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(A) Distribution of cell types in the glomeruli of healthy and IgAN patients. Endocapillary cells (Ecs). (B) Dot plot showing gene expression in luminal <t>mesangial</t> cells of TfR1 receptor and mTOR after scRNAseq analysis. (C) Mesangial TfR1 is overexpressed in kidneys from cIgAN patients compared to healthy control. Data were obtained by immunohistochemistry in childhood biopsies.
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(A) Distribution of cell types in the glomeruli of healthy and IgAN patients. Endocapillary cells (Ecs). (B) Dot plot showing gene expression in luminal <t>mesangial</t> cells of TfR1 receptor and mTOR after scRNAseq analysis. (C) Mesangial TfR1 is overexpressed in kidneys from cIgAN patients compared to healthy control. Data were obtained by immunohistochemistry in childhood biopsies.
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(A) Distribution of cell types in the glomeruli of healthy and IgAN patients. Endocapillary cells (Ecs). (B) Dot plot showing gene expression in luminal <t>mesangial</t> cells of TfR1 receptor and mTOR after scRNAseq analysis. (C) Mesangial TfR1 is overexpressed in kidneys from cIgAN patients compared to healthy control. Data were obtained by immunohistochemistry in childhood biopsies.
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(A) Distribution of cell types in the glomeruli of healthy and IgAN patients. Endocapillary cells (Ecs). (B) Dot plot showing gene expression in luminal <t>mesangial</t> cells of TfR1 receptor and mTOR after scRNAseq analysis. (C) Mesangial TfR1 is overexpressed in kidneys from cIgAN patients compared to healthy control. Data were obtained by immunohistochemistry in childhood biopsies.
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(A) Distribution of cell types in the glomeruli of healthy and IgAN patients. Endocapillary cells (Ecs). (B) Dot plot showing gene expression in luminal <t>mesangial</t> cells of TfR1 receptor and mTOR after scRNAseq analysis. (C) Mesangial TfR1 is overexpressed in kidneys from cIgAN patients compared to healthy control. Data were obtained by immunohistochemistry in childhood biopsies.
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Procell Inc primary human glomerular mesangial cell
( A , B ) The metabolites of glycine, serine and threonine metabolism, pyrimidine metabolism in the pIgA + si-NC and pIgA + si-GLDC groups were analyzed. ( A ) Unpaired t test, N = 3, No. 1: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0078. No. 3: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0013. No. 4: pIgA+si-GLDC/Control vs . pIgA/Control, * P = 0.0482. Error bar: mean ± SEM. ( B ) Unpaired t test, N = 3, No. 1: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0075. No. 2: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0006. No. 5: pIgA+si-GLDC/Control vs . pIgA/Control, ** P = 0.0002; pIgA+si-GLDC/Control vs. pIgA+si-NC/Control, ## P = 0.0100. Error bar: mean ± SEM. ( C , D ) Glycine, thymidine, thymine, uracil levels in the WT, G776R, K759A groups were detected by ELISA. ( C ) Unpaired t test, N = 3, G776R/NC vs . WT/NC, ** P = 0.0006; K759A/NC vs . WT/NC, ** P = 0.0017. Error bar: mean ± SEM. ( D ) Unpaired t test, N = 3, Thymidine: G776R/NC vs . WT/NC, ** P = 0.0005; K759A/NC vs . WT/NC, ** P = 0.0006. Thymine: G776R/NC vs . WT/NC, * P = 0.0200; K759A/NC vs . WT/NC, * P = 0.0141. Uracil: G776R/NC vs . WT/NC, * P = 0.0162; K759A/NC vs . WT/NC, ** P = 0.0067. Error bar: mean ± SEM. ( E , F ) SV40-MES13 cells treated with methotrexate (0.5, 1.0, 2.0 μM) were grouped into control and pIgA groups, NC and GLDC groups. Cell proliferation assay was performed. ( E ) One-way ANOVA with Tukey’s post-hoc test, N = 3, pIgA: Methotrexate 2 μM vs . Methotrexate 0 μM, ** P < 0.0001. ( F ) One-way ANOVA with