hours, exerts cardioprotective effects through the cGMP pathway and nitric oxide production in endothelial cells, and controls oxidative stress and apoptosis in myocardial tissue. Melatonin through MT2 receptors increases lipolysis and thermogenesis, which have a positive effect on weight reduction in obese individuals. Currently, most drugs that target melatonin receptors are primarily used to treat neurological disorders. A detailed investigation to explore the role of melatonin and its signalling pathway in peripheral organs is essential to develop therapeutic molecules for managing metabolic disorders.

Background: Gastric cancer (GC) remains a significant global health burden, particularly in East Asia, where it is a leading cause of cancer-related morbidity and mortality. Despite advancements in chemotherapy, the development of chemoresistance continues to undermine the efficacy of standard treatments such as Docetaxel and Oxaliplatin. Arsenic trioxide (ATO) has emerged as a potential therapeutic agent capable of overcoming resistance by targeting DNA repair mechanisms, particularly through the downregulation of Checkpoint Kinase 1 (Chk1). This study investigates the cytotoxic effects of ATO and its capacity to enhance chemotherapy efficacy in GC cells.

Methods: AGS and MKN-45 gastric cancer cell lines were exposed to ATO, Docetaxel, Oxaliplatin, and their combinations. Cell viability was assessed via the MTT assay, while Chk1 and CDC25 expressions at the mRNA and protein levels was analyzed using real-time PCR and Western blotting. Statistical analyses were performed using ANOVA and Tukey's post hoc test.

Results: The MTT assay revealed significant dose- and time-dependent reductions in cell viability, with combination treatments achieving the most pronounced effects. The greatest cytotoxicity was observed with 4 µM ATO combined with 2500 µM Docetaxel or 100 µM Oxaliplatin, showing a high level of statistical significance (p < 0.0001). Additionally, ATO monotherapy significantly downregulated Chk1 and CDC25 expressions (p < 0.05), while its combination with chemotherapeutic agents further enhanced Chk1 and CDC25 suppressions, with ATO-Docetaxel demonstrating the most pronounced effect (p < 0.01).

Conclusions: These findings highlight ATO's potential to sensitize GC cells to chemotherapy by impairing DNA repair mechanisms and inducing synergistic cytotoxicity. ATO holds promise as an adjuvant therapeutic agent for overcoming chemoresistance in gastric cancer.

Hepatitis B virus surface antigen (HBsAg), IgM and IgG antibodies to hepatitis B virus core antigen (anti-HBcIgM and anti-HBcIgG) comprise serological markers of hepatitis B virus (HBV) infection of great importance in the epidemiological surveillance of hepatitis B, since they have been routinely considered for classifying the acute and chronic clinical forms of HBV infection. This classification is established according to the expression and dynamics of these markers in the infected person's bloodstream, which serves as the basis for the differential diagnosis between the two clinical entities. However, in certain circumstances, both acute and chronic infection, the detection of these markers may not occur in the bloodstream, favoring the occurrence of atypical serological profiles of infection, and compromising the correct infection clinical classification. In addition, the complex and varied nature of hepatitis B serological profiles may compromise the health professional's ability to analyze the case and, thus, correctly classify the infection's clinical form. Since the expression of these markers in the bloodstream occurs dynamically, with consequent changes in the patient's serological profile as he progresses towards recovery or chronicity, the diagnosis of acute or chronic infection may also be compromised, if it is established based on the collection of a single sample and without knowing the patient's clinical history and their epidemiological antecedents. This manuscript addresses the sensitivity and specificity of HBsAg, anti-HBcIgM, and anti-HBcIgG serological markers detection in the clinical classification of HBV infection and in the epidemiological surveillance of hepatitis B. This review is covering the clinical and epidemiological interpretations of the markers in and of themselves, not in reference to any specific assays.

