CONTROL OF INFLAMMATORY PROCESSES BY CERAMID 1-PHOSPHATE. INVOLVEMENT IN ATEROGENESIS AND ADIPOGENESIS (Q3151089): Difference between revisions

From EU Knowledge Graph
Jump to navigation Jump to search
(‎Changed label, description and/or aliases in en: translated_label)
(‎Removed claim: summary (P836): CERAMID 1-PHOSPHATE (C1P) IS A BIOACTIVE PHOSPHORUSPHYLICIDE THAT REGULATES VITAL CELLULAR FUNCTIONS. IT IS MITOGENIC, ANTIAPOPTOTIC, PRO-INFLAMMATORY AND INDUCES CELLULAR MIGRATION. PRECISELY, THESE FUNCTIONS HAVE BEEN ASSOCIATED WITH ATEROGENICAL AND ADIPOGENICAL RESPONSES, ESPECIALLY WHEN THESE PROCESSES OCCUR IN MACROPHAGES AND ADIPOCYTES. HOWEVER, THE MOLECULAR MECHANISMS BY WHICH C1P CARRIES OUT ITS ACTIONS ARE NOT CLEAR. MACROPHAGES PLA...)
Property / summary
CERAMID 1-PHOSPHATE (C1P) IS A BIOACTIVE PHOSPHORUSPHYLICIDE THAT REGULATES VITAL CELLULAR FUNCTIONS. IT IS MITOGENIC, ANTIAPOPTOTIC, PRO-INFLAMMATORY AND INDUCES CELLULAR MIGRATION. PRECISELY, THESE FUNCTIONS HAVE BEEN ASSOCIATED WITH ATEROGENICAL AND ADIPOGENICAL RESPONSES, ESPECIALLY WHEN THESE PROCESSES OCCUR IN MACROPHAGES AND ADIPOCYTES. HOWEVER, THE MOLECULAR MECHANISMS BY WHICH C1P CARRIES OUT ITS ACTIONS ARE NOT CLEAR. MACROPHAGES PLAY A CRUCIAL ROLE IN THE IMMUNE RESPONSE AND HAVE BEEN DESCRIBED AS THE MOST IMPORTANT CELLS IN THE ONSET AND PROGRESS OF ATHEROSCLEROSIS. OBESITY IS KNOWN TO BE ONE OF THE MOST IMPORTANT RISK FACTORS TO PROMOTE ATEROGENESIS AND THAT INFLAMMATORY PROCESSES ARE THE MAIN CONNECTION BETWEEN OBESITY AND ATHEROSCLEROSIS. HIGH LEVELS OF PRO-INFLAMMATORY CYTOKINES PREVAIL IN BOTH ATHEROSCLEROSIS AND OBESITY. IT IS KNOWN THAT CERAMIDS, WHICH ARE THE PRECURSORS OF C1P, ARE INVOLVED IN VASCULAR LESIONS THROUGH MECHANISMS THAT INTERFERE WITH CELL PROLIFERATION, CELL SURVIVAL AND INFLAMMATORY PROCESSES. IT HAS RECENTLY BEEN POSTULATED THAT THE ENZYME PHOSPHATIDILETHANOLAMINE METHYL TRANSFERASE (PEMT), WHICH CATALYSES THE CONVERSION OF PHOSPHATIDYLETHANOLAMINE TO PHOSPHATIDYLCHOLINE, IS POSITIVELY ASSOCIATED WITH OBESITY INDUCED BY HIGH-FAT DIETS, AND WITH ATHEROSCLEROSIS. IN ADDITION, ANIMALS LACKING THE PEMT GENE ARE PROTECTED AGAINST WEIGHT GAIN AND DEVELOPMENT OF CARDIOVASCULAR DISEASE. OUR PRELIMINARY RESULTS INDICATE THAT IN ADIPOSE TISSUE IN MICE LACKING THE PEMT GENE, THE LEVELS OF CERAMIDE KINASE (CERK), AN ENZYME THAT CATALYSES THE SYNTHESIS OF C1P IN MAMMALS, ARE MUCH LOWER THAN THOSE OF NORMAL MICE. This suggests that CERK as C1P are a remote FACTOR in the INFLAMATOR ASSOCIATE TO Aterogenesis AND ADIPOGENESIS._x000D_ The present research project has been set up with the end of elucidateing some of the mechanisms involved in the proceedings common INFLAMATORIES TO Aterogenesis and Adipogenesis with the End of Stabilising New Therapeutic STRATEGIES against ATEROSCLEROSIS and OBESITY. In order to consecrate this project, the following tasks have been established:_x000D_ Determining some of the mechanisms that have been implemented in the status of the C1P MIGRATION AND CLULAR SUPERVIVENCE: In particular, the FUNCTIONS that disempress the METALOPROTEINS OF CELL MATRIZ (MMPS) and RUTA JAK/STAT in the CELL MIGRATION AND IMPLICATION OF THE TRANSCRIPCIONAL FACTOR FKHRL1 AND YOUR INTRACULAR DIANAS IN THE CELULAR SUPERVIVENCE._x000D_ DETERMINAR DETERMINATE if CERK and C1P play an important role in the ADIPOGENESIS._x000D_ STUDY THE IMPLEMENTATION OF CERK/C1P IN THE REGULATION OF THE LEVEL OF CITOQUINAS PRO AND ANTIINFLAMATORIAS._x000D_ Determining PEMT’s paddle in flammable processes in macrophages and additives: SPECIFICALLY, IT WILL BE DETERMINED WHETHER PEMT IS NECESSARY FOR THE MIGRATION OF MACROPHAGES AND PRE-ADIPOCYTES. It will also be examined whether the STIMULE OF THE CELL MIGRATION REQUIRES PEMT PARTICIPATION AND DETERMINATION Whether antisense oligonucleotides SPECIFIC OF PEMT may counteract the proinflammatory effects of PEMT._x000D_ Whether the proposed STUDIES PROPOSES PROPERTY CONTROL on the C1P CELULAR SYNALISM MECHANISMS that may be introduced into the treatment of atherosclerosis and obsessity. (English)
 
