Neuropeptides produced in neurosecretory cells are the largest group of insect hormones. They regulate various physiological functions, such as fat body homeostasis, feeding, digestion, excretion, circulation, reproduction, metamorphosis, and behavior throughout all life stages. The PRXamide peptide family (X, a variable amino acid) is a well-characterized neuropeptide component with a common amino acid sequence, PRXamide (NH2), at the C-terminal end conserved across Insecta. The PRXamide peptides are classified into three subfamilies, each having diverse biological roles in insects: (1) pyrokinin (PK) includes the pheromone biosynthesis activating neuropeptide (PBAN) and the diapause hormone (DH), (2) the capability (CAPA) peptides, and (3) the ecdysis-triggering hormone (ETH). PBAN as a member of PK subfamily was first identified to stimulate pheromone biosynthesis in moths three decades ago. Since then, PBAN peptides have been extensively studied by various research groups from a broad spectrum of arthropods. In this paper, we briefly review insect PBAN molecules with emphasis on gene structure and expression, signal transduction, physiological mechanism in sex pheromone biosynthesis, and application for pest management.
Hongming Lv;Yvxi He;Jingjing Wu; Li Zhen ;Yvwei Zheng
Journal of Veterinary Science
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v.24
no.1
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pp.2.1-2.14
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2023
Background: Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear. Objectives: This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms. Methods: In this study, a chronic CS-induced myocardial injury model was used; mice were subjected to chronic CS (4℃) for three hours per day for three weeks. Results: CS could result in myocardial injury by inducing the levels of heat shock proteins 70 (HSP70), enhancing the generation of creatine phosphokinase-isoenzyme (CKMB) and malondialdehyde (MDA), increasing the contents of tumor necrosis factor-α (TNF-α), high mobility group box 1 (HMGB1) interleukin1b (IL-1β), IL-18, IL-6, and triggering the depletion of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Multiple signaling pathways were activated by cold exposure, including pyroptosis-associated NOD-like receptor 3 (NLRP3)-regulated caspase-1-dependent/Gasdermin D (GSDMD), inflammation-related toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), as well as oxidative stressinvolved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia. Conclusions: These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures.
C. U. Han;Lee, C. H.;K. S. Jang;Park, Y. H.;H. K. Lim;Kim, J.C.;Park, G. J.;J.S. Cha;Park, J. E.
Proceedings of the Korean Society of Plant Pathology Conference
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2003.10a
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pp.66.2-66
/
2003
A gain-of-function mutant, SHM-11 obtained through gamma-ray mutagenesis, is resistant to rice blast caused by Magnaporthe grisea while wild type Sanghaehyanghyella is highly susceptible to the same disease. The resistance in the mutant was not race-specific when we tested with four races (KJ-201, KI-1113a, KI-313, KI-409) of M. grisea. To identify genes involved disease resistance in the gain-of-function mutant, genes specifically expressed in the mutant were selected by suppression subtractive hybridization using cDNAS of blast-inoculated mutant and wild type as a tester and a driver, respectively, Random 200 clones from the subtracted library were selected and analyzed by DNA sequencing. The sequenced genes represented three major groups related with disease resistance; genes encoding PR proteins, genes probably for phytoalexin biosynthesis, and genes involved in disease resistance signal transduction. A gene encoding a putative receptor-like protein kinase was identified as highly expressed only in the gain-of-function mutant after blast infection. The role of the putative receptor-like protein kinase gene during blast resistance will be further studied.
Many of the adverse effects of solar UV exposure appear to be directly attributable to damage to epidermal DNA. In particular, cyclobutane pyrimidine dimers (CPD) may initiate mutagenic changes as well as induce signal transduction responses that lead to a loss of skin immune surveillance and micro-destruction of skin structure. Our approach is to reverse the DNA damage using prokaryotic DNA repair enzymes delivered into skin using specially engineered liposomes. T4 endonuclease V encapsulated in liposomes (T4N5 liposome lotion) enhanced DNA repair by shifting repair of CPD from the nucleotide excision to the base excision repair pathway. Following topical application to humans, increased repair limited UV-induction of cytokines, many of which are immunosuppressive. In a recent clinical study, topical treatment of UV-irradiated human skin with T4N5 liposome lotion reduced the suppression of the nickel sulfate contact hypersensitivity response. Similarly, the photoreactivating enzyme enhances repair by directly reversing CPDs after absorbing activating light. Here also treatment of UV-irradiated human skin with photoreactivating enzyme in liposomes and photoreactivating light restored the response to the contact allergen nickel sulfate. These findings confirm in humans the observation in mice that UV induced suppression of contact hypersensitivity is caused in part by CPDs. We have tested the ability of T4N5 liposome lotion to prevent UV-induced skin cancer in patients with xeroderma pigmentosum (XP), who have an elevated incidence of skin cancer resulting from a genetic defect in DNA repair. Daily use of the lotion for one year in a group of 20 XP patients reduced the average number of actinic keratoses by 68% and basal cell cancers by 30% compared to 9 patients in the placebo control group. Delivery of DNA repair enzymes to skin is a promising new approach to photoprotection.
