Intestine Cell

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Stefan Offermanns - One of the best experts on this subject based on the ideXlab platform.

  • adhesion receptor adgrg2 gpr64 is in the gi tract selectively expressed in mature intestinal tuft Cells
    Molecular metabolism, 2021
    Co-Authors: Kaare V. Grunddal, Sarah Tonack, Kristoffer L. Egerod, Jonathan James Thompson, Natalia Petersen, Maja S. Engelstoft, Constance Vagne, Céline Keime, Gérard Gradwohl, Stefan Offermanns
    Abstract:

    Abstract Objective GPR64/ADGRG2 is an orphan Adhesion G protein-coupled receptor (ADGR) known to be mainly expressed in the parathyroid gland and epididymis. This investigation aimed to delineate the Cellular expression of GPR64 throughout the body with focus on the gastrointestinal (GI) tract. Methods Transgenic Gpr64mCherry reporter mice were histologically examined throughout the body and reporter protein expression in intestinal tuft Cells was confirmed by specific Cell ablation. The GPCR repertoire of intestinal Gpr64mCherry-positive tuft Cells was analyzed by quantitative RT-PCR analysis and in situ hybridization. The Gpr64mCherry was crossed into the general tuft Cell reporter Trpm5GFP to generate small intestinal organoids for time-lapse imaging. Intestinal tuft Cells were isolated from small Intestine, FACS-purified and transcriptionally compared using RNA-seq analysis. Results Expression of the Gpr64mCherry reporter was identified in multiple organs and specifically in olfactory microvillous Cells, enteric nerves, and importantly in respiratory and GI tuft Cells. In the small Intestine, Cell ablation targeting Gpr64-expressing epithelial Cells eliminated tuft Cells. Transcriptional analysis of small intestinal Gpr64mCherry -positive tuft Cells confirmed expression of Gpr64 and the chemo-sensors Sucnr1, Gprc5c, Drd3, and Gpr41/Ffar3. Time-lapse studies of organoids from Trpm5GFP:Gpr64mCherry mice revealed sequential expression of initially Trpm5GFP and subsequently also Gpr64mCherry in maturing intestinal tuft Cells. RNA-seq analysis of small intestinal tuft Cells based on these two markers demonstrated a dynamic change in expression of transcription factors and GPCRs from young to mature tuft Cells. Conclusions GPR64 is expressed in chemosensory epithelial Cells across a broad range of tissues; however, in the GI tract, GPR64 is remarkably selectively expressed in mature versus young immunoregulatory tuft Cells.

  • Adhesion receptor ADGRG2/GPR64 is in the GI-tract selectively expressed in mature intestinal tuft Cells
    'Elsevier BV', 2021
    Co-Authors: Kaare V. Grunddal, Sarah Tonack, Kristoffer L. Egerod, Jonathan James Thompson, Natalia Petersen, Maja S. Engelstoft, Constance Vagne, Céline Keime, Gérard Gradwohl, Stefan Offermanns
    Abstract:

    Objective: GPR64/ADGRG2 is an orphan Adhesion G protein-coupled receptor (ADGR) known to be mainly expressed in the parathyroid gland and epididymis. This investigation aimed to delineate the Cellular expression of GPR64 throughout the body with focus on the gastrointestinal (GI) tract. Methods: Transgenic Gpr64mCherry reporter mice were histologically examined throughout the body and reporter protein expression in intestinal tuft Cells was confirmed by specific Cell ablation. The GPCR repertoire of intestinal Gpr64mCherry-positive tuft Cells was analyzed by quantitative RT-PCR analysis and in situ hybridization. The Gpr64mCherry was crossed into the general tuft Cell reporter Trpm5GFP to generate small intestinal organoids for time-lapse imaging. Intestinal tuft Cells were isolated from small Intestine, FACS-purified and transcriptionally compared using RNA-seq analysis. Results: Expression of the Gpr64mCherry reporter was identified in multiple organs and specifically in olfactory microvillous Cells, enteric nerves, and importantly in respiratory and GI tuft Cells. In the small Intestine, Cell ablation targeting Gpr64-expressing epithelial Cells eliminated tuft Cells. Transcriptional analysis of small intestinal Gpr64mCherry -positive tuft Cells confirmed expression of Gpr64 and the chemo-sensors Sucnr1, Gprc5c, Drd3, and Gpr41/Ffar3. Time-lapse studies of organoids from Trpm5GFP:Gpr64mCherry mice revealed sequential expression of initially Trpm5GFP and subsequently also Gpr64mCherry in maturing intestinal tuft Cells. RNA-seq analysis of small intestinal tuft Cells based on these two markers demonstrated a dynamic change in expression of transcription factors and GPCRs from young to mature tuft Cells. Conclusions: GPR64 is expressed in chemosensory epithelial Cells across a broad range of tissues; however, in the GI tract, GPR64 is remarkably selectively expressed in mature versus young immunoregulatory tuft Cells