Tukey’s post-hoc test, N = 3. GLDC: Methotrexate 2 μM vs . Methotrexate 0 μM, ** P < 0.0001. Error bar: mean ± SD. ( G , H ) Thymidine, thymine, uracil levels in the pIgA, pIgA + Methotrexate, GLDC, GLDC + Methotrexate groups were detected by ELISA. ( G ) Unpaired T test, N = 3, Thymine, * P = 0.0228. ( H ) Unpaired t test, N = 3, Thymine, * P = 0.0254; Thymidine, * P = 0.0303. Error bar: mean ± SEM. ( I , J ) SV40-MES13 cells were grouped into NC, GLDC, GLDC + si-CAD, GLDC + si-DHODH, pIgA + si-NC, pIgA + si-GLDC, pIgA + si-GLDC + si-CAD, pIgA + si-GLDC + si-DHODH. Cell viability assay was performed. ( I ) One-way ANOVA with Tukey’s post-hoc test, N = 3, NC vs . GLDC, ** P = 0.0059; GLDC+si-NC vs . GLDC+si-CAD, ** P = 0.0018; GLDC+si-NC vs . GLDC+si-DHODH, ** P = 0.0022. ( J ) One-way ANOVA with Tukey’s post-hoc test, N = 3, pIgA+si-NC vs . pIgA+si-GLDC, ** P = 0.0014. Error bar: mean ± SD. ( K ) The mechanism diagram of GLDC promoting pyrimidine metabolism leading to increased proliferation of <t>glomerular</t> <t>mesangial</t> cells under pIgA treatment. .
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ScienCell human mesangial cells
( A , B ) The metabolites of glycine, serine and threonine metabolism, pyrimidine metabolism in the pIgA + si-NC and pIgA + si-GLDC groups were analyzed. ( A ) Unpaired t test, N = 3, No. 1: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0078. No. 3: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0013. No. 4: pIgA+si-GLDC/Control vs . pIgA/Control, * P = 0.0482. Error bar: mean ± SEM. ( B ) Unpaired t test, N = 3, No. 1: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0075. No. 2: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0006. No. 5: pIgA+si-GLDC/Control vs . pIgA/Control, ** P = 0.0002; pIgA+si-GLDC/Control vs. pIgA+si-NC/Control, ## P = 0.0100. Error bar: mean ± SEM. ( C , D ) Glycine, thymidine, thymine, uracil levels in the WT, G776R, K759A groups were detected by ELISA. ( C ) Unpaired t test, N = 3, G776R/NC vs . WT/NC, ** P = 0.0006; K759A/NC vs . WT/NC, ** P = 0.0017. Error bar: mean ± SEM. ( D ) Unpaired t test, N = 3, Thymidine: G776R/NC vs . WT/NC, ** P = 0.0005; K759A/NC vs . WT/NC, ** P = 0.0006. Thymine: G776R/NC vs . WT/NC, * P = 0.0200; K759A/NC vs . WT/NC, * P = 0.0141. Uracil: G776R/NC vs . WT/NC, * P = 0.0162; K759A/NC vs . WT/NC, ** P = 0.0067. Error bar: mean ± SEM. ( E , F ) SV40-MES13 cells treated with methotrexate (0.5, 1.0, 2.0 μM) were grouped into control and pIgA groups, NC and GLDC groups. Cell proliferation assay was performed. ( E ) One-way ANOVA with Tukey’s post-hoc test, N = 3, pIgA: Methotrexate 2 μM vs . Methotrexate 0 μM, ** P < 0.0001. ( F ) One-way ANOVA with Tukey’s post-hoc test, N = 3. GLDC: Methotrexate 2 μM vs . Methotrexate 0 μM, ** P < 0.0001. Error bar: mean ± SD. ( G , H ) Thymidine, thymine, uracil levels in the pIgA, pIgA + Methotrexate, GLDC, GLDC + Methotrexate groups were detected by ELISA. ( G ) Unpaired T test, N = 3, Thymine, * P = 0.0228. ( H ) Unpaired t test, N = 3, Thymine, * P = 0.0254; Thymidine, * P = 0.0303. Error bar: mean ± SEM. ( I , J ) SV40-MES13 cells were grouped into NC, GLDC, GLDC + si-CAD, GLDC + si-DHODH, pIgA + si-NC, pIgA + si-GLDC, pIgA + si-GLDC + si-CAD, pIgA + si-GLDC + si-DHODH. Cell viability assay was performed. ( I ) One-way ANOVA with Tukey’s post-hoc test, N = 3, NC vs . GLDC, ** P = 0.0059; GLDC+si-NC vs . GLDC+si-CAD, ** P = 0.0018; GLDC+si-NC vs . GLDC+si-DHODH, ** P = 0.0022. ( J ) One-way ANOVA with Tukey’s post-hoc test, N = 3, pIgA+si-NC vs . pIgA+si-GLDC, ** P = 0.0014. Error bar: mean ± SD. ( K ) The mechanism diagram of GLDC promoting pyrimidine metabolism leading to increased proliferation of <t>glomerular</t> <t>mesangial</t> cells under pIgA treatment. .
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Image Search Results