Jae-Gyun Choi;Sheu-Ran Choi;Dong-Wook Kang;Hyun Jin Shin;Miae Lee;Jungmo Hwang;Hyun-Woo Kim
Journal of Veterinary Science
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v.24
no.2
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pp.26.1-26.11
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2023
Background: Angiotensin-converting enzyme inhibitor (ACEi) inhibits the catalysis of angiotensin I to angiotensin II and the degradation of substance P (SP) and bradykinin (BK). While the possible relationship between ACEi and SP in nociceptive mice was recently suggested, the effect of ACEi on signal transduction in astrocytes remains unclear. Objectives: This study examined whether ACE inhibition with captopril or enalapril modulates the levels of SP and BK in primary cultured astrocytes and whether this change modulates PKC isoforms (PKCα, PKCβI, and PKCε) expression in cultured astrocytes. Methods: Immunocytochemistry and Western blot analysis were performed to examine the changes in the levels of SP and BK and the expression of the PKC isoforms in primary cultured astrocytes, respectively. Results: The treatment of captopril or enalapril increased the immunoreactivity of SP and BK significantly in glial fibrillary acidic protein-positive cultured astrocytes. These increases were suppressed by a pretreatment with an angiotensin-converting enzyme. In addition, treatment with captopril increased the expression of the PKCβI isoform in cultured astrocytes, while there were no changes in the expression of the PKCα and PKCε isoforms after the captopril treatment. The captopril-induced increased expression of the PKCβI isoform was inhibited by a pretreatment with the neurokinin-1 receptor antagonist, L-733,060, the BK B1 receptor antagonist, R 715, or the BK B2 receptor antagonist, HOE 140. Conclusions: These results suggest that ACE inhibition with captopril or enalapril increases the levels of SP and BK in cultured astrocytes and that the activation of SP and BK receptors mediates the captopril-induced increase in the expression of the PKCβI isoform.
Kyoung Rok Geem ;Jaewook Kim ;Wonsil Bae ;Moo-Geun Jee ;Jin Yu ;Inbae Jang;Dong-Yun Lee ;Chang Pyo Hong ;Donghwan Shim;Hojin Ryu
Journal of Ginseng Research
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v.47
no.3
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pp.469-478
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2023
Background: Nitrogen (N) is an essential macronutrient for plant growth and development. To support agricultural production and enhance crop yield, two major N sources, nitrate and ammonium, are applied as fertilizers to the soil. Although many studies have been conducted on N uptake and signal transduction, the molecular genetic mechanisms of N-mediated physiological roles, such as the secondary growth of storage roots, remain largely unknown. Methods: One-year-old P. ginseng seedlings treated with KNO3 were analyzed for the secondary growth of storage roots. The histological paraffin sections were subjected to bright and polarized light microscopic analysis. Genome-wide RNA-seq and network analysis were carried out to dissect the molecular mechanism of nitrate-mediated promotion of ginseng storage root thickening. Results: Here, we report the positive effects of nitrate on storage root secondary growth in Panax ginseng. Exogenous nitrate supply to ginseng seedlings significantly increased the root secondary growth. Histological analysis indicated that the enhancement of root secondary growth could be attributed to the increase in cambium stem cell activity and the subsequent differentiation of cambium-derived storage parenchymal cells. RNA-seq and gene set enrichment analysis (GSEA) revealed that the formation of a transcriptional network comprising auxin, brassinosteroid (BR)-, ethylene-, and jasmonic acid (JA)-related genes mainly contributed to the secondary growth of ginseng storage roots. In addition, increased proliferation of cambium stem cells by a N-rich source inhibited the accumulation of starch granules in storage parenchymal cells. Conclusion: Thus, through the integration of bioinformatic and histological tissue analyses, we demonstrate that nitrate assimilation and signaling pathways are integrated into key biological processes that promote the secondary growth of P. ginseng storage roots.
Jinsu Lee;Minsoo Han;Yesol Shin;Jung-Min Lee;Geon Heo;Yuree Lee
Molecules and Cells
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v.46
no.6
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pp.329-336
/
2023
Reactive oxygen species (ROS) serve as secondary messengers that regulate various developmental and signal transduction processes, with ROS primarily generated by NADPH OXIDASEs (referred to as RESPIRATORY BURST OXIDASE HOMOLOGs [RBOHs] in plants). However, the types and locations of ROS produced by RBOHs are different from those expected to mediate intracellular signaling. RBOHs produce O2•- rather than H2O2 which is relatively long-lived and able to diffuse through membranes, and this production occurs outside the cell instead of in the cytoplasm, where signaling cascades occur. A widely accepted model explaining this discrepancy proposes that RBOH-produced extracellular O2•- is converted to H2O2 by superoxide dismutase and then imported by aquaporins to reach its cytoplasmic targets. However, this model does not explain how the specificity of ROS targeting is ensured while minimizing unnecessary damage during the bulk translocation of extracellular ROS (eROS). An increasing number of studies have provided clues about eROS action mechanisms, revealing various mechanisms for eROS perception in the apoplast, crosstalk between eROS and reactive nitrogen species, and the contribution of intracellular organelles to cytoplasmic ROS bursts. In this review, we summarize these recent advances, highlight the mechanisms underlying eROS action, and provide an overview of the routes by which eROS-induced changes reach the intracellular space.