Glen K. Andrews - One of the best experts on this subject based on the ideXlab platform.

  • A mouse model of acrodermatitis enteropathica: Loss of Intestine zinc transporter ZIP4 (Slc39a4) disrupts the stem Cell niche and Intestine integrity. PLoS Genet
    2016
    Co-Authors: Jim Geiser, Koen J. T. Venken, Robert C. De Lisle, Glen K. Andrews
    Abstract:

    Mutations in the human Zip4 gene cause acrodermatitis enteropathica, a rare, pseudo-dominant, lethal genetic disorder. We created a tamoxifen-inducible, enterocyte-specific knockout of this gene in mice which mimics this human disorder. We found that the enterocyte Zip4 gene in mice is essential throughout life, and loss-of-function of this gene rapidly leads to wasting and death unless mice are nursed or provided excess dietary zinc. An initial effect of the knockout was the reprogramming of Paneth Cells, which contribute to the intestinal stem Cell niche in the crypts. Labile zinc in Paneth Cells was lost, followed by diminished Sox9 (sex determining region Y-box 9) and lysozyme expression, and accumulation of mucin, which is normally found in goblet Cells. This was accompanied by dysplasia of the intestinal crypts and significantly diminished small Intestine Cell division, and attenuated mTOR1 activity in villus enterocytes, indicative of increased catabolic metabolism, and diminished protein synthesis. This was followed by disorganization of the absorptive epithelium. Elemental analyses of small Intestine, liver, and pancreas from Zip4-Intestine knockout mice revealed that total zinc was dramatically and rapidly decreased in these organs whereas iron, manganese, and copper slowly accumulated to high levels in the liver as the disease progressed. These studies strongly suggest that wasting and lethality in acrodermatitis enteropathica patients reflects the loss-of-function of the Intestine zinc transporter ZIP4, which leads to abnormal Paneth Cell gene expression, disruption of the intestinal stem Cell niche, and diminished function of the intestinal mucosa. These changes, i

  • a mouse model of acrodermatitis enteropathica loss of Intestine zinc transporter zip4 slc39a4 disrupts the stem Cell niche and Intestine integrity
    PLOS Genetics, 2012
    Co-Authors: Jim Geiser, Koen J. T. Venken, Robert C. De Lisle, Glen K. Andrews
    Abstract:

    Mutations in the human Zip4 gene cause acrodermatitis enteropathica, a rare, pseudo-dominant, lethal genetic disorder. We created a tamoxifen-inducible, enterocyte-specific knockout of this gene in mice which mimics this human disorder. We found that the enterocyte Zip4 gene in mice is essential throughout life, and loss-of-function of this gene rapidly leads to wasting and death unless mice are nursed or provided excess dietary zinc. An initial effect of the knockout was the reprogramming of Paneth Cells, which contribute to the intestinal stem Cell niche in the crypts. Labile zinc in Paneth Cells was lost, followed by diminished Sox9 (sex determining region Y-box 9) and lysozyme expression, and accumulation of mucin, which is normally found in goblet Cells. This was accompanied by dysplasia of the intestinal crypts and significantly diminished small Intestine Cell division, and attenuated mTOR1 activity in villus enterocytes, indicative of increased catabolic metabolism, and diminished protein synthesis. This was followed by disorganization of the absorptive epithelium. Elemental analyses of small Intestine, liver, and pancreas from Zip4-Intestine knockout mice revealed that total zinc was dramatically and rapidly decreased in these organs whereas iron, manganese, and copper slowly accumulated to high levels in the liver as the disease progressed. These studies strongly suggest that wasting and lethality in acrodermatitis enteropathica patients reflects the loss-of-function of the Intestine zinc transporter ZIP4, which leads to abnormal Paneth Cell gene expression, disruption of the intestinal stem Cell niche, and diminished function of the intestinal mucosa. These changes, in turn, cause a switch from anabolic to catabolic metabolism and altered homeostasis of several essential metals, which, if untreated by excess dietary zinc, leads to dramatic weight loss and death.

