Molecular Biology Reports最新文献

Background: To tolerate biotic stress, plants employ phytohormones such as jasmonic acid (JA), salicylic acid (SA), and ethylene (ET) to regulate the immune response against different pathogens. Phytohormone-responsive genes, known as "Defense signaling marker genes," are used to evaluate plant disease resistance during pathogen infection. Most information on these marker genes derives from studies on the model plant Arabidopsis thaliana. The present study was aimed analyze the effect of hormonal elicitation at different concentrations at 24 h pos-treatment in the transcript level of 8 traditional genes selected for molecular studies plant-pathogen interactions in Capsicum.

Methods and results: Chemical treatment was achieved by spraying leaves of in vitro seedlings C. annuum L. with 0.1 mM, 1 mM or 2.5 mM ET; 1 mM, 2.5 mM, or 5 mM SA; 2.5 mM BABA; or 0.150 mM MeJA. Twenty-four hours after treatments were applied molecular analyses were carried out using qPCR to investigate the expression. Results revealed that 1 mM of ET or 0.15 mM of MeJA activated the expression CaPR1 (18--11.64-fold change), CaLOX2 (13.80-fold), CaAP2/ERF06 (22- 5.3- fold change), and CaPDF1.2 (2.3-1.5- fold). While, 5 mM of SA present effect of negative regulation on the expression in most of these genes.

Conclusions: Our results show that the expression profile induced by phytohormones in CaPR1 are particular in C. annuum, because were significantly induced for ET/MeJA, and dow-regulation with SA Contrary to Arabidopsis. Although, on both plants it is observed the cross talk between JA/ET and SA mediated signal pathways for the regulation of this gene.

Infertility is a reproductive health problem in the male or female reproductive system. Traditional assisted reproductive technology (ART) has been unable to solve various cases of infertility for years. Clinical researchers have sought to treat infertility using new methods that are more effective and noninvasive than the old methods. Recently, Mesenchymal stem cells (MSCs) and MSCs-derived Exosomes (MSC-Exos) via paracrine activity play an important role in treating various causes of infertility and improving pregnancy outcomes. In this review, we focus on the roles of MSCs and MSC-Exos cell therapy in female infertility in the different types of female reproductive disorders.

Background: Spinocerebellar ataxia with axonal neuropathy type 1 (OMIM: 607250) is an extremely rare autosomal recessive disorder caused by a mutation in the tyrosyl-DNA phosphodiesterase 1 (TDP1) gene. Only a single missense variant (p.His493Arg) in this gene has been reported. This variant was found in three Arab families with a possible common founder effect.

Methods and results: We report a female patient born to a consanguineous Pakistani family segregating autosomal recessive spinocerebellar ataxia with axonal neuropathy type 1. The patient presents additional clinical features distinct from previously reported Arab families including congenital onset of the disease. We performed whole exome sequencing with the patient's DNA and identified a novel missense variant (NC_000014.9:g.89991982C > T; p.His478Tyr) in exon 13 of the TDP1 gene. Sanger sequencing was performed to verify the autosomal recessive segregation of the p.His478Tyr variant in the family.

Conclusion: The current study expands both the clinical and mutation spectrum of the TDP1 associated spinocerebellar ataxia with axonal neuropathy type 1 and increases the body of evidence that supports the pathogenic role of TDP1 in cerebellar ataxias with peripheral neuropathy.

Melanoma is an aggressive cancer that disregards both the MAPK and Hippo signaling pathways. This systematic review explores STK3 function in the Hippo pathway to regulate networks and its therapeutic potential in melanoma. From 1991 to 2024, we studied how STK3 interacts with the MAPK/ERK pathway to promote apoptosis and inhibit tumor growth. STK3 controls cell growth, apoptosis, and metastasis via the Hippo and MAPK pathways. It is a melanoma tumor suppressor. Some ways to target STK3 are to directly activate it, stop downstream effectors like YAP/TAZ from working, or use existing BRAF inhibitors together with other methods. Despite advancements, challenges in STK3 drug development persist, warranting further investigation. This review examined the role of STK3 in the development of melanoma and identified potential vulnerabilities for therapeutic intervention.