Background: Cold atmospheric plasma is a novel innovative approach for wound care, and it is currently underrepresented in veterinary medicine. Objectives: To investigate the efficacy and safety of using cold atmospheric microwave plasma (CAMP) as an adjunct therapy for wound healing in dogs and cats. Methods: Wound healing outcomes were retrospectively analyzed using clinical records of client-owned dogs and cats who were first managed through standard wound care alone (pre-CAMP period) and subsequently via CAMP therapy (CAMP period). The degree of wound healing was estimated based on wound size and a modified wound scoring system. Results: Of the 27 acute and chronic wounds included in the analysis, 81.48% showed complete healing after the administration of CAMP as an adjunct therapy to standard care. Most wounds achieved complete healing in < 5 weeks. Compared with the pre-CAMP period, the rate of wound healing significantly increased every week in the CAMP period in terms of in wound size (first week, p < 0.001; second week, p = 0.012; third week, p < 0.001) and wound score (first week, p < 0.001; second week, p < 0.001; third week, p = 0.001). No adverse events were noted except for mild discomfort and transient erythema. Conclusions: CAMP is a well-tolerated therapeutic option with immense potential to support the treatment of wounds of diverse etiology in small animal practice. Further research is warranted to establish specific criteria for CAMP treatment according to wound characteristics.
Objectives : While treatments for cancer are advancing, the development of effective treatments for cancer metastasis, the main cause of cancer patient death, remains insufficient. Recent studies on Dichroae Radix have revealed that its active ingredients have the potential to inhibit cancer metastasis. This study aimed to investigate the cancer metastasis inhibitory effect of Dichroae Radix using network pharmacological analysis. Methods : The active compounds of Dichroae Radix have been identified using Traditional Chinese Medicine System Pharmacology Database and Analysis Platform. The UniProt database was used to collect each of information of all target proteins associated with the active compounds. To find the bio-metabolic processes associated with each target, the DAVID6.8 Gene Functional classifier tool was used. Compound-Target and Target-Pathway networks were analyzed via Cytoscape 3.40. Results : In total, 25 active compounds and their 62 non-redundant targets were selected through the TCMSP database and analysis platform. The target genes underwent gene ontology and pathway enrichment analysis. The gene list applied to the gene ontology analysis revealed associations with various biological processes, including signal transduction, chemical synaptic transmission, G-protein-coupled receptor signaling pathways, response to xenobiotic stimulus, and response to drugs, among others. A total of eleven genes, including HSP90AB1, CALM1, F2, AR, PAKACA, PTGS2, NOS2, RXRA, ESR1, ESR2, and NCOA1, were found to be associated with biological pathways related to cancer metastasis. Furthermore, nineteen of the active compounds from Dichroae Radix were confirmed to interact with these genes. Conclusions : The results provide valuable insights into the mechanism of action and molecular targets of Dichroae Radix. Notably, Berberine, the main active ingredient of Dichroae Radix, plays a significant role in degrading AR proteins in advanced prostate cancer. Further studies and validations can provide crucial data to advance cancer metastasis prevention and treatment strategies.
Objective: The main objective of this study was to define molecular mechanisms associated with thermal stress responses of chickens from commercial broilers (BR, Ross 308), Thai native chickens (NT) and crossbreeds between BR×NT (H75). Methods: Twenty days before reaching specific market age, chickens from each breed were divided into control and thermal-stressed groups. The stressed groups were exposed to a cyclic thermal challenge (35℃±1℃ for 6 h, followed by 26℃±1℃ for 18 h) for 20 days. Control group was raised under a constant temperature of 26℃±1℃. Pectoralis major (n = 4) from each group was collected for transcriptome analysis using HiSeq Illumina and analysis of glycogen and lactate. Gene expression patterns between control and thermal-stressed groups were compared within the same breeds. Results: Differentially expressed transcripts of 65, 59, and 246 transcripts for BR, NT, and H75, respectively, were revealed by RNA-Seq and recognized by Kyoto encyclopedia of genes and genomes database. Pathway analysis underlined altered glucose homeostasis and protein metabolisms in all breeds. The signals centered around phosphatidylinositol 3-kinase (PI3K)/Akt signaling, focal adhesion, and MAPK signaling in all breeds with slight differences in molecular signal transduction patterns among the breeds. An extensive apoptosis was underlined for BR. Roles of AMPK, MAPK signaling and regulation of actin cytoskeleton in adaptive response were suggested for H75 and NT chickens. Lower glycogen content was observed in the breast muscles of BR and NT (p<0.01) compared to their control counterparts. Only BR muscle exhibited increased lactate (p<0.01) upon exposure to the stress. Conclusion: The results provided a better comprehension regarding the associated biological pathways in response to the cyclic thermal stress in each breed and in chickens with different growth rates.
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