Kaare V. Grunddal - One of the best experts on this subject based on the ideXlab platform.

  • adhesion receptor adgrg2 gpr64 is in the gi tract selectively expressed in mature intestinal tuft Cells
    Molecular metabolism, 2021
    Co-Authors: Kaare V. Grunddal, Sarah Tonack, Kristoffer L. Egerod, Jonathan James Thompson, Natalia Petersen, Maja S. Engelstoft, Constance Vagne, Céline Keime, Gérard Gradwohl, Stefan Offermanns
    Abstract:

    Abstract Objective GPR64/ADGRG2 is an orphan Adhesion G protein-coupled receptor (ADGR) known to be mainly expressed in the parathyroid gland and epididymis. This investigation aimed to delineate the Cellular expression of GPR64 throughout the body with focus on the gastrointestinal (GI) tract. Methods Transgenic Gpr64mCherry reporter mice were histologically examined throughout the body and reporter protein expression in intestinal tuft Cells was confirmed by specific Cell ablation. The GPCR repertoire of intestinal Gpr64mCherry-positive tuft Cells was analyzed by quantitative RT-PCR analysis and in situ hybridization. The Gpr64mCherry was crossed into the general tuft Cell reporter Trpm5GFP to generate small intestinal organoids for time-lapse imaging. Intestinal tuft Cells were isolated from small Intestine, FACS-purified and transcriptionally compared using RNA-seq analysis. Results Expression of the Gpr64mCherry reporter was identified in multiple organs and specifically in olfactory microvillous Cells, enteric nerves, and importantly in respiratory and GI tuft Cells. In the small Intestine, Cell ablation targeting Gpr64-expressing epithelial Cells eliminated tuft Cells. Transcriptional analysis of small intestinal Gpr64mCherry -positive tuft Cells confirmed expression of Gpr64 and the chemo-sensors Sucnr1, Gprc5c, Drd3, and Gpr41/Ffar3. Time-lapse studies of organoids from Trpm5GFP:Gpr64mCherry mice revealed sequential expression of initially Trpm5GFP and subsequently also Gpr64mCherry in maturing intestinal tuft Cells. RNA-seq analysis of small intestinal tuft Cells based on these two markers demonstrated a dynamic change in expression of transcription factors and GPCRs from young to mature tuft Cells. Conclusions GPR64 is expressed in chemosensory epithelial Cells across a broad range of tissues; however, in the GI tract, GPR64 is remarkably selectively expressed in mature versus young immunoregulatory tuft Cells.

  • Adhesion receptor ADGRG2/GPR64 is in the GI-tract selectively expressed in mature intestinal tuft Cells
    'Elsevier BV', 2021
    Co-Authors: Kaare V. Grunddal, Sarah Tonack, Kristoffer L. Egerod, Jonathan James Thompson, Natalia Petersen, Maja S. Engelstoft, Constance Vagne, Céline Keime, Gérard Gradwohl, Stefan Offermanns
    Abstract:

    Objective: GPR64/ADGRG2 is an orphan Adhesion G protein-coupled receptor (ADGR) known to be mainly expressed in the parathyroid gland and epididymis. This investigation aimed to delineate the Cellular expression of GPR64 throughout the body with focus on the gastrointestinal (GI) tract. Methods: Transgenic Gpr64mCherry reporter mice were histologically examined throughout the body and reporter protein expression in intestinal tuft Cells was confirmed by specific Cell ablation. The GPCR repertoire of intestinal Gpr64mCherry-positive tuft Cells was analyzed by quantitative RT-PCR analysis and in situ hybridization. The Gpr64mCherry was crossed into the general tuft Cell reporter Trpm5GFP to generate small intestinal organoids for time-lapse imaging. Intestinal tuft Cells were isolated from small Intestine, FACS-purified and transcriptionally compared using RNA-seq analysis. Results: Expression of the Gpr64mCherry reporter was identified in multiple organs and specifically in olfactory microvillous Cells, enteric nerves, and importantly in respiratory and GI tuft Cells. In the small Intestine, Cell ablation targeting Gpr64-expressing epithelial Cells eliminated tuft Cells. Transcriptional analysis of small intestinal Gpr64mCherry -positive tuft Cells confirmed expression of Gpr64 and the chemo-sensors Sucnr1, Gprc5c, Drd3, and Gpr41/Ffar3. Time-lapse studies of organoids from Trpm5GFP:Gpr64mCherry mice revealed sequential expression of initially Trpm5GFP and subsequently also Gpr64mCherry in maturing intestinal tuft Cells. RNA-seq analysis of small intestinal tuft Cells based on these two markers demonstrated a dynamic change in expression of transcription factors and GPCRs from young to mature tuft Cells. Conclusions: GPR64 is expressed in chemosensory epithelial Cells across a broad range of tissues; however, in the GI tract, GPR64 is remarkably selectively expressed in mature versus young immunoregulatory tuft Cells

Jim Geiser - One of the best experts on this subject based on the ideXlab platform.

  • A mouse model of acrodermatitis enteropathica: Loss of Intestine zinc transporter ZIP4 (Slc39a4) disrupts the stem Cell niche and Intestine integrity. PLoS Genet
    2016
    Co-Authors: Jim Geiser, Koen J. T. Venken, Robert C. De Lisle, Glen K. Andrews
    Abstract:

    Mutations in the human Zip4 gene cause acrodermatitis enteropathica, a rare, pseudo-dominant, lethal genetic disorder. We created a tamoxifen-inducible, enterocyte-specific knockout of this gene in mice which mimics this human disorder. We found that the enterocyte Zip4 gene in mice is essential throughout life, and loss-of-function of this gene rapidly leads to wasting and death unless mice are nursed or provided excess dietary zinc. An initial effect of the knockout was the reprogramming of Paneth Cells, which contribute to the intestinal stem Cell niche in the crypts. Labile zinc in Paneth Cells was lost, followed by diminished Sox9 (sex determining region Y-box 9) and lysozyme expression, and accumulation of mucin, which is normally found in goblet Cells. This was accompanied by dysplasia of the intestinal crypts and significantly diminished small Intestine Cell division, and attenuated mTOR1 activity in villus enterocytes, indicative of increased catabolic metabolism, and diminished protein synthesis. This was followed by disorganization of the absorptive epithelium. Elemental analyses of small Intestine, liver, and pancreas from Zip4-Intestine knockout mice revealed that total zinc was dramatically and rapidly decreased in these organs whereas iron, manganese, and copper slowly accumulated to high levels in the liver as the disease progressed. These studies strongly suggest that wasting and lethality in acrodermatitis enteropathica patients reflects the loss-of-function of the Intestine zinc transporter ZIP4, which leads to abnormal Paneth Cell gene expression, disruption of the intestinal stem Cell niche, and diminished function of the intestinal mucosa. These changes, i

  • a mouse model of acrodermatitis enteropathica loss of Intestine zinc transporter zip4 slc39a4 disrupts the stem Cell niche and Intestine integrity
    PLOS Genetics, 2012
    Co-Authors: Jim Geiser, Koen J. T. Venken, Robert C. De Lisle, Glen K. Andrews
    Abstract:

    Mutations in the human Zip4 gene cause acrodermatitis enteropathica, a rare, pseudo-dominant, lethal genetic disorder. We created a tamoxifen-inducible, enterocyte-specific knockout of this gene in mice which mimics this human disorder. We found that the enterocyte Zip4 gene in mice is essential throughout life, and loss-of-function of this gene rapidly leads to wasting and death unless mice are nursed or provided excess dietary zinc. An initial effect of the knockout was the reprogramming of Paneth Cells, which contribute to the intestinal stem Cell niche in the crypts. Labile zinc in Paneth Cells was lost, followed by diminished Sox9 (sex determining region Y-box 9) and lysozyme expression, and accumulation of mucin, which is normally found in goblet Cells. This was accompanied by dysplasia of the intestinal crypts and significantly diminished small Intestine Cell division, and attenuated mTOR1 activity in villus enterocytes, indicative of increased catabolic metabolism, and diminished protein synthesis. This was followed by disorganization of the absorptive epithelium. Elemental analyses of small Intestine, liver, and pancreas from Zip4-Intestine knockout mice revealed that total zinc was dramatically and rapidly decreased in these organs whereas iron, manganese, and copper slowly accumulated to high levels in the liver as the disease progressed. These studies strongly suggest that wasting and lethality in acrodermatitis enteropathica patients reflects the loss-of-function of the Intestine zinc transporter ZIP4, which leads to abnormal Paneth Cell gene expression, disruption of the intestinal stem Cell niche, and diminished function of the intestinal mucosa. These changes, in turn, cause a switch from anabolic to catabolic metabolism and altered homeostasis of several essential metals, which, if untreated by excess dietary zinc, leads to dramatic weight loss and death.

Sarah Tonack - One of the best experts on this subject based on the ideXlab platform.

  • adhesion receptor adgrg2 gpr64 is in the gi tract selectively expressed in mature intestinal tuft Cells
    Molecular metabolism, 2021
    Co-Authors: Kaare V. Grunddal, Sarah Tonack, Kristoffer L. Egerod, Jonathan James Thompson, Natalia Petersen, Maja S. Engelstoft, Constance Vagne, Céline Keime, Gérard Gradwohl, Stefan Offermanns
    Abstract:

    Abstract Objective GPR64/ADGRG2 is an orphan Adhesion G protein-coupled receptor (ADGR) known to be mainly expressed in the parathyroid gland and epididymis. This investigation aimed to delineate the Cellular expression of GPR64 throughout the body with focus on the gastrointestinal (GI) tract. Methods Transgenic Gpr64mCherry reporter mice were histologically examined throughout the body and reporter protein expression in intestinal tuft Cells was confirmed by specific Cell ablation. The GPCR repertoire of intestinal Gpr64mCherry-positive tuft Cells was analyzed by quantitative RT-PCR analysis and in situ hybridization. The Gpr64mCherry was crossed into the general tuft Cell reporter Trpm5GFP to generate small intestinal organoids for time-lapse imaging. Intestinal tuft Cells were isolated from small Intestine, FACS-purified and transcriptionally compared using RNA-seq analysis. Results Expression of the Gpr64mCherry reporter was identified in multiple organs and specifically in olfactory microvillous Cells, enteric nerves, and importantly in respiratory and GI tuft Cells. In the small Intestine, Cell ablation targeting Gpr64-expressing epithelial Cells eliminated tuft Cells. Transcriptional analysis of small intestinal Gpr64mCherry -positive tuft Cells confirmed expression of Gpr64 and the chemo-sensors Sucnr1, Gprc5c, Drd3, and Gpr41/Ffar3. Time-lapse studies of organoids from Trpm5GFP:Gpr64mCherry mice revealed sequential expression of initially Trpm5GFP and subsequently also Gpr64mCherry in maturing intestinal tuft Cells. RNA-seq analysis of small intestinal tuft Cells based on these two markers demonstrated a dynamic change in expression of transcription factors and GPCRs from young to mature tuft Cells. Conclusions GPR64 is expressed in chemosensory epithelial Cells across a broad range of tissues; however, in the GI tract, GPR64 is remarkably selectively expressed in mature versus young immunoregulatory tuft Cells.

  • Adhesion receptor ADGRG2/GPR64 is in the GI-tract selectively expressed in mature intestinal tuft Cells
    'Elsevier BV', 2021
    Co-Authors: Kaare V. Grunddal, Sarah Tonack, Kristoffer L. Egerod, Jonathan James Thompson, Natalia Petersen, Maja S. Engelstoft, Constance Vagne, Céline Keime, Gérard Gradwohl, Stefan Offermanns
    Abstract:

    Objective: GPR64/ADGRG2 is an orphan Adhesion G protein-coupled receptor (ADGR) known to be mainly expressed in the parathyroid gland and epididymis. This investigation aimed to delineate the Cellular expression of GPR64 throughout the body with focus on the gastrointestinal (GI) