Expression characteristics of lipid metabolism-related genes and correlative immune infiltration landscape in acute myocardial infarction.

Lipid metabolism is an important part of the heart's energy supply. The expression pattern and molecular mechanism of lipid metabolism-related genes (LMRGs) in acute myocardial infarction (AMI) are still unclear, and the link between lipid metabolism and immunity is far from being elucidated. In this study, 23 Common differentially expressed LMRGs were discovered in the AMI-related mRNA microarray datasets GSE61144 and GSE60993. These genes were mainly related to "leukotriene production involved in inflammatory response", "lipoxygenase pathway", "metabolic pathways", and "regulation of lipolysis in adipocytes" pathways. 12 LMRGs (ACSL1, ADCY4, ALOX5, ALOX5AP, CCL5, CEBPB, CEBPD, CREB5, GAB2, PISD, RARRES3, and ZNF467) were significantly differentially expressed in the validation dataset GSE62646 with their AUC > 0.7 except for ALOX5AP (AUC = 0.699). Immune infiltration analysis and Pearson correlation analysis explored the immune characteristics of AMI, as well as the relationship between these identified LMRGs and immune response. Lastly, the up-regulation of ACSL1, ALOX5AP, CEBPB, and GAB2 was confirmed in the mouse AMI model. Taken together, LMRGs ACSL1, ALOX5AP, CEBPB, and GAB2 are significantly upregulated in AMI patients' blood, peripheral blood of AMI mice, myocardial tissue of AMI mice, and therefore might be new potential biomarkers for AMI.

Injectable and Sprayable Fluorescent Nanoprobe for Rapid Real-Time Detection of Human Colorectal Tumors.

The development of minimally invasive surgery has greatly advanced precision tumor surgery, but sometimes suffers from restricted visualization of the surgical field, especially during the removal of abdominal tumors. A 3-D inspection of tumors could be achieved by intravenously injecting tumor-selective fluorescent probes, whereas most of which are unable to instantly distinguish tumors via in situ spraying, which is urgently needed in the process of surgery in a convenient manner. In this study, we have designed an injectable and sprayable fluorescent nanoprobe, termed Poly-g-BAT, to realize rapid tumor imaging in freshly dissected human colorectal tumors and animal models. Mechanistically, the incorporation of γ-glutamyl group facilitates the rapid internalization of Poly-g-BAT, and these internalized nanoprobes can be subsequently activated by intracellular NAD(P)H: quinone oxidoreductase-1 to release near-infrared fluorophores. As a result, Poly-g-BAT can achieve a superior tumor-to-normal ratio (TNR) up to 12.3 and enable a fast visualization (3 min after in situ spraying) of tumor boundaries in the xenograft tumor models, Apcmin/+ mice models and fresh human tumor tissues. In addition, Poly-g-BAT is capable of identifying minimal premalignant lesions via intravenous injection. This article is protected by copyright. All rights reserved.

Transcriptomic analysis reveals the lipid metabolism-related gene regulatory characteristics and potential therapeutic agents for myocardial ischemia-reperfusion injury.

Background: Impaired energy balance caused by lipid metabolism dysregulation is an essential mechanism of myocardial ischemia-reperfusion injury (MI/RI). This study aims to explore the lipid metabolism-related gene (LMRG) expression patterns in MI/RI and to find potential therapeutic agents. Methods: Differential expression analysis was performed to screen the differentially expressed genes (DEGs) and LMRGs in the MI/RI-related dataset GSE61592. Enrichment and protein-protein interaction (PPI) analyses were performed to identify the key signaling pathways and genes. The expression trends of key LMRGs were validated by external datasets GSE160516 and GSE4105. The corresponding online databases predicted miRNAs, transcription factors (TFs), and potential therapeutic agents targeting key LMRGs. Finally, the identified LMRGs were confirmed in the H9C2 cell hypoxia-reoxygenation (H/R) model and the mouse MI/RI model. Results: Enrichment analysis suggested that the "lipid metabolic process" was one of the critical pathways in MI/RI. Further differential expression analysis and PPI analysis identified 120 differentially expressed LMRGs and 15 key LMRGs. 126 miRNAs, 55 TFs, and 51 therapeutic agents were identified targeting these key LMRGs. Lastly, the expression trends of Acadm, Acadvl, and Suclg1 were confirmed by the external datasets, the H/R model and the MI/RI model. Conclusion: Acadm, Acadvl, and Suclg1 may be the key genes involved in the MI/RI-related lipid metabolism dysregulation; and acting upon these factors may serve as a potential therapeutic strategy.

A Pluripotential Neutrophil-Mimic Nanovehicle Modulates Immune Microenvironment with Targeted Drug Delivery for Augmented Antitumor Chemotherapy.

The limited therapeutic outcomes and severe systemic toxicity of chemotherapy remain major challenges to the current clinical antitumor therapeutic regimen. Tumor-targeted drug delivery that diminishes the undifferentiated systemic distribution is a practical solution to ameliorating systemic toxicity. However, the tumor adaptive immune microenvironment still poses a great threat that compromises the therapeutic efficacy of chemotherapy by promoting the tolerance of the tumor cells. Herein, a pluripotential neutrophil-mimic nanovehicle (Neutrosome(L)) composed of an activated neutrophil membrane-incorporated liposome is proposed to modulate the immune microenvironment and synergize antitumor chemotherapy. The prominent tumor targeting capability inherited from activated neutrophils and the improved tumor penetration ability of Neutrosome(L) enable considerable drug accumulation in tumor tissues (more than sixfold that of free drug). Importantly, Neutrosome(L) can modulate the immune microenvironment by restricting neutrophil infiltration in tumor tissue, which may be attributed to the neutralization of inflammatory cytokines, thus potentiating antitumor chemotherapy. As a consequence, the treatment of cisplatin-loaded Neutrosome(L) performs prominent tumor suppression effects, reduces systemic drug toxicity, and prolongs the survival period of tumor-bearing mice. The pluripotential neutrophil-mimic nanovehicle proposed in this study can not only enhance the tumor accumulation of chemotherapeutics but also modulate the immune microenvironment, providing a compendious strategy for augmented antitumor chemotherapy.

Initial IL-10 production dominates the therapy of mesenchymal stem cell scaffold in spinal cord injury.

Rationale: Spinal cord injury (SCI) is an acute damage to the central nervous system that results in severe morbidity and permanent disability. Locally implanted scaffold systems with immobilized mesenchymal stem cells (MSCs) have been widely proven to promote locomotor function recovery in SCI rats; however, the underlying mechanism remains elusive. Methods and Results: In this study, we constructed a hyaluronic acid scaffold system (HA-MSC) to accelerate the adhesive growth of human MSCs and prolong their survival time in SCI rat lesions. MSCs regulate local immune responses by upregulating the expression of anti-inflammatory cytokines. Interestingly, the dramatically increased, but transient expression of interleukin 10 (IL-10) is found to be secreted by MSCs in the first week. Blocking the function of the initially produced IL-10 by the antibody completely abolished the neurological and behavioral recovery of SCI rats, indicating a core role of IL-10 in SCI therapy with HA-MSC implantation. Transcriptome analyses indicated that IL-10 selectively promotes the migration and cytokine secretion-associated programs of MSCs, which in turn helps MSCs exert their anti-inflammatory therapeutic effects. Conclusion: Our findings highlight a novel role of IL-10 in regulating MSC migration and cytokine secretion-associated programs, and determine the vital role of IL-10 in the domination of MSC treatment for spinal cord repair.

Identification of the communal pathogenesis and immune landscape between viral myocarditis and dilated cardiomyopathy.

AIMS: Studies have confirmed that viral myocarditis (VMC) is one of the risk factors for dilated cardiomyopathy (DCM). The molecular mechanisms underlying the progression from VMC to DCM remain unclear and require further investigation. METHODS AND RESULTS: The mRNA microarray datasets GSE57338 (DCM) and GSE1145 (VMC) were obtained from the Gene Expression Omnibus database. The candidate key genes were further screened using weighted correlation network analysis (WGCNA), protein-protein interaction and external dataset validation, and the correlation between the candidate key genes and immune cells and the signalling pathways of the candidate key genes were observed by enrichment analysis and immune infiltration analysis. The expression of key genes was validated in the external dataset GSE35182. The crosstalk genes between DCM and VMC were mainly enriched in 'transcriptional misregulation in cancer', 'FoxO signalling pathway', 'AGE-RAGE signalling pathway in diabetic complications', 'thyroid hormone signalling pathway', 'AMPK signalling pathway', and other signalling pathways. The immune infiltration analysis indicated that VMC was mainly associated with resting dendritic cells and M0 macrophages, while DCM was mainly associated with monocytes, M0 macrophages, CD8+ T cells, resting CD4 memory T cells, naive CD4+ T cells, and resting mast cells. In DCM-related dataset GSE57338 and VMC-related dataset GSE1145, a total of 18 candidate key genes were differentially expressed. BLC6, FOXO1, and UBE2M were identified as the key genes that lead to the progression from VMC to DCM by GSE35182. CONCLUSIONS: Three key genes (BLC6, FOXO1, and UBE2M) were identified and provided new insights into the diagnosis and treatment of VMC with DCM.