Background: The European flounder is readily chosen as an experimental subject and model in physiological and ecotoxicological studies mostly because of its adaptability to laboratory conditions. Many studies utilise a quantitative PCR (qPCR) approach to ascertain the expression of target genes under experimental conditions. Such an approach relies heavily on the selection of reference genes with stable expression. Yet certain housekeeping genes are commonly used in this role, often without due consideration of their overall expression patterns. Therefore, new approaches should be developed to identify stable reference genes for a given species and to expand the general pool of genes suitable for the reference in qPCR analysis.

Methods and results: Here RNA-seq data of nine flounder organs led to identify four candidate genes of the most stable expression. It was achieved by differential expression analysis and tritoconstrictor script. Specific primers were designed for the complete ORF as well as for qPCR analysis. RT-qPCR efficiencies were tested on ORF amplicon templates. Most of the genes tested showed good amplification in a wide range of template dilutions (10⁷-10¹), with a correlation coefficient (R²) ranging from 0.991 to 0.998 and a consistent efficiency (E) (Sybr Green I staining and TaqMan molecular probe).

Conclusions: The proposed approach based on differential expression analysis and a new bioinformatic tool is an appropriate selection method of candidates for reference genes in qPCR. The proposed approach, combining differential expression analysis with a new bioinformatics tool, provides an effective method for selecting reference gene candidates for qPCR. As a result, we can propose four genes (polr2f, yif1a, sf3b6, uba52), each with a set of validated primers, as suitable for consideration as reference genes in qPCR analysis in European flounder, an emerging model species.

Background: Remote limb ischemic pre-conditioning (RIPreC) can invoke potent renal protection. The involvement of oxidative stress and inflammatory pathways in renal ischemia/reperfusion injury (I/RI) was also confirmed. This study was designed to investigate the RIPreC effects on IRI-induced kidney dysfunction in rats through NFĸB/TNF-α/TGF-ꞵ/apelin signaling pathway.

Methods: Renal I/RI was induced by occluding the kidney arteries for 45 min, then reperfusion for 24 h. Four similar cycles of left femoral artery ischemia (2 min)/reperfusion (3 min) before the onset of kidney ischemia were performed to create RIPreC. Animals were randomly divided into three groups: sham, I/R, and RIPreC + I/R. Following the reperfusion phase, urine and blood samples were taken, and the kidney was removed for functional, molecular, and histological examination.

Results: When compared to sham rats, renal IRI resulted in decreased creatinine clearance and increased sodium fractional excretion, lower antioxidant enzyme activities, higher malondialdehyde content and higher nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), transforming growth factor-betta (TGF-β), and Apelin expression levels, and histologically damaged kidney tissue. All of the alterations, as mentioned earlier, were alleviated using the RIPreC treatment.

Conclusion: Thus, RIPreC can protect against renal dysfunction after renal I/RI via modulation of the TNF-α/NF-κB/TGF-ꞵ/Apelin signaling pathway and strengthening the antioxidant defense system.

Background: Myocardial ischemia-reperfusion injury (MI/RI) significantly impacts the patients with acute myocardial infarction (AMI), with the NLRP3-mediated necrosis exacerbates the pathological progression of myocardial infarction. Exercise, recognized as a crucial approach for both disease prevention and treatment, is widely utilized in clinical practice worldwide and has demonstrated broad effectiveness in cardiovascular disease (CVD) prevention.

Purpose: To explore the cardio protective effect of exercise preconditioning and the mechanism by which exercise modulation of NLRP3 improves myocardial ischemia and reperfusion injury.

Methods and results: In this study, C57BL/6 N mice were employed to establish an exercise preconditioning model and a MI/RI model. The exercise intervention involved moderate-intensity aerobic exercise on a treadmill (50-70% VO2max) for small animals. Our research findings indicate that moderate-intensity aerobic exercise intervention improved cardiac function, reduced myocardial injury and inflammatory response, decreased myocardial infarction area and degree of cell apoptosis in mice compared to those raised under conventional conditions. Additionally, the expression of NLRP3 in the myocardial tissue of mice with MI/RI was reduced after exercise intervention. Moreover, exercise inhibited the activation of apoptosis related proteins such as Caspase-1 and GSDMD, while reducing the levels of inflammatory factors such as IL-1β and IL-18.

Conclusions: This study found that moderate-intensity aerobic exercise can reduce the inflammatory response, reduce the degree of cell pyroptosis, reduce myocardial ischemia and reperfusion injury, and achieve endogenous protective effects on the myocardium.