Emerging studies have identified ferroptosis as a promising therapeutic target, the inhibition of which is hypothesized to mitigate brain injury and subsequent neuronal death following stroke. Zerumbone, a phytochemical sesquiterpene isolated from Zingiber zerumbet Smith, exhibit diverse therapeutic properties across a range of neurological disorders. This study aimed to elucidate the postischemic neuroprotective effects and regulatory impact of zerumbone on ferroptosis-mediated cell death following oxygen‒glucose deprivation/reperfusion (OGD/R) injury. We employed an in vitro OGD/R SH-SY5Y cell model of stroke to evaluate the postischemic neuroprotective effects of zerumbone, a lead molecule identified through literature studies. Moreover, assays were performed to assess how zerumbone affects lipid peroxide levels, intracellular reactive oxygen species (ROS), and mitochondrial membrane integrity. Furthermore, molecular docking simulations were carried out to determine the targets, and western blotting was performed to examine TFR1 protein expression. Zerumbone (0.5 µM) treatment at 1-hour postischemia increased cell viability (72.11 ± 0.98) and mitigated OGD/R-induced ischemic injury. Zerumbone significantly decreased intracellular ROS levels and lipid peroxide production while increasing mitochondrial membrane integrity, suggesting that zerumbone ameliorated OGD/R-induced ischemic injury by inhibiting ferroptosis in vitro. This finding was corroborated by our western blot analysis, which revealed that the antiferroptotic role of zerumbone was distinctly mediated through the downregulation of transferrin receptor 1 (TFR1) protein expression. This communication, for the first time, highlights the feasibility of zerumbone as a promising adjunctive neuroprotective agent against ferroptosis cell death in the context of cerebral stroke. This study lays the groundwork for subsequent in-depth investigations to fully elucidate its therapeutic potential in ischemic stroke treatment.

This review focuses on dental pulp stem cells (DPSCs) which are mesenchymal stem cells (MSCs) and originating from the neural crest. These cells possess a high capacity for self-renewal and multilineage differentiation. Because of these traits, they represent promising sources for tissue engineering, regenerative medicine, and clinical applications. The objective of this study was to assess the extrinsic and intrinsic factors influencing DPSC characteristics and their potential in tissue engineering. This review discusses the external and internal factors affecting DPSC properties, including proliferation, migration, differentiation, and gene expression post extraction. Additionally, it explores the impact of the microenvironment-its composition and physical properties-and genetic and epigenetic regulation on DPSC behavior. Variations in the microenvironment and genetic regulation play pivotal roles in modulating DPSC functions, including their proliferation and differentiation potential. Intrinsic and extrinsic factors are key barriers to realizing the full therapeutic potential of DPSCs. A deeper understanding of the extrinsic and intrinsic factors affecting DPSC behavior is critical for optimizing their use in regenerative medicine, particularly for dental and craniofacial applications. Although DPSCs hold significant promise, challenges remain, and this review provides insights into the current limitations and future directions for DPSC-based therapies. Researchers and clinicians are offered a comprehensive resource for advancing the field.

Background: SERPINB5, also known as Maspin, is a non-inhibitory member of the serine protease inhibitor superfamily. SERPINB5 exerts diverse effects on a variety of human cancers, including cell proliferation, angiogenesis, apoptosis, tumor invasion, and metastasis. SERPINB5 has traditionally been regarded as a tumor suppressor gene, but emerging evidences supports its oncogenic properties.

Methods: We conducted a comprehensive review of the existing literature on SERPINB5 in gastrointestinal cancers, synthesizing data on its expression patterns, subcellular localization, epigenetic modifications, and clinical significance.

Results: Depending on its subcellular localization and epigenetic modifications, SERPINB5 demonstrate either protumor or antitumor activity in different gastrointestinal cancers, such as colorectal cancer, gastric cancer, pancreatic cancer, gallbladder cancer and liver cancer. We elucidate its potential as a predictive and prognostic biomarker, with a focus on its implications for diagnosis, prognosis, and therapeutic intervention, emphasizing its utility in early lesion detection and treatment.

Conclusions: SERPINB5 plays a complex and context-dependent role in gastrointestinal cancers, highlighting further research to dissect the true significance of SERPINB5 expression and the molecular mechanisms underlying its divergent clinical behaviors in cancer.

Background: The filamentation temperature-sensitive H (FtsH) gene family, which is known to play a critical role in plant growth and development by regulating photosynthesis, chloroplast development, and response to plant stress, has been extensively studied in various species. However, the FtsH gene family in wheat has not been previously documented.

Methods and results: In this study, 38 TaFtsH gene family members were identified, divided into eight groups and unevenly distributed across various chromosomes. Analysis of gene structure and conserved motifs revealed that TaFtsH genes within the same taxon share similar gene structures and conserved motifs. Further collinearity analysis provided insights into the evolutionary history of TaFtsH genes. Examination of cis-acting elements in the promoter region of TaFtsH genes revealed the presence of developmental and stress response elements in genes. The expression pattern of the wheat FtsH gene under various abiotic stresses was analyzed using real-time fluorescence quantitative PCR. Additionally, transient expression in tobacco verified the localization of the TaFtsH11-B protein in chloroplasts.

Conclusions: These findings collectively contribute to laying the groundwork for the functional characterization of TaFtsH genes.