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PubMed1998

Inherited cytokine and cytokine receptor deficiencies in man.

Over the past decades, cytokines and their receptors have been shown to play a decisive role in the differentiation of both innate and adaptive immunity. The essential roles of cytokine/receptor pathways in vivo, however, have remained elusive and poorly defined. In some cases, primary immunodeficiency syndromes have provided the natural models in which the role of cytokines and their receptors in the development and function of the immune system have been elucidated. Animal models of cytokine/receptor deficiencies generated through gene targeting have also played a decisive factor in identifying the true biological roles of cytokine/receptor pathways. The end result of these approaches has been an enormous advance in our understanding of the cytokine control of normal and pathological human conditions, as well as the advent of new diagnostic tools and novel therapies.

Animals↗

PubMed2006

Quantitative phosphotyrosine proteomics of EphB2 signaling by stable isotope labeling with amino acids in cell culture (SILAC).

Eph-related receptor tyrosine kinases (RTK) have been implicated in several biological functions including synaptic plasticity, axon guidance, and morphogenesis, yet the details of the signal transduction pathways that produce these specific biological functions after ligand-receptor interaction remain unclear. We used Stable Isotope Labeling by Amino Acids in Cell Culture (SILAC) in combination with LC-MS/MS to characterize cellular signaling following stimulation by ephrinB1-Fc of NG-108 cells that overexpress EphB2 receptors. Because tyrosine phosphorylation functions as a key regulatory event in RTK signaling, we used anti-phosphotyrosine immunoprecipitation (pY IP) of cell lysates to isolate potential participants in the EphB2 pathway. Our SILAC experiments identified 127 unique proteins, 40 of which demonstrated increased abundance in pY IPs from ephrinB1-Fc stimulated cells as compared with unstimulated cells. Six proteins demonstrated decreased abundance, and 81 did not change significantly in relative abundance. Western blotting analysis of five proteins after pY IP verified their SILAC results. On the basis of previously published work and use of PathwayAssist software, we proposed an interaction network downstream of EphB2 for the proteins with changed ratios.

Amino Acid Sequence↗

PubMed2004

Promotion and attenuation of FGF signaling through the Ras-MAPK pathway.

The fibroblast growth factors (FGFs) represent a large family of ligands that activate signal transduction pathways leading to diverse biological responses, including many involved in various processes during development. Here, we discuss the discovery of a subset of conserved FGF target genes that encode feedback regulators of FGF signaling itself. Members of the Sprouty, Sef, and mitogen-activated protein kinase phosphatase families are negative modulators of FGF signaling, whereas positive factors that promote FGF signaling include the ETS transcription factors ERM and PEA3 and the transmembrane protein XFLRT3. These molecules affect the FGF signaling cascade at different levels to regulate the final output of the pathway. This multilayered regulation suggests that precise adjustment of FGF signaling is critical in development.

Animals↗

PubMed2004

Multi-tissue gene-expression analysis in a mouse model of thyroid hormone resistance.

BACKGROUND: Resistance to thyroid hormone (RTH) is caused by mutations of the thyroid hormone receptor beta (TRbeta) gene. To understand the transcriptional program underlying TRbeta mutant-induced phenotypic expression of RTH, cDNA microarrays were used to profile the expression of 11,500 genes in a mouse model of human RTH. RESULTS: We analyzed transcript levels in cerebellum, heart and white adipose tissue from a knock-in mouse (TRbetaPV/PV mouse) that harbors a human mutation (referred to as PV) and faithfully reproduces human RTH. Because TRbetaPV/PV mice have elevated thyroid hormone (T3), to define T3-responsive genes in the context of normal TRbeta, we also analyzed T3 effects in hyperthyroid wild-type gender-matched littermates. Microarray analysis revealed 163 genes responsive to T3 treatment and 187 genes differentially expressed between TRbetaPV/PV mice and wild-type littermates. Both the magnitude and gene make-up of the transcriptional response varied widely across tissues and conditions. We identified genes modulated in T3-dependent PV-independent, T3- and PV-dependent, and T3-independent PV-dependent pathways that illuminated the biological consequences of PV action in vivo. Most T3-responsive genes that were dysregulated in the heart and white adipose tissue of TRbetaPV/PV mice were repressed in T3-treated wild-type mice and upregulated in TRbetaPV/PV mice, suggesting the inappropriate activation of T3-suppressed genes in RTH. CONCLUSIONS: Comprehensive multi-tissue gene-expression analysis uncovered complex multiple signaling pathways that mediate the molecular actions of TRbeta mutants in vivo. In particular, the T3-independent mutant-dependent genomic response unveiled the contribution of a novel 'change-of-function' of TRbeta mutants to the pathogenesis of RTH. Thus, the molecular actions of TRbeta mutants are more complex than previously envisioned.

Adipose Tissue↗

PubMed2024

Transcriptome analysis of the diseased intervertebral disc tissue in patients with spinal tuberculosis.

OBJECTIVE: To investigate the differential expression genes (DEGs) in spinal tuberculosis using transcriptomics, with the aim of identifying novel therapeutic targets and prognostic indicators for the clinical management of spinal tuberculosis. METHODS: Patients who visited the Department of Orthopedics at the Second Hospital, Lanzhou University from January 2021 to May 2023 were enrolled. Based on the inclusion and exclusion criteria, there were 5 patients in the test group and 5 patients in the control group. Total RNA was extracted and paired-end sequencing was conducted on the sequencing platform. After processing the sequencing data with clean reads and annotating the reference genome, FPKM normalization and differential expression analysis were performed. The DEGs and long non-coding RNAs (LncRNAs) were analyzed for Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment. The cis-regulation of differentially expressed mRNAs (DE mRNAs) by LncRNAs was predicted and analyzed to establish a co-expression network. RESULTS: This study identified 2366 DEGs, with 974 genes significantly upregulated and 1392 genes significantly downregulated. The upregulated genes are associated with cytokine-cytokine receptor interactions, tuberculosis, and TNF-α signaling pathways, primarily enriched in biological processes such as immunity and inflammation. The downregulated genes are related to muscle development, contraction, fungal defense response, and collagen metabolism processes. Analysis of LncRNAs from bone tuberculosis RNA-seq data detected a total of 3652 LncRNAs, with 356 significantly upregulated and 184 significantly downregulated. Further analysis identified 311 significantly different LncRNAs that could cis-regulate 777 target genes, enriched in pathways such as muscle contraction, inflammatory response, and immune response, closely related to bone tuberculosis. There are 51 genes enriched in the immune response pathway regulated by cis-acting LncRNAs. LncRNAs that regulate immune response-related genes, such as upregulated RP11-451G4.2, RP11-701P16.5, AC079767.4, AC017002.1, LINC01094, CTA-384D8.35, and AC092484.1, as well as downregulated RP11-2C24.7, may serve as potential prognostic and therapeutic targets. CONCLUSION: The DE mRNAs and LncRNAs in spinal tuberculosis are both associated with immune regulatory pathways. These pathways promote or inhibit the tuberculosis infection and development at the mechanistic level and play an important role in the process of tuberculosis transferring to bone tissue.

Humans↗

PubMed2025

Mechanism of action of curculigoside ameliorating osteoporosis: an analysis based on network pharmacology and experimental validation.

OBJECTIVE: This study aimed to predict and verify the mechanism of curculigoside in treating osteoporosis using network pharmacology, molecular docking technology, and micro-CT technology. METHODS: Herb databases were searched to identify and screen potential targets of curculigoside. The GeneCards platform was utilized to mine osteoporosis-related targets. Cytoscape 3.6.0 software was employed to construct a compound-target-disease network. A protein-protein interaction (PPI) network for curculigoside in osteoporosis treatment was established, and core targets were screened. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and GO biological process analyses were performed using the Metascape database. Finally, molecular docking and micro-CT were used to validate core targets relevant to osteoporosis. RESULTS: A total of 166 potential curculigoside targets and 4,313 osteoporosis-related targets were identified, with 91 common targets. Ten key targets, including matrix metalloproteinase (MMP)3, MMP9, interleukin (IL)-6, and caspase-3, were screened. KEGG pathway enrichment analysis indicated involvement in 10 pathways, such as the Rap1 signaling pathway and tumor necrosis factor (TNF) signaling pathway. Molecular docking results demonstrated strong binding affinity between curculigoside and the core targets. Micro-CT analysis revealed that curculigoside not only improved BMD, BV/TV, BS/BV, and Tb.Th but also reduced Tb.Sp in osteoporotic bone. CONCLUSIONS: Curculigoside is likely to treat osteoporosis through targets such as MMP3, MMP9, IL-6, and caspase-3, acting on signaling pathways including Rap1 and TNF. These results indicate that curculigoside exhibits multitarget and multipathway characteristics in osteoporosis treatment, providing a theoretical basis for further clinical investigation.

Osteoporosis↗

PubMedDate not supplied

Advances in human chronopharmacology.

Regular and thus predictable changes in biologic susceptibility and response to a large variety of physical as well as chemical agents can now be viewed as rather common phenomena. Chronopharmacology involves both the investigation of drug effects as a function of biologic timing and the investigation of drug effects upon rhythm characteristics (the period, tau, the acrophase, phi, the amplitude, A, and the mesor, M). Illustrative examples of circadian (tau congruent to 24 hrs) chronopharmacology in man are summarized in up-dated tables, keeping in mind that the objective demonstration of chronopharmacologic facts demands the use of an appropriate methodology. Circadian changes in the effects of various chemical agents have been documented: histamine, sodium salicylate, acetylcholine, halothane, prostaglandin F2alpha, reserpine, cyproheptadine, ethanol, insulin, chlorothiazide, oxymetholone, orcinprenaline and SCH 1000 (the latter being bronchodilators), Indomethacin, lignocaine, ACTH, cortisol and various synthetic corticosteroids. Despite that pharmacological facts are well documented in man for circadian rhythms, studies are not only restricted to the 24-h period but have been already extended to rhythms of periods of e.g. approximately 30 days as well as approximately 1 year. For a better understanding of chronopharmacologic findings, three new concepts must be considered: a) the chronokinetics of a drug, defined as both rhythmic (circadian) changes in the drug bioavailability (and/or pharmacokinetic effects) and its excretion (urinary, among others); b) the chronesthesy of a biosystem to a drug, or the circadian change in the susceptibility of any biosystem to a drug (including organ systems, tumors, parasites, etc.); and c) The chronergy of a drug, or the rhythmic change in the overall effects and the effectiveness of a drug. This term takes into consideration the chronokinetics and the chronesthesies of the organismic biosystems involved. Presently, one of the aims of chronopharmacology is to solve problems of drug optimization, i.e. to enhance the desired efficiency of a corticosteroid or other medications, while reducing undesired effects. In the human organism, among other animal species, the metabolic fate of a pharmacologic agent (as well as that of a nutrient) is not constant as a function of biological time. The metabolic pathways are neither open permanently, nor open with a constant patency along the 24-h scale, among other bioperiodic domains. Thus, the chronobiologic approach concerning pharmacologic phenomena involves a lesser risk of errors and/or false information than the conventional homeostatic approach.

Biological Clocks↗

PubMed2026

Sex-specific associations of the plasma-proteome with incident coronary artery disease.

AIMS: The etiology of coronary artery Disease (CAD) appears different for men and women, yet insights into underlying sex-specific biological mechanisms are limited. We integrated genomic and proteomic analyses to investigate sex-specific associations of the plasma-proteome with CAD. METHODS AND RESULTS: In 40,829 UK Biobank participants (free-of-CAD, baseline-365 days thereafter; 55% women; mean age 56.9 ± 8.1 years), we examined associations between 2,922 plasma proteins and incident CAD over a median follow-up of 13.7 years (IQR 13.1-14.4) using multivariable-adjusted Cox proportional hazards models. Sex-specific analyses identified 440 female exclusive and 32 male exclusive proteins associated with incident CAD (FDR-corrected p < 0.05), revealing distinct pathway enrichments, including innate immune response in women and angiogenesis in men. Causality was assessed through combined and sex-stratified two-sample Mendelian randomization (MR) using inverse-variance-weighted analyses with genome wide association summary statistics from 422,108 men (61,969 cases) and 521,695 women (27,128 cases) (UK Biobank, FinnGen freeze 9). Integration of direct sex-protein interaction analyses with sex-combined MR identified 59 proteins with evidence for sex-specific causal effects. Four proteins demonstrated concordant directionality in sex-stratified MR analyses (n = 943,803) and multivariable regression models, namely CDKN2D, MYH9, and SKAP2 (women), and CTSH (men). To assess translational relevance, prioritized targets were further evaluated in secondary major adverse cardiovascular events among carotid endarterectomy patients (MACE; Athero-Express) and acute myocardial infarction (AMI; MISSION!) using plasma proteomics and ELISA. After further top-target identification in the context of MACE and AMI, clinical drug candidates were identified through a machine learning framework, including CTSH (men), and TNFRSF4 (both sexes). CONCLUSIONS: We identified sex-specific associations of proteins and biological pathways with incident CAD. Whereas the majority of proteins had consistent associations in both men and women, our findings suggest a degree of sex-specific pathogenesis with evidence for potential causality, opening new alleys for tailored prevention strategies and clinical cardiovascular risk management.

Journal Article↗

PubMed1984

A quantitative analysis of the spatial organization of the vestibulo-ocular reflexes in lateral- and frontal-eyed animals--II. Neuronal networks underlying vestibulo-oculomotor coordination.

The neuronal connectivity underlying the vestibulo-ocular reflexes in cat and rabbit was evaluated in the light of quantitative data of the spatial orientation on semicircular canals and extraocular muscles. Neuronal connectivity was calculated using a matrix-analysis of the sensory and motor periphery, and of the brain stem pathways connecting semicircular canals and extraocular muscles. Two cases of vestibulo-ocular reflex compensation were considered. In the first case, vestibulo-oculor reflex compensation was assumed to be isotropic, i.e. the vestibulo-ocular reflex gain is the same for all directions of rotation. In the second case, the vestibulo-oculor reflex gain was assumed to be anisotropic with the "torsional" gain smaller than the "horizontal" and "vertical" gains. The theoretical calculation predicts that besides the principal vestibulo-ocular reflex pathways (classical three-neuron-arc connectivity), several accessory connections (other than principal connections, regardless of the synapses involved) exist which are characteristic for each species. These accessory connections were compared to physiological and anatomical data. In the cat theoretical connections for an isotropic vestibulo-ocular reflex gain agree with pathways observed experimentally, of which the most characteristic are excitatory connections to the superior rectus and inhibitory connections to the inferior rectus muscle from both of the anterior canals, and a mirror image pattern of connections from the posterior canals. In the rabbit experimentally obtained data and calculated connections rarely agree. However, for an anisotropic gain we find a higher rate of coincidence between experimental and theoretical connections. Our evaluation indicates, that accessory vestibulo-ocular reflex pathways serve to compensate for the incongruence between semicircular canal and extraocular muscle planes, at least in the cat. Available experimental data suggest an important role of a special subclass of accessory pathways via axon collaterals of principal projections (three-neuron-arc nature). With certain restrictions, the presented method of calculation promises to be a useful tool for a quantitative analysis of the vestibulo-ocular reflex.

Animals↗

PubMedDate not supplied

Ligands for the vitamin D endocrine system: different shapes function as agonists and antagonists for genomic and rapid response receptors or as a ligand for the plasma vitamin D binding protein.

The integrated operation of the vitamin D endocrine system which produces the steroid hormone 1alpha,25(OH)(2)-vitamin D(3) (1alpha,25(OH)(2)D(3)) is dependent on four classes of proteins each of which have inherent in their secondary and tertiary structure a ligand binding domain (LBD) that allows the stereospecific binding of 1alpha,25(OH)(2)D(3) or related analogs as a substrate or ligand. These LBDs include: (a) the cytochrome P450 enzymes in the liver, kidney, and other tissues which metabolize vitamin D(3) into biologically active metabolites; (b) the plasma vitamin D binding protein (DBP) which selectively transports these hydrophobic molecules to the various target organs of the vitamin D endocrine system; (c) the nuclear receptor VDR(nuc) that is involved in regulation of gene transcription in over 30 cell types which possess this receptor; and (d) a plasma membrane receptor, VDR(mem), that is involved in initiation of signal transduction pathways which generate rapid biological responses. This article reviews the evidence that supports the conclusions that the LBD of the DBP, VDR(mem) and VDR(nuc) each select as their preferred ligand a unique shape of the conformationally flexible 1alpha,25(OH)(2)D(3). Two critical aspects of the conformationally flexible 1alpha,25(OH)(2)D(3) molecule which defines the optimum ligand shape are (a) the orientation and relative rigidity of the flexible 8 carbon side chain and (b) the position of the A ring in relation to the C/D rings as determined by the extent of rotation around the 6,7 single carbon bond of the seco B ring. These conclusions are based on consideration of structure-function studies of over 300 analogs of 1alpha,25(OH)(2)D(3), of these, 22 analogs are highlighted in this presentation.

Animals↗

PubMed1999

Structure and function of Fas/Fas ligand.

Fas is a member of the TNF receptor family, that contain 2-6 cysteine-rich domains (CRDs) in their extracellular regions, a single transmembrane domain and variably sized intracytoplasmic domains. Fas belongs to a subgroup of family members that have a "death domain" near the carboxy-terminal region of the molecule. This domain binds to adaptor molecules that transmit a death signal to the cell. Signal transduction is complex and involves caspases, ceramides and stress pathways. Fas ligand is biologically active as a homotrimer. Receptor binding has been localized to the C-terminus and a self-association motif to the N-terminus of the ligand extracellular domain. Expression of ligand in a functionally active form is highly regulated at the transcriptional level as well as by cleavage by metalloproteinases. Since Fas/Fas ligand delete activated cells in the peripheral immune system, defects in this pathway predispose to autoimmune disorders.

Animals↗

PubMed2004

Enterostatin and its target mechanisms during regulation of fat intake.

A high-fat diet easily promotes hyperphagia giving an impression of an uncontrolled process. Fat digestion itself however provides control of fat intake through the digestion itself, carried out by pancreatic lipase and its protein cofactor colipase, and through enterostatin, a peptide released from procolipase during fat digestion. Procolipase (-/-) knockout mice have a severely reduced fat digestion and fat uptake, pointing to a major role of the digestive process itself. With a normal fat digestion, enterostatin basically restricts fat intake by preventing the overconsumption of fat. The mechanism for enterostatin might be an inhibition of a mu-opioid-mediated pathway, demonstrated through binding studies on SK-N-MC-cells and crude brain membranes. Another target protein of enterostatin is the beta-subunit of F1F0-ATPase, displaying a distinct binding of enterostatin, established through an aqueous two-phase partition system. The binding of enterostatin to F1-ATPase was partially displaced by beta-casomorphin, a peptide stimulating fat intake and acting competitively to enterostatin. We frame a hypothesis that regulation of fat intake through enterostatin contains a reward component, which is an F1-ATPase-mediated pathway, possibly complemented with an opioidergic pathway.

Analgesics, Opioid↗

PubMed2006

Resources for integrative systems biology: from data through databases to networks and dynamic system models.

In systems biology, biologically relevant quantitative modelling of physiological processes requires the integration of experimental data from diverse sources. Recent developments in high-throughput methodologies enable the analysis of the transcriptome, proteome, interactome, metabolome and phenome on a previously unprecedented scale, thus contributing to the deluge of experimental data held in numerous public databases. In this review, we describe some of the databases and simulation tools that are relevant to systems biology and discuss a number of key issues affecting data integration and the challenges these pose to systems-level research.

Animals↗

PubMed2002

HIV-1 Tat protein and endothelium: from protein/cell interaction to AIDS-associated pathologies.

Tat protein, the transactivating factor of the human immunodeficiency virus type 1 (HIV-1), is a small cationic polypeptide that can be released from HIV-1 infected cells. Extracellular Tat elicits different biological responses in several types of target cells, including endothelial cells (ECs). In the present paper, we will review the various aspects from the laboratory bench to the bedside that characterize the tight relationship that exists between HIV-1 Tat and the endothelium. Tat interacts with at least three different types of receptors present on the surface of ECs. This leads to the activation of several signal transduction pathways and triggers various biological responses in the endothelium. The bioavailability, cell interaction, intracellular signaling, and biological activity of Tat are tightly regulated by components of the extracellular matrix and circulating molecules. Thus, Tat is at the center of a complex network of interactions that occur at the surface of ECs and that greatly affect the functions of the endothelium, possibly resulting in some of the pathological processes that occur in AIDS patients.

Acquired Immunodeficiency Syndrome↗

PubMed2002

mSprouty2 inhibits FGF10-activated MAP kinase by differentially binding to upstream target proteins.

Murine Sprouty2 (mSpry2) is a conserved ortholog of Drosophila Sprouty, a gene that inhibits several tyrosine kinase receptor pathways, resulting in net reduction of mitogen-activated protein (MAP) kinase activation. However, the precise mechanism mediating mSpry2 function as a negative regulator in tyrosine kinase growth factor pathways that regulate diverse biological functions remains incompletely characterized. Fibroblast growth factor 10 (FGF10) is a key positive regulator of lung branching morphogenesis and induces epithelial expression of mSpry2 adjacent to mesenchymal sites of FGF10. Herein, we demonstrate that FGF10 stimulation of mouse lung epithelial cells (MLE15) overexpressing mSpry2 results in both mSpry2 tyrosine phosphorylation and differential binding of mSpry2 to several key upstream target proteins in the MAP kinase-activating pathway. Thus FGF receptor (FGFR) activation results in increased association of mSpry2 with growth factor receptor-binding protein 2, suc-1-associated nuerotrophic factor target 2, and Raf but decreased binding to protein tyrosine phosphatase 2 and GTPase-activating protein 1, resulting in a net reduction of MAP kinase activation. mSpry2 also spatially translocates to the plasma membrane and intracellular membrane structures in response to FGF10 stimulation. Our data demonstrate novel intracellular mechanisms mediating mSpry2 function as a negative regulator of uncontrolled FGF-induced MAP kinase signaling.

Amino Acid Sequence↗

PubMed2001

[Activation of PKA pathway inhibits reactivity of human myeloma cell line-U266 to IL-6].

OBJECTIVE: To study the effects of PKA pathway activation on the biological function and signal transduction of IL-6 in a human myeloma cell line-U266. METHODS: The effect of IL-6 on the growth of U266 cells was shown by MTT; electrophoretic mobility shift assay (EMSA) was used to detect the activation of two transcription factors(TFs)-STAT3 and the NF-IL-6 by IL-6, which were involved in the JAK/STAT and Ras/NF-IL-6 signal transduction pathways. Then, the cells were treated with IL-6 and Forskolin (FK), an agonist of the PKA pathway. The changes in the cell growth and activation of the two TFs were exhibited by MTT and EMSA. RESULTS: (1) IL-6 could promote the proliferation of U266 cells, (2) both JAK/STAT and Ras/NF-IL-6 signal transduction pathways were activated by IL-6 in the U266 cells and (3) Cell proliferation and activation of the two IL-6 signal transduction pathways were inhibited by Forskolin; down-regulating the actiration of these two signal transduction pathways at the same time. CONCLUSION: The inhibition of cell growth, mediated by the activation of the PKA pathway, is related to the down-regulated activation of the two IL-6 signal transduction pathways.

CCAAT-Enhancer-Binding Protein-beta↗

PubMed2004

Smoking, nicotine and Parkinson's disease.

Epidemiological studies show that smoking is associated with a lower incidence of Parkinson's disease (PD). This finding is important because it could provide clues about therapeutic strategies for protection against this debilitating movement disorder. Smoke contains numerous chemicals that could be responsible for the apparent protective effect. Here, a role for nicotine is considered, because this chemical stimulates brain dopaminergic systems and provides some symptomatic benefit in PD. Nicotine also has a neuroprotective action. Putative factors and signaling pathways involved in the actions of nicotine are discussed. An understanding of the molecular basis for the reduced occurrence of PD in tobacco users is crucial for the development of intervention strategies to reduce or halt disease progression.

Animals↗

PubMed2002

Drosophila melanogaster myotropins have unique functions and signaling pathways.

Drosophila melanogaster TDVDHVFLRFamide (DMS), SDNFMRFamide, and pEVRFRQCYFNPISCF (FLT) represent three structurally distinct peptide families. Each peptide decreases heart rate albeit with different magnitudes and time-dependent responses. DMS and FLT are expressed in the crop and decrease crop motility; however, SDNFMRFamide expression and effect on the crop has not been reported. These data suggest the peptides have different physiological roles. The peptides have non-overlapping expression patterns in neural tissue, which suggests different mechanisms regulate their synthesis and release. The structures, expression patterns, and activities of the myotropins suggest they have important but different roles in biology and different signaling pathways.

Animals↗