Q3139752 (Q3139752): Difference between revisions
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(Created claim: summary (P836): Extracapillary glomerulonephritis (GNE) is the most serious form of kidney injury with morphological manifestations of glomerular lesion in the form of “semilunas” (multilayer accumulations of cells) leading to the deterioration in renal function within weeks. Infiltrating macrophages have been classically described as the potential origin of cellular semimoons. But studies currently place the parietal epithelial cells of the Bowman capsule (PEC...) |
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Extracapillary glomerulonephritis (GNE) is the most serious form of kidney injury with morphological manifestations of glomerular lesion in the form of “semilunas” (multilayer accumulations of cells) leading to the deterioration in renal function within weeks. Infiltrating macrophages have been classically described as the potential origin of cellular semimoons. But studies currently place the parietal epithelial cells of the Bowman capsule (PECs) as the overwhelmingly predominant cell type. Thus, macrophages would participate in glomerular inflammation and PECS are the origin of semiluna and extracappilarity, although signaling pathways that activate their proliferation are not fully understood. Based on preliminary in vitro data obtained in our laboratory, we hypothesised that PECs express tM-CSF and their receptor and that this fact is key in their own proliferation and consequently in the pathogenesis of NGs. With this project, we will decipher the signaling pathway of the M-CSF and its receiver in the activation and proliferation of human PECs in cultivation. We will determine the role of the M-CSF/M-CSF_R system in the expansion of PECS in the pathogenesis of the experimental GE murine model and correlate the serum levels of M-CSF with the glomerular expression of M-CSR-R in different types of human glomerular disease in biopsies from our Biobank at Bellvitge Hospital. If confirmed, we could design therapeutic strategies against SGPs to reduce the severity of the lesion and improve its prognosis. (English) | |||||||||||||||
Property / summary: Extracapillary glomerulonephritis (GNE) is the most serious form of kidney injury with morphological manifestations of glomerular lesion in the form of “semilunas” (multilayer accumulations of cells) leading to the deterioration in renal function within weeks. Infiltrating macrophages have been classically described as the potential origin of cellular semimoons. But studies currently place the parietal epithelial cells of the Bowman capsule (PECs) as the overwhelmingly predominant cell type. Thus, macrophages would participate in glomerular inflammation and PECS are the origin of semiluna and extracappilarity, although signaling pathways that activate their proliferation are not fully understood. Based on preliminary in vitro data obtained in our laboratory, we hypothesised that PECs express tM-CSF and their receptor and that this fact is key in their own proliferation and consequently in the pathogenesis of NGs. With this project, we will decipher the signaling pathway of the M-CSF and its receiver in the activation and proliferation of human PECs in cultivation. We will determine the role of the M-CSF/M-CSF_R system in the expansion of PECS in the pathogenesis of the experimental GE murine model and correlate the serum levels of M-CSF with the glomerular expression of M-CSR-R in different types of human glomerular disease in biopsies from our Biobank at Bellvitge Hospital. If confirmed, we could design therapeutic strategies against SGPs to reduce the severity of the lesion and improve its prognosis. (English) / rank | |||||||||||||||
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Property / summary: Extracapillary glomerulonephritis (GNE) is the most serious form of kidney injury with morphological manifestations of glomerular lesion in the form of “semilunas” (multilayer accumulations of cells) leading to the deterioration in renal function within weeks. Infiltrating macrophages have been classically described as the potential origin of cellular semimoons. But studies currently place the parietal epithelial cells of the Bowman capsule (PECs) as the overwhelmingly predominant cell type. Thus, macrophages would participate in glomerular inflammation and PECS are the origin of semiluna and extracappilarity, although signaling pathways that activate their proliferation are not fully understood. Based on preliminary in vitro data obtained in our laboratory, we hypothesised that PECs express tM-CSF and their receptor and that this fact is key in their own proliferation and consequently in the pathogenesis of NGs. With this project, we will decipher the signaling pathway of the M-CSF and its receiver in the activation and proliferation of human PECs in cultivation. We will determine the role of the M-CSF/M-CSF_R system in the expansion of PECS in the pathogenesis of the experimental GE murine model and correlate the serum levels of M-CSF with the glomerular expression of M-CSR-R in different types of human glomerular disease in biopsies from our Biobank at Bellvitge Hospital. If confirmed, we could design therapeutic strategies against SGPs to reduce the severity of the lesion and improve its prognosis. (English) / qualifier | |||||||||||||||