A novel hypoxia-associated gene signature for prognosis prediction in head and neck squamous cell carcinoma.

BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) is the most common malignant tumor of head and neck, which seriously threatens human life and health. However, the mechanism of hypoxia-associated genes (HAGs) in HNSCC remains unelucidated. This study aims to establish a hypoxia-associated gene signature and the nomogram for predicting the prognosis of patients with HNSCC. METHODS: Previous literature reports provided a list of HAGs. The TCGA database provided genetic and clinical information on HNSCC patients. First, a hypoxia-associated gene risk model was constructed for predicting overall survival (OS) in HNSCC patients and externally validated in four GEO datasets (GSE27020, GSE41613, GSE42743, and GSE117973). Then, immune status and metabolic pathways were analyzed. A nomogram was constructed and assessed the predictive value. Finally, experimental validation of the core genes was performed by qRT-PCR. RESULTS: A HNSCC prognostic model was constructed based on 8 HAGs. This risk model was validated in four external datasets and exhibited high predictive value in various clinical subgroups. Significant differences in immune cell infiltration levels and metabolic pathways were found between high and low risk subgroups. The nomogram was highly accurate for predicting OS in HNSCC patients. CONCLUSIONS: The 8 hypoxia-associated gene signature can serve as novel independent prognostic indicators in HNSCC patients. The nomogram combining the risk score and clinical stage enhanced predictive performance in predicting OS compared to the risk model and clinical characteristics alone.

Transcriptome analysis reveals the mechanism of pyroptosis-related genes in septic cardiomyopathy.

Background: Septic cardiomyopathy (SC) is characterized by myocardial dysfunction caused by sepsis and constitutes one of the serious complications of sepsis. Pyroptosis is a unique proinflammatory programmed cell death process. However, the role of pyroptosis in the development of SC remains unclear, and further study is required. The purpose of this study is to identify pyroptosis-related genes (PRGs) in SC and explore the mechanism of pyroptosis involved in the regulation of SC formation and progression. Methods: Differential expression analysis and enrichment analysis were performed on the SC-related dataset GSE79962 to identify differentially expressed genes (DEGs). PRGs were screened by intersecting genes associated with pyroptosis in previous studies with the DEGs obtained from GSE79962. The expression pattern of them was studied based on their raw expression data. Additionally, corresponding online databases were used to predict miRNAs, transcription factors (TFs) and therapeutic agents of PRGs. Lipopolysaccharide (LPS)-induced cell damage models in H9C2 and AC16 cell lines were constructed, cell activity was detected by CCK-8 and cell pyroptosis were detected by Hoechst33342/PI staining. Furthermore, these PRGs were verified in the external datasets (GSE53007 and GSE142615) and LPS-induced cell damage model. Finally, the effect of siRNA-mediated PRGs knockdown on the pyroptosis phenotype was examined. Results: A total of 1,206 DEGs were screened, consisting of 663 high-expressed genes and 543 low-expressed genes. Among them, ten PRGs (SOD2, GJA1, TIMP3, TAP1, TIMP1, NOD1, TP53, CPTP, CASP1 and SAT1) were identified, and they were mainly enriched in "Pyroptosis", "Ferroptosis", "Longevity regulating pathway", and "NOD-like receptor signaling pathway". A total of 147 miRNAs, 31 TFs and 13 therapeutic drugs were predicted targeting the PRGs. The expression trends of SOD2 were confirmed in both the external datasets and LPS-induced cell damage models. Knockdown of SOD2 induced increased pyroptosis in the AC16 LPS-induced cell damage model. Conclusions: In this study, we demonstrated that SOD2 is highly expressed in both the SC and LPS-induced cell damage models. Knockdown of SOD2 led to a significant increase in pyroptosis in the AC16 LPS-induced cell damage model. These findings suggest that SOD2 may serve as a potential target for the diagnosis and treatment of SC.

The cotton miR171a-SCL6 module mediates plant resistance through regulating GhPR1 expression.

Plants have developed intricate defense mechanisms in response to fluctuating environmental cues, including the use of microRNA (miRNA) as post-transcriptional regulators. However, the specific mechanisms through which miRNA contributes to disease resistance remain largely elusive. While the miR171-SCLs have been investigated in an eclectic array of plants, there has been a notable scarcity of research specifically focused on cotton (Gossypium hirsutum). In our previous miRNA-sequencing analysis, we found that ghr-miR171a displayed a differential response to infections by Verticillium dahliae. In this study, we further investigated the function of the miR171a-SCL6 module in cotton during V. dahliae infection. The ghr-miR171a was confirmed to direct the cleavage of GhSCL6 mRNA in the post-transcriptional process, as evidenced by 5' RLM-RACE, ß-glucuronidase (GUS) histochemical staining and enzyme activity assay. Interestingly, we found that overexpressing ghr-miR171a reduced cotton plants' resistance to V. dahliae, while suppressing ghr-miR171a increased the plants' defense capacity. The GhSCL6 protein, when fused with green fluorescent protein (GFP), localizes in the cell nucleus, indicating its potential role in gene regulation. This was further corroborated by yeast two-hybrid assays, which verified GhSCL6's transcriptional activation ability. Through quantitative reverse transcriptase PCR (qRT-PCR), luciferase (LUC) fluorescence, and yeast one-hybrid assays, we found that GhSCL6 binds to the GT-box element of the GhPR1 promoter, activating its expression and thereby enhancing plant disease resistance. Taken together, our findings demonstrate that the cotton miR171a-SCL6 module regulates Verticillium wilt resistance in plants through the post-transcriptional process. This insight may offer new perspectives for disease resistance strategies in cotton.

Immune Cell Infiltration Analysis Based on Bioinformatics Reveals Novel Biomarkers of Coronary Artery Disease.

Background: Coronary artery disease (CAD) is a multifactorial immune disease, but research into the specific immune mechanism is still needed. The present study aimed to identify novel immune-related markers of CAD. Methods: Three CAD-related datasets (GSE12288, GSE98583, GSE113079) were downloaded from the Gene Expression Integrated Database. Gene ontology annotation, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis and weighted gene co-expression network analysis were performed on the common significantly differentially expressed genes (DEGs) of these three data sets, and the most relevant module genes for CAD obtained. The immune cell infiltration of module genes was evaluated with the CIBERSORT algorithm, and characteristic genes accompanied by their diagnostic effectiveness were screened by the machine-learning algorithm least absolute shrinkage and selection operator (LASSO) regression analysis. The expression levels of characteristic genes were evaluated in the peripheral blood mononuclear cells of CAD patients and healthy controls for verification. Results: A total of 204 upregulated and 339 downregulated DEGs were identified, which were mainly enriched in the following pathways: "Apoptosis", "Th17 cell differentiation", "Th1 and Th2 cell differentiation", "Glycerolipid metabolism", and "Fat digestion and absorption". Five characteristic genes, LMAN1L, DOK4, CHFR, CEL and CCDC28A, were identified by LASSO analysis, and the results of the immune cell infiltration analysis indicated that the proportion of immune infiltrating cells (activated CD8 T cells and CD56 DIM natural killer cells) in the CAD group was lower than that in the control group. The expressions of CHFR, CEL and CCDC28A in the peripheral blood of the healthy controls and CAD patients were significantly different. Conclusion: We identified CHFR, CEL and CCDC28A as potential biomarkers related to immune infiltration in CAD based on public data sets and clinical samples. This finding will contribute to providing a potential target for early noninvasive diagnosis and immunotherapy of CAD.

Cotton RSG2 Mediates Plant Resistance against Verticillium dahliae by miR482b Regulation.

Cotton Verticillium wilt, mainly caused by Verticillium dahliae, has a serious impact on the yield and quality of cotton fiber. Many microRNAs (miRNAs) have been identified to participate in plant resistance to V. dahliae infection, but the exploration of miRNA's function mechanism in plant defense is needed. Here, we demonstrate that the ghr-miR482b-GhRSG2 module mediates cotton plant resistance to V. dahliae infection. Based on the mRNA degradation data and GUS fusion experiments, ghr-miR482b directedly bonds to GhRSG2 mRNA to lead to its degradation. The knockdown and overexpression of ghr-miR482b through virus-induced gene silencing strategies enhanced (decreased by 0.39-fold in disease index compared with the control) and weakened (increased by 0.46-fold) the plant resistance to V. dahliae, respectively. In addition, silencing GhRSG2 significantly increased (increased by 0.93-fold in disease index) the plant sensitivity to V. dahliae compared with the control plants treated with empty vector. The expression levels of two SA-related disease genes, GhPR1 and GhPR2, significantly decreased in GhRSG2-silenced plants by 0.71 and 0.67 times, respectively, and in ghr-miR482b-overexpressed (OX) plants by 0.59 and 0.75 times, respectively, compared with the control, whereas the expression levels of GhPR1 and GhPR2 were significantly increased by 1.21 and 2.59 times, respectively, in ghr-miR482b knockdown (KD) plants. In sum, the ghr-miR482b-GhRSG2 module participates in the regulation of plant defense against V. dahliae by inducing the expression of PR1 and PR2 genes.

Nanozyme-Integrated Thermoresponsive In Situ Forming Hydrogel Enhances Mesenchymal Stem Cell Viability and Paracrine Effect for Efficient Spinal Cord Repair.

Mesenchymal stem cell (MSC)-based therapy has emerged as a promising strategy for the treatment of spinal cord injury (SCI). However, the hostile microenvironment of SCI, which can adversely affect the survival and paracrine effect of the implanted MSCs, severely limits the therapeutic efficacy of this approach. Here, we report on a ceria nanozyme-integrated thermoresponsive in situ forming hydrogel (CeNZ-gel) that can enable dual enhancement of MSC viability and paracrine effect, leading to highly efficient spinal cord repair. The sol-gel transition property of the CeNZ-gel at body temperature ensures uniform coverage of the hydrogel in injured spinal cord tissues. Our results demonstrate that the CeNZ-gel significantly increases the viability of transplanted MSCs in the microenvironment by attenuating oxidative stress and, more importantly, promotes the secretion of angiogenic factors from MSCs by inducing autophagy of MSCs. The synergy between the oxidative stress-relieving effect of CeNZs and the paracrine effect of MSCs accelerates angiogenesis, nerve repair, and motor function recovery after SCI, providing an efficient strategy for MSC-based SCI therapy.

Recent advances of magnetic chitosan hydrogel: Preparation, properties and applications.

Magnetic chitosan hydrogels are organic-inorganic composite material with the characteristics of both magnetic materials and natural polysaccharides. Due to its biocompatibility, low toxicity and biodegradability, chitosan, a natural polymer has been widely used for preparing magnetic hydrogels. The addition of magnetic nanoparticles to chitosan hydrogels not only improves their mechanical strength, but also endows them with magnetic thermal effects, targeting capabilities, magnetically-sensitive release characteristics, easy separation and recovery, thus enabling them to be used in various applications including drug delivery, magnetic resonance imaging, magnetothermal therapy, and adsorption of heavy metals and dyes. In this review, the physical and chemical crosslinking methods of chitosan hydrogels and the methods for binding magnetic nanoparticles in hydrogel networks are first introduced. Subsequently, the properties of magnetic chitosan hydrogels were summarized including mechanical properties, self-healing, pH responsiveness and properties in magnetic fields. Finally, the potential for further technological and applicative advancements of magnetic chitosan hydrogels is discussed.

Genome-wide identification of terpenoid synthase family genes in Gossypium hirsutum and functional dissection of its subfamily cadinene synthase A in gossypol synthesis.

Plant terpenoid synthase (TPS) family genes participate in metabolite synthesis, hormones, gossypol, etc. Here, we genome-widely identified TPS family genes in 12 land plant species. Four hundred and thirty TPS-related genes were divided into seven subfamilies. The TPS-c in Bryophytes was suggested to be the earliest subfamily, followed by the TPS-e/f and TPS-h presence in ferns. TPS-a, the largest number of genes, was derived from monocotyledonous and dicotyledonous plants. Collinearity analysis showed that 38 out of the 76 TPS genes in G. hirsutum were collinear within G. arboreum and G. raimondii. Twenty-one GhTPS-a genes belong to the cadinene synthase (GhCDN) subfamily and were divided into five groups, A, B, C, D, and E. The special cis-elements in the promoters of 12 GhCDN-A genes suggested that the JA and ethylene signaling pathways may be involved in their expression regulation. When 12 GhCDN-A genes were simultaneously silenced through virus-induced gene silencing, the glandular color of GhCDN-A-silenced plants was lighter than that of the control, supported by a gossypol content decrease based on HPLC testing, suggesting that GhCDN-A subgroup genes participate in gossypol synthesis. According to RNA-seq analysis, gossypol synthesis-related genes and disease-resistant genes in the glandular variety exhibited upregulated expression compared to the glandless variety, whereas hormone signaling-related genes were downregulated. All in all, these results revealed plant TPS gene evolution rules and dissected the TPS subfamily, GhCDN-A, function in gossypol synthesis in cotton.

CRISPR/Cas9 and Agrobacterium tumefaciens virulence proteins synergistically increase efficiency of precise genome editing via homology directed repair in plants.

CRISPR/Cas9 genome editing and Agrobacterium tumefaciens-mediated genetic transformation are widely-used plant biotechnology tools derived from bacterial immunity-related systems, each involving DNA modification. The Cas9 endonuclease introduces DNA double-strand breaks (DSBs), and the A. tumefaciens T-DNA is released by the VirD2 endonuclease assisted by VirDl and attached by VirE2, transferred to the plant nucleus and integrated into the genome. Here, we explored the potential for synergy between the two systems and found that Cas9 and three virulence (Vir) proteins achieve precise genome editing via the homology directed repair (HDR) pathway in tobacco and rice plants. Compared with Cas9T (Cas9, VirD1, VirE2) and CvD (Cas9-VirD2) systems, the HDR frequencies of a foreign GFPm gene in the CvDT system (Cas9-VirD2, VirD1, VirE2) increased 52-fold and 22-fold, respectively. Further optimization of the CvDT process with a donor linker (CvDTL) achieved a remarkable increase in the efficiency of HDR-mediated genome editing. Additionally, the HDR efficiency of the three rice endogenous genes ACETOLACTATE SYNTHASE (ALS), PHYTOENE DESATURASE (PDS), and NITROGEN TRANSPORTER 1.1 B (NRT1.1B) increased 24-, 32- and 16-fold, respectively, in the CvDTL system, compared with corresponding Cas9TL (Cas9T process with a donor linker). Our results suggest that collaboration between CRISPR/Cas9 and Agrobacterium-mediated genetic transformation can make great progress towards highly efficient and precise genome editing via the HDR pathway.

Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia-Reperfusion Injury.

(1) Background: The molecular mechanism of oxidative stress-related genes (OSRGs) in myocardial ischemia-reperfusion injury (MIRI) has not been fully elucidated. (2) Methods: Differential expression analysis, enrichment analysis, and PPI analysis were performed on the MIRI-related datasets GSE160516 and GSE61592 to find key pathways and hub genes. OSRGs were obtained from the Molecular Signatures Database (MSigDB). The expression pattern and time changes of them were studied on the basis of their raw expression data. Corresponding online databases were used to predict miRNAs, transcription factors (TFs), and therapeutic drugs targeting common differentially expressed OSRGs. These identified OSRGs were further verified in the external dataset GSE4105 and H9C2 cell hypoxia-reoxygenation (HR) model. (3) Results: A total of 134 DEGs of MIRI were identified which were enriched in the pathways of "immune response", "inflammatory response", "neutrophil chemotaxis", "phagosome", and "platelet activation". Six hub genes and 12 common differentially expressed OSRGs were identified. A total of 168 miRNAs, 41 TFs, and 21 therapeutic drugs were predicted targeting these OSRGs. Lastly, the expression trends of Aif1, Apoe, Arg1, Col1a1, Gpx7, and Hmox1 were confirmed in the external dataset and HR model. (4) Conclusions: Aif1, Apoe, Arg1, Col1a1, Gpx7, and Hmox1 may be involved in the oxidative stress mechanism of MIRI, and the intervention of these genes may be a potential therapeutic strategy.

The cotton miR530-SAP6 module activated by systemic acquired resistance mediates plant defense against Verticillium dahliae.

Many cotton miRNAs in root responding to Verticillium dahliae infection have been identified. Conversely, the miRNAs in leaf distantly responding to this fungal infection from roots via systemic acquired resistance (SAR) remain to be explored. Here, we constructed two groups of leaf sRNA libraries in cotton treated with V. dahliae via root-dipped method at 7- and 10-day post inoculation. Analysis of high-throughput sRNA sequencing identified 75 known and 379 novel miRNAs, of which 41 miRNAs significantly differentially expressed in fungal treatment plant leaves compared to the mock treatment at two time points. Then we characterized the cotton miR530-SAP6 module as a representative in the distant response to V. dahliae infection in roots. Based on degradome data and a luciferase (LUC) fusion reporter analysis, ghr-miR530 directedly cleaved GhSAP6 mRNA during the post-transcriptional process. Silencing of ghr-miR530 increased plant defense to this fungus, while its overexpression attenuated plant resistance. In link with ghr-miR530 function, the knockdown of GhSAP6 also decreased the plant resistance, resulting from down-regulation of SA-relative gene expression including GhNPR1 and GhPR1. In all, these results demonstrated that there are numerous miRNAs in leaf distantly responding to V. dahliae infection in roots mediate plant immunity.

Recent nanotechnology-based strategies for interfering with the life cycle of bacterial biofilms.

Biofilm formation plays an important role in the resistance development in bacteria to conventional antibiotics. Different properties of the bacterial strains within biofilms compared with their planktonic states and the protective effect of extracellular polymeric substances contribute to the insusceptibility of bacterial cells to conventional antimicrobials. Although great effort has been devoted to developing novel antibiotics or synthetic antibacterial compounds, their efficiency is overshadowed by the growth of drug resistance. Developments in nanotechnology have brought various feasible strategies to combat biofilms by interfering with the biofilm life cycle. In this review, recent nanotechnology-based strategies for interfering with the biofilm life cycle according to the requirements of different stages are summarized. Additionally, the importance of strategies that modulate the bacterial biofilm microenvironment is also illustrated with specific examples. Lastly, we discussed the remaining challenges and future perspectives on nanotechnology-based strategies for the treatment of bacterial infection.

Iris lactea var. chinensis plant drought tolerance depends on the response of proline metabolism, transcription factors, transporters and the ROS-scavenging system.

BACKGROUND: Iris lactea var. chinensis, a perennial herbaceous species, is widely distributed and has good drought tolerance traits. However, there is little information in public databases concerning this herb, so it is difficult to understand the mechanism underlying its drought tolerance. RESULTS: In this study, we used Illumina sequencing technology to conduct an RNA sequencing (RNA-seq) analysis of I. lactea var. chinensis plants under water-stressed conditions and rehydration to explore the potential mechanisms involved in plant drought tolerance. The resulting de novo assembled transcriptome revealed 126,979 unigenes, of which 44,247 were successfully annotated. Among these, 1187 differentially expressed genes (DEGs) were identified from a comparison of the water-stressed treatment and the control (CK) treatment (T/CK); there were 481 upregulated genes and 706 downregulated genes. Additionally, 275 DEGs were identified in the comparison of the rehydration treatment and the water-stressed treatment (R/T). Based on Quantitative Real-time Polymerase Chain Reaction (qRT-PCR) analysis, the expression levels of eight randomly selected unigenes were consistent with the transcriptomic data under water-stressed and rehydration treatment, as well as in the CK. According to Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, proline metabolism-related DEGs, including those involved in the 'proline catabolic process', the 'proline metabolic process', and 'arginine and proline metabolism', may play important roles in plant drought tolerance. Additionally, these DEGs encoded 43 transcription factors (TFs), 46 transporters, and 22 reactive oxygen species (ROS)-scavenging system-related proteins. Biochemical analysis and histochemical detection showed that proline and ROS were accumulated under water-stressed conditions, which is consistent with the result of the transcriptomic analysis. CONCLUSIONS: In summary, our transcriptomic data revealed that the drought tolerance of I. lactea var. chinensis depends on proline metabolism, the action of TFs and transporters, and a strong ROS-scavenging system. The related genes found in this study could help us understand the mechanisms underlying the drought tolerance of I. lactea var. chinensis.