Property / summary: CERAMID 1-PHOSPHATE (C1P) IS A BIOACTIVE PHOSPHORUSPHYLICIDE THAT REGULATES VITAL CELLULAR FUNCTIONS. IT IS MITOGENIC, ANTIAPOPTOTIC, PRO-INFLAMMATORY AND INDUCES CELLULAR MIGRATION. PRECISELY, THESE FUNCTIONS HAVE BEEN ASSOCIATED WITH ATEROGENICAL AND ADIPOGENICAL RESPONSES, ESPECIALLY WHEN THESE PROCESSES OCCUR IN MACROPHAGES AND ADIPOCYTES. HOWEVER, THE MOLECULAR MECHANISMS BY WHICH C1P CARRIES OUT ITS ACTIONS ARE NOT CLEAR. MACROPHAGES PLAY A CRUCIAL ROLE IN THE IMMUNE RESPONSE AND HAVE BEEN DESCRIBED AS THE MOST IMPORTANT CELLS IN THE ONSET AND PROGRESS OF ATHEROSCLEROSIS. OBESITY IS KNOWN TO BE ONE OF THE MOST IMPORTANT RISK FACTORS TO PROMOTE ATEROGENESIS AND THAT INFLAMMATORY PROCESSES ARE THE MAIN CONNECTION BETWEEN OBESITY AND ATHEROSCLEROSIS. HIGH LEVELS OF PRO-INFLAMMATORY CYTOKINES PREVAIL IN BOTH ATHEROSCLEROSIS AND OBESITY. IT IS KNOWN THAT CERAMIDS, WHICH ARE THE PRECURSORS OF C1P, ARE INVOLVED IN VASCULAR LESIONS THROUGH MECHANISMS THAT INTERFERE WITH CELL PROLIFERATION, CELL SURVIVAL AND INFLAMMATORY PROCESSES. IT HAS RECENTLY BEEN POSTULATED THAT THE ENZYME PHOSPHATIDILETHANOLAMINE METHYL TRANSFERASE (PEMT), WHICH CATALYSES THE CONVERSION OF PHOSPHATIDYLETHANOLAMINE TO PHOSPHATIDYLCHOLINE, IS POSITIVELY ASSOCIATED WITH OBESITY INDUCED BY HIGH-FAT DIETS, AND WITH ATHEROSCLEROSIS. IN ADDITION, ANIMALS LACKING THE PEMT GENE ARE PROTECTED AGAINST WEIGHT GAIN AND DEVELOPMENT OF CARDIOVASCULAR DISEASE. OUR PRELIMINARY RESULTS INDICATE THAT IN ADIPOSE TISSUE IN MICE LACKING THE PEMT GENE, THE LEVELS OF CERAMIDE KINASE (CERK), AN ENZYME THAT CATALYSES THE SYNTHESIS OF C1P IN MAMMALS, ARE MUCH LOWER THAN THOSE OF NORMAL MICE. This suggests that CERK as C1P are a remote FACTOR in the INFLAMATOR ASSOCIATE TO Aterogenesis AND ADIPOGENESIS._x000D_ The present research project has been set up with the end of elucidateing some of the mechanisms involved in the proceedings common INFLAMATORIES TO Aterogenesis and Adipogenesis with the End of Stabilising New Therapeutic STRATEGIES against ATEROSCLEROSIS and OBESITY. In order to consecrate this project, the following tasks have been established:_x000D_ Determining some of the mechanisms that have been implemented in the status of the C1P MIGRATION AND CLULAR SUPERVIVENCE: In particular, the FUNCTIONS that disempress the METALOPROTEINS OF CELL MATRIZ (MMPS) and RUTA JAK/STAT in the CELL MIGRATION AND IMPLICATION OF THE TRANSCRIPCIONAL FACTOR FKHRL1 AND YOUR INTRACULAR DIANAS IN THE CELULAR SUPERVIVENCE._x000D_ DETERMINAR DETERMINATE if CERK and C1P play an important role in the ADIPOGENESIS._x000D_ STUDY THE IMPLEMENTATION OF CERK/C1P IN THE REGULATION OF THE LEVEL OF CITOQUINAS PRO AND ANTIINFLAMATORIAS._x000D_ Determining PEMT’s paddle in flammable processes in macrophages and additives: SPECIFICALLY, IT WILL BE DETERMINED WHETHER PEMT IS NECESSARY FOR THE MIGRATION OF MACROPHAGES AND PRE-ADIPOCYTES. It will also be examined whether the STIMULE OF THE CELL MIGRATION REQUIRES PEMT PARTICIPATION AND DETERMINATION Whether antisense oligonucleotides SPECIFIC OF PEMT may counteract the proinflammatory effects of PEMT._x000D_ Whether the proposed STUDIES PROPOSES PROPERTY CONTROL on the C1P CELULAR SYNALISM MECHANISMS that may be introduced into the treatment of atherosclerosis and obsessity. (English) / rank
Normal rank
 
Property / summary: CERAMID 1-PHOSPHATE (C1P) IS A BIOACTIVE PHOSPHORUSPHYLICIDE THAT REGULATES VITAL CELLULAR FUNCTIONS. IT IS MITOGENIC, ANTIAPOPTOTIC, PRO-INFLAMMATORY AND INDUCES CELLULAR MIGRATION. PRECISELY, THESE FUNCTIONS HAVE BEEN ASSOCIATED WITH ATEROGENICAL AND ADIPOGENICAL RESPONSES, ESPECIALLY WHEN THESE PROCESSES OCCUR IN MACROPHAGES AND ADIPOCYTES. HOWEVER, THE MOLECULAR MECHANISMS BY WHICH C1P CARRIES OUT ITS ACTIONS ARE NOT CLEAR. MACROPHAGES PLAY A CRUCIAL ROLE IN THE IMMUNE RESPONSE AND HAVE BEEN DESCRIBED AS THE MOST IMPORTANT CELLS IN THE ONSET AND PROGRESS OF ATHEROSCLEROSIS. OBESITY IS KNOWN TO BE ONE OF THE MOST IMPORTANT RISK FACTORS TO PROMOTE ATEROGENESIS AND THAT INFLAMMATORY PROCESSES ARE THE MAIN CONNECTION BETWEEN OBESITY AND ATHEROSCLEROSIS. HIGH LEVELS OF PRO-INFLAMMATORY CYTOKINES PREVAIL IN BOTH ATHEROSCLEROSIS AND OBESITY. IT IS KNOWN THAT CERAMIDS, WHICH ARE THE PRECURSORS OF C1P, ARE INVOLVED IN VASCULAR LESIONS THROUGH MECHANISMS THAT INTERFERE WITH CELL PROLIFERATION, CELL SURVIVAL AND INFLAMMATORY PROCESSES. IT HAS RECENTLY BEEN POSTULATED THAT THE ENZYME PHOSPHATIDILETHANOLAMINE METHYL TRANSFERASE (PEMT), WHICH CATALYSES THE CONVERSION OF PHOSPHATIDYLETHANOLAMINE TO PHOSPHATIDYLCHOLINE, IS POSITIVELY ASSOCIATED WITH OBESITY INDUCED BY HIGH-FAT DIETS, AND WITH ATHEROSCLEROSIS. IN ADDITION, ANIMALS LACKING THE PEMT GENE ARE PROTECTED AGAINST WEIGHT GAIN AND DEVELOPMENT OF CARDIOVASCULAR DISEASE. OUR PRELIMINARY RESULTS INDICATE THAT IN ADIPOSE TISSUE IN MICE LACKING THE PEMT GENE, THE LEVELS OF CERAMIDE KINASE (CERK), AN ENZYME THAT CATALYSES THE SYNTHESIS OF C1P IN MAMMALS, ARE MUCH LOWER THAN THOSE OF NORMAL MICE. This suggests that CERK as C1P are a remote FACTOR in the INFLAMATOR ASSOCIATE TO Aterogenesis AND ADIPOGENESIS._x000D_ The present research project has been set up with the end of elucidateing some of the mechanisms involved in the proceedings common INFLAMATORIES TO Aterogenesis and Adipogenesis with the End of Stabilising New Therapeutic STRATEGIES against ATEROSCLEROSIS and OBESITY. In order to consecrate this project, the following tasks have been established:_x000D_ Determining some of the mechanisms that have been implemented in the status of the C1P MIGRATION AND CLULAR SUPERVIVENCE: In particular, the FUNCTIONS that disempress the METALOPROTEINS OF CELL MATRIZ (MMPS) and RUTA JAK/STAT in the CELL MIGRATION AND IMPLICATION OF THE TRANSCRIPCIONAL FACTOR FKHRL1 AND YOUR INTRACULAR DIANAS IN THE CELULAR SUPERVIVENCE._x000D_ DETERMINAR DETERMINATE if CERK and C1P play an important role in the ADIPOGENESIS._x000D_ STUDY THE IMPLEMENTATION OF CERK/C1P IN THE REGULATION OF THE LEVEL OF CITOQUINAS PRO AND ANTIINFLAMATORIAS._x000D_ Determining PEMT’s paddle in flammable processes in macrophages and additives: SPECIFICALLY, IT WILL BE DETERMINED WHETHER PEMT IS NECESSARY FOR THE MIGRATION OF MACROPHAGES AND PRE-ADIPOCYTES. It will also be examined whether the STIMULE OF THE CELL MIGRATION REQUIRES PEMT PARTICIPATION AND DETERMINATION Whether antisense oligonucleotides SPECIFIC OF PEMT may counteract the proinflammatory effects of PEMT._x000D_ Whether the proposed STUDIES PROPOSES PROPERTY CONTROL on the C1P CELULAR SYNALISM MECHANISMS that may be introduced into the treatment of atherosclerosis and obsessity. (English) / qualifier
point in time: 12 October 2021
Timestamp+2021-10-12T00:00:00Z
Timezone+00:00
CalendarGregorian
Precision1 day
Before0
After0
 

Revision as of 15:40, 12 October 2021

Project Q3151089 in Spain
Language Label Description Also known as
English
CONTROL OF INFLAMMATORY PROCESSES BY CERAMID 1-PHOSPHATE. INVOLVEMENT IN ATEROGENESIS AND ADIPOGENESIS
Project Q3151089 in Spain

    Statements

    contained in NUTS
    Biscay
    0 references
    country
    Spain
    0 references
    EU contribution
    72,600.0 Euro
    0 references
    budget
    145,200.0 Euro
    0 references
    co-financing rate
    50.0 percent
    0 references
    start time
    30 December 2016
    0 references
    end time
    31 December 2020
    0 references
    beneficiary name (string)
    UNIVERSIDAD DEL PAIS VASCO/EUSKAL HERRIKO UNIBERTSITATEA
    0 references
    beneficiary
    Q3134714
    0 references
    coordinate location

    43°19'37.56"N, 2°59'4.60"W
    0 references
    postal code
    48054
    0 references
    summary
    EL CERAMIDO 1-FOSFATO (C1P) ES UN FOSFOESFINGOLIPIDO BIOACTIVO QUE REGULA FUNCIONES CELULARES VITALES. ES MITOGENICO, ANTIAPOPTOTICO, PROINFLAMATORIO E INDUCE LA MIGRACION CELULAR. PRECISAMENTE, ESTAS FUNCIONES SE HAN ASOCIADO A RESPUESTAS ATEROGENICAS Y ADIPOGENICAS, SOBRE TODO CUANDO ESTOS PROCESOS OCURREN EN MACROFAGOS Y ADIPOCITOS. SIN EMBARGO, LOS MECANISMOS MOLECULARES POR LOS CUALES EL C1P LLEVA A CABO SUS ACCIONES NO ESTAN CLAROS. LOS MACROFAGOS JUEGAN UN PAPEL CRUCIAL EN LA RESPUESTA INMUNITARIA Y SE HAN DESCRITO COMO LAS CELULAS MAS IMPORTANTES EN EL INICIO Y PROGRESO DE LA ATEROSCLEROSIS. SE SABE QUE LA OBESIDAD ES UNO DE LOS FACTORES DE RIESGO MAS IMPORTANTES PARA PROMOVER LA ATEROGENESIS Y QUE LOS PROCESOS INFLAMATORIOS SON LA CONEXION PRINCIPAL ENTRE OBESIDAD Y ATEROSCLEROSIS. TANTO EN LA ATEROSCLEROSIS COMO EN LA OBESIDAD PREVALECEN ELEVADOS LOS NIVELES DE CITOQUINAS PROINFLAMATORIAS. SE SABE QUE LOS CERAMIDOS, QUE SON LOS PRECURSORES DE C1P, ESTAN IMPLICADOS EN LAS LESIONES VASCULARES MEDIANTE MECANISMOS QUE INTERFIEREN CON LA PROLIFERACION CELULAR, LA SUPERVIVIENCIA CELULAR Y LOS PROCESOS INFLAMATORIOS. RECIENTEMENTE SE HA POSTULADO QUE EL ENZIMA FOSFATIDILETANOLAMINA METIL TRANSFERASA (PEMT), EL CUAL CATALIZA LA CONVERSION DE FOSFATIDILETANOLAMINA EN FOSFATIDILCOLINA, ESTA POSITIVAMENTE ASOCIADO A LA OBESIDAD INDUCIDA POR DIETAS DE CONTENIDO GRASO ELEVADO, Y CON LA ATEROSCLEROSIS. ADEMAS, ANIMALES CARENTES DEL GEN PEMT ESTAN PROTEGIDOS CONTRA LA GANANCIA DE PESO Y EL DESARROLLO DE ENFERMEDAD CARDIOVASCULAR. NUESTROS RESULTADOS PRELIMINARES INDICAN QUE EN EL TEJIDO ADIPOSO DE RATONES CARENTES DEL GEN PEMT LOS NIVELES DE CERAMIDA QUINASA (CERK), ENZIMA QUE CATALIZA LA SINTESIS DE C1P EN MAMIFEROS, SON MUCHO MENORES QUE LOS DE RATONES NORMALES. ESTO SUGIERE QUE TANTO LA CERK COMO EL C1P SON UN FACTOR RELEVANTE EN LAS RESPUESTAS INFLAMATORIAS ASOCIADAS A LA ATEROGENESIS Y LA ADIPOGENESIS._x000D_ EL PRESENTE PROYECTO DE INVESTIGACION SE HA ESTABLECIDO CON EL FIN DE ELUCIDAR ALGUNOS DE LOS MECANISMOS IMPLICADOS EN LOS PROCESOS INFLAMATORIOS COMUNES A LA ATEROGENESIS Y LA ADIPOGENESIS CON EL FIN DE ESTABLECER NUEVAS ESTRATEGIAS TERAPEUTICAS CONTRA LA ATEROSCLEROSIS Y LA OBESIDAD. PARA CONSEGUIR ESTE PROPOSITO, SE HAN ESTABLECIDO LOS SIGUIENTES OBJETIVOS:_x000D_ DETERMINAR ALGUNOS DE LOS MECANISMOS IMPLICADOS EN LA ESTIMULACION DE LA MIGRACION Y SUPERVIVENCIA CELULAR POR C1P: CONCRETAMENTE SE ESTUDIARAN LAS FUNCIONES QUE DESEMPEÑAN LAS METALOPROTEINASAS DE LA MATRIZ CELULAR (MMPS) Y DE LA RUTA JAK/STAT EN LA MIGRACION CELULAR Y LA IMPLICACION DEL FACTOR TRANSCRIPCIONAL FKHRL1 Y SUS DIANAS INTRACELULARES EN LA SUPERVIVENCIA CELULAR._x000D_ DETERMINAR SI CERK Y C1P JUEGAN UN PAPEL IMPORTANTE EN LA ADIPOGENESIS._x000D_ ESTUDIAR LA IMPLICACION DE CERK/C1P EN LA REGULACION DE LOS NIVELES DE CITOQUINAS PRO Y ANTIINFLAMATORIAS._x000D_ DETERMINAR EL PAPEL DE LA PEMT EN PROCESOS INFLAMATORIOS EN MACROFAGOS Y ADIPOCITOS: CONCRETAMENTE SE DETERMINARA SI LA PEMT ES NECESARIA PARA LA MIGRACION DE MACROFAGOS Y PRE-ADIPOCITOS. ASIMISMO, SE EXAMINARA SI LA ESTIMULACION DE LA MIGRACION CELULAR REQUIERE LA PARTICIPACION DE PEMT Y SE DETERMINARA SI OLIGONUCLEOTIDOS ANTISENTIDO ESPECIFICOS DE PEMT PUEDEN CONTRARRESTAR LOS EFECTOS PROINFLAMATORIOS DE LA PEMT._x000D_ SE ESPERA QUE LOS ESTUDIOS PROPUESTOS PROPORCIONEN RESULTADOS SIGNIFICATIVOS SOBRE LOS MECANISMOS DE SEÑALIZACION CELULAR DEL C1P QUE PUEDAN POSTERIORMENTE INCIDIR EN EL TRATAMIENTO DE LA ATEROSCLEROSIS Y LA OBESIDAD. (Spanish)
    0 references
    location (string)
    Leioa
    0 references

    Identifiers

    Spanish Kohesio ID
    SAF2016-79695-R
    0 references
     
    Retrieved from "https://linkedopendata.eu/w/index.php?title=Item:Q3151089&oldid=12814623"