Background: Major Human Histocompatibility complex (MHC or HLA in humans) has been associated to autoimmune diseases. However, only statistical phenomenological and no pathogenetic description has been reached after decades. This shows that MHC single locus association studies are probably useless for HLA/diseases association. Extended HLA (class I and class II genes) haplotypes should also be studied conjointly with class III or complement alleles (complotypes). Complotypes in humans are defined as alleles belonging to C2, C4 and Bf (Factor B) genes/proteins (class III). Also, the placing of MHC class I and class II genes close together with complement genes from at least birds to humans shows existence of a strong selection to gather conjointly these loci that fight microbes, help self-maintenance and avoid autoimmunity. In this paper we aim to study Bf alleles in primates in order to rise again interest to study the role of Bf alleles together with other MHC genes in their physiopathology and evolution.

Methods: Orangutan (Pongo pygmaeus, Popy) cell lines RNA from 6 different individuals were retrotranscribed, PCR amplified, cloned and DNA sequenced in order to study Bf alleles.

Results: A Bf allele identical to that found in chimpanzee (Patr-Bf*A01) and human (rs641153) was found in two of the six studied orangutans: Popy-Bf*A01 and Popy-Bf*A02. This polymorphism is placed in Factor B codon 32 that defines BF*S and Bf*F proteins in man and produce Leu instead of Arg (Bf*S) or Gln (Bf*F). In addition, each new orangutan allele present synonymous differences with each other at codon 25: Popy-Bf*A01 shows ACG while Popy-Bf*A02 bears ACA, both codifying for Thr.

Conclusions: The selection for about 15 million years (time gap of evolutionary appearance between orangutan and hominids) shows the importance of this particular allele conservation in immune and self defense in primates. The complotypes (Bf,C2 and C4 loci) alleles together with other MHC class I and Cass II loci alleles are often transmitted in block to the germinal line: this indicates that all specific alleles from the MHC different loci may work together to accomplish MHC functions. All MHC loci alleles should be studied together to unveil their physiopathology and also maintenance of specific alleles (like the one described in this paper) for so long time in evolution should be further studied in Bf and the other neighbouring complement loci (C2 and C4).

Background: As a multifunctional ecosystem, the human digestive system contains a complex network of microorganisms, collectively known as gut microbiota. This consortium composed of more than 10¹³ microorganisms and Firmicutes and Bacteroidetes are the dominant microbes. Gut microbiota is increasingly recognized for its critical role in physiological processes beyond digestion. Gut microbiota participates in a symbiotic relationship with the host and takes advantage of intestinal nutrients and mutually participates in the digestion of complex carbohydrates and maintaining intestinal functions.

Method and result: We reviewed the neuroactive components produced by gut microbiota. Interestingly, microbiota plays a crucial role in regulating the activity of the intestinal lymphatic system, regulation of the intestinal epithelial barrier, and maintaining the tolerance to food immunostimulating molecules. The gut-brain axis is a two-way communication pathway that links the gut microbiota to the central nervous system (CNS) and importantly is involved in neurodevelopment, cognition, emotion and synaptic transmissions. The connections between gut microbiota and CNS are via endocrine system, immune system and vagus nerve.

Conclusion: The gut microbiota produces common neurotransmitters and neuromodulators of the nervous system. These compounds play a role in neuronal functions, immune system regulation, gastrointestinal homeostasis, permeability of the blood brain barrier and other physiological processes. This review investigates the essential aspects of the neurotransmitters and neuromodulators produced by gut microbiota and their implications in health and disease.

One of the most famous and heterogeneous cancers worldwide is breast cancer (BC). Owing to differences in the gene expression profiles and clinical features of distinct BC subtypes, different treatments are prescribed for patients. However, even with more thorough pathological evaluations of tumors than in the past, available treatments do not perform equally well for all individuals. Precision medicine is a new approach that considers the effects of patients' genes, lifestyle, and environment to choose the right treatment for an individual patient. As a powerful tool, the organoid culture system can maintain the morphological and genetic characteristics of patients' tumors. Evidence also shows that organoids have high predictive value for patient treatment. In this review, a variety of BC studies performed on organoid culture systems are evaluated. Additionally, the potential of using organoid models in BC translational research, especially in immunotherapy, drug screening, and precision medicine, has been reported.