point in time: 12 October 2021
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Revision as of 13:01, 12 October 2021
Project Q3139752 in Spain
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English | No label defined |
Project Q3139752 in Spain |
Statements
43,500.0 Euro
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87,000.0 Euro
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50.0 percent
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1 January 2018
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31 March 2021
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INSTITUTO DE INVESTIGACION BIOMEDICA DE BELLVITGE
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08101
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La glomerulonefritis extracapilar (GNE) es la forma más grave de lesión renal con manifestaciones morfológicas de lesión glomerular en forma de “semilunas” (acumulaciones en multicapa de células) que conllevan al deterioro en semanas de la función renal. Los macrófagos infiltrantes han sido clásicamente descritos como el origen potencial de las semilunas celulares. Pero, actualmente los estudios sitúan a las células epiteliales parietales de la cápsula de Bowman (PECs) como el tipo celular abrumadoramente predominante. Así, los macrófagos participarían en la inflamación glomerular y las PECS son originarían la semiluna y la extracapilaridad, aunque las vías de señalización que activan su proliferación no se entienden completamente. En base a datos preliminares in vitro obtenidos en nuestro laboratorio, hipotetizamos que las PECs expresan tM-CSF y su receptor y que este hecho es clave en su propia proliferación y consecuentemente en la patogenia de las GNE. Con este proyecto, descifraremos la vía de señalización del M-CSF y de su receptor en la activación y proliferación de las PECs humanas en cultivo. Determinaremos papel del sistema M-CSF /M-CSF_R en la expansión de las PECS en la patogenia de modelo experimental murino de GE y correlacionaremos los niveles séricos de M-CSF con la expresión glomerular de M-CSR-R en diferentes tipos de enfermedad glomerular humanas en biopsias procedentes de nuestro Biobanco en el Hospital de Bellvitge. De confirmarse, podríamos diseñar estrategias terapéuticas frente a las PECs para reducir la gravedad de la lesión y mejorar su pronóstico. (Spanish)
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Extracapillary glomerulonephritis (GNE) is the most serious form of kidney injury with morphological manifestations of glomerular lesion in the form of “semilunas” (multilayer accumulations of cells) leading to the deterioration in renal function within weeks. Infiltrating macrophages have been classically described as the potential origin of cellular semimoons. But studies currently place the parietal epithelial cells of the Bowman capsule (PECs) as the overwhelmingly predominant cell type. Thus, macrophages would participate in glomerular inflammation and PECS are the origin of semiluna and extracappilarity, although signaling pathways that activate their proliferation are not fully understood. Based on preliminary in vitro data obtained in our laboratory, we hypothesised that PECs express tM-CSF and their receptor and that this fact is key in their own proliferation and consequently in the pathogenesis of NGs. With this project, we will decipher the signaling pathway of the M-CSF and its receiver in the activation and proliferation of human PECs in cultivation. We will determine the role of the M-CSF/M-CSF_R system in the expansion of PECS in the pathogenesis of the experimental GE murine model and correlate the serum levels of M-CSF with the glomerular expression of M-CSR-R in different types of human glomerular disease in biopsies from our Biobank at Bellvitge Hospital. If confirmed, we could design therapeutic strategies against SGPs to reduce the severity of the lesion and improve its prognosis. (English)
12 October 2021
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Hospitalet de Llobregat, L'
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Identifiers
PI17_01411
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