(A) Distribution of cell types in the glomeruli of healthy and IgAN patients. Endocapillary cells (Ecs). (B) Dot plot showing gene expression in luminal mesangial cells of TfR1 receptor and mTOR after scRNAseq analysis. (C) Mesangial TfR1 is overexpressed in kidneys from cIgAN patients compared to healthy control. Data were obtained by immunohistochemistry in childhood biopsies.

Journal: PLOS One

Article Title: Blockade of mTOR ameliorates IgA nephropathy by correcting CD89 and CD71 dysfunctions in humanized mice

doi: 10.1371/journal.pone.0318581

Figure Lengend Snippet: (A) Distribution of cell types in the glomeruli of healthy and IgAN patients. Endocapillary cells (Ecs). (B) Dot plot showing gene expression in luminal mesangial cells of TfR1 receptor and mTOR after scRNAseq analysis. (C) Mesangial TfR1 is overexpressed in kidneys from cIgAN patients compared to healthy control. Data were obtained by immunohistochemistry in childhood biopsies.

Article Snippet: Human mesangial cells (HMCs, Innoprot # P10661 ) were obtained from healthy human kidney tissue.

Techniques: Gene Expression, Control, Immunohistochemistry

( A , B ) The metabolites of glycine, serine and threonine metabolism, pyrimidine metabolism in the pIgA + si-NC and pIgA + si-GLDC groups were analyzed. ( A ) Unpaired t test, N = 3, No. 1: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0078. No. 3: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0013. No. 4: pIgA+si-GLDC/Control vs . pIgA/Control, * P = 0.0482. Error bar: mean ± SEM. ( B ) Unpaired t test, N = 3, No. 1: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0075. No. 2: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0006. No. 5: pIgA+si-GLDC/Control vs . pIgA/Control, ** P = 0.0002; pIgA+si-GLDC/Control vs. pIgA+si-NC/Control, ## P = 0.0100. Error bar: mean ± SEM. ( C , D ) Glycine, thymidine, thymine, uracil levels in the WT, G776R, K759A groups were detected by ELISA. ( C ) Unpaired t test, N = 3, G776R/NC vs . WT/NC, ** P = 0.0006; K759A/NC vs . WT/NC, ** P = 0.0017. Error bar: mean ± SEM. ( D ) Unpaired t test, N = 3, Thymidine: G776R/NC vs . WT/NC, ** P = 0.0005; K759A/NC vs . WT/NC, ** P = 0.0006. Thymine: G776R/NC vs . WT/NC, * P = 0.0200; K759A/NC vs . WT/NC, * P = 0.0141. Uracil: G776R/NC vs . WT/NC, * P = 0.0162; K759A/NC vs . WT/NC, ** P = 0.0067. Error bar: mean ± SEM. ( E , F ) SV40-MES13 cells treated with methotrexate (0.5, 1.0, 2.0 μM) were grouped into control and pIgA groups, NC and GLDC groups. Cell proliferation assay was performed. ( E ) One-way ANOVA with Tukey’s post-hoc test, N = 3, pIgA: Methotrexate 2 μM vs . Methotrexate 0 μM, ** P < 0.0001. ( F ) One-way ANOVA with Tukey’s post-hoc test, N = 3. GLDC: Methotrexate 2 μM vs . Methotrexate 0 μM, ** P < 0.0001. Error bar: mean ± SD. ( G , H ) Thymidine, thymine, uracil levels in the pIgA, pIgA + Methotrexate, GLDC, GLDC + Methotrexate groups were detected by ELISA. ( G ) Unpaired T test, N = 3, Thymine, * P = 0.0228. ( H ) Unpaired t test, N = 3, Thymine, * P = 0.0254; Thymidine, * P = 0.0303. Error bar: mean ± SEM. ( I , J ) SV40-MES13 cells were grouped into NC, GLDC, GLDC + si-CAD, GLDC + si-DHODH, pIgA + si-NC, pIgA + si-GLDC, pIgA + si-GLDC + si-CAD, pIgA + si-GLDC + si-DHODH. Cell viability assay was performed. ( I ) One-way ANOVA with Tukey’s post-hoc test, N = 3, NC vs . GLDC, ** P = 0.0059; GLDC+si-NC vs . GLDC+si-CAD, ** P = 0.0018; GLDC+si-NC vs . GLDC+si-DHODH, ** P = 0.0022. ( J ) One-way ANOVA with Tukey’s post-hoc test, N = 3, pIgA+si-NC vs . pIgA+si-GLDC, ** P = 0.0014. Error bar: mean ± SD. ( K ) The mechanism diagram of GLDC promoting pyrimidine metabolism leading to increased proliferation of glomerular mesangial cells under pIgA treatment. .

Journal: EMBO Molecular Medicine

Article Title: Glycine decarboxylase advances IgA nephropathy by boosting mesangial cell proliferation through the pyrimidine pathway

doi: 10.1038/s44321-025-00315-2

Figure Lengend Snippet: ( A , B ) The metabolites of glycine, serine and threonine metabolism, pyrimidine metabolism in the pIgA + si-NC and pIgA + si-GLDC groups were analyzed. ( A ) Unpaired t test, N = 3, No. 1: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0078. No. 3: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0013. No. 4: pIgA+si-GLDC/Control vs . pIgA/Control, * P = 0.0482. Error bar: mean ± SEM. ( B ) Unpaired t test, N = 3, No. 1: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0075. No. 2: pIgA+si-GLDC/Control vs . pIgA+si-NC/Control, ## P = 0.0006. No. 5: pIgA+si-GLDC/Control vs . pIgA/Control, ** P = 0.0002; pIgA+si-GLDC/Control vs. pIgA+si-NC/Control, ## P = 0.0100. Error bar: mean ± SEM. ( C , D ) Glycine, thymidine, thymine, uracil levels in the WT, G776R, K759A groups were detected by ELISA. ( C ) Unpaired t test, N = 3, G776R/NC vs . WT/NC, ** P = 0.0006; K759A/NC vs . WT/NC, ** P = 0.0017. Error bar: mean ± SEM. ( D ) Unpaired t test, N = 3, Thymidine: G776R/NC vs . WT/NC, ** P = 0.0005; K759A/NC vs . WT/NC, ** P = 0.0006. Thymine: G776R/NC vs . WT/NC, * P = 0.0200; K759A/NC vs . WT/NC, * P = 0.0141. Uracil: G776R/NC vs . WT/NC, * P = 0.0162; K759A/NC vs . WT/NC, ** P = 0.0067. Error bar: mean ± SEM. ( E , F ) SV40-MES13 cells treated with methotrexate (0.5, 1.0, 2.0 μM) were grouped into control and pIgA groups, NC and GLDC groups. Cell proliferation assay was performed. ( E ) One-way ANOVA with Tukey’s post-hoc test, N = 3, pIgA: Methotrexate 2 μM vs . Methotrexate 0 μM, ** P < 0.0001. ( F ) One-way ANOVA with Tukey’s post-hoc test, N = 3. GLDC: Methotrexate 2 μM vs . Methotrexate 0 μM, ** P < 0.0001. Error bar: mean ± SD. ( G , H ) Thymidine, thymine, uracil levels in the pIgA, pIgA + Methotrexate, GLDC, GLDC + Methotrexate groups were detected by ELISA. ( G ) Unpaired T test, N = 3, Thymine, * P = 0.0228. ( H ) Unpaired t test, N = 3, Thymine, * P = 0.0254; Thymidine, * P = 0.0303. Error bar: mean ± SEM. ( I , J ) SV40-MES13 cells were grouped into NC, GLDC, GLDC + si-CAD, GLDC + si-DHODH, pIgA + si-NC, pIgA + si-GLDC, pIgA + si-GLDC + si-CAD, pIgA + si-GLDC + si-DHODH. Cell viability assay was performed. ( I ) One-way ANOVA with Tukey’s post-hoc test, N = 3, NC vs . GLDC, ** P = 0.0059; GLDC+si-NC vs . GLDC+si-CAD, ** P = 0.0018; GLDC+si-NC vs . GLDC+si-DHODH, ** P = 0.0022. ( J ) One-way ANOVA with Tukey’s post-hoc test, N = 3, pIgA+si-NC vs . pIgA+si-GLDC, ** P = 0.0014. Error bar: mean ± SD. ( K ) The mechanism diagram of GLDC promoting pyrimidine metabolism leading to increased proliferation of glomerular mesangial cells under pIgA treatment. .

Article Snippet: Primary human glomerular mesangial cell ( H. sapiens ) , Procell Life Science & Technology , CP-H067.

Techniques: Control, Enzyme-linked Immunosorbent Assay, Proliferation Assay, Viability Assay

This upregulation of GLDC modulates the glycolytic pathway through pyrimidine metabolism, thereby promoting the proliferation of glomerular mesangial cells. Concurrently, the secretions from glomerular mesangial cells, such as C3, TGF-β1, and MCP-1, are increased. These secreted factors contribute to enhanced inflammatory responses, recruitment of macrophages, and fibrotic reactions in the surrounding interstitium.

Journal: EMBO Molecular Medicine

Article Title: Glycine decarboxylase advances IgA nephropathy by boosting mesangial cell proliferation through the pyrimidine pathway

doi: 10.1038/s44321-025-00315-2

Figure Lengend Snippet: This upregulation of GLDC modulates the glycolytic pathway through pyrimidine metabolism, thereby promoting the proliferation of glomerular mesangial cells. Concurrently, the secretions from glomerular mesangial cells, such as C3, TGF-β1, and MCP-1, are increased. These secreted factors contribute to enhanced inflammatory responses, recruitment of macrophages, and fibrotic reactions in the surrounding interstitium.

Article Snippet: Primary human glomerular mesangial cell ( H. sapiens ) , Procell Life Science & Technology , CP-H067.

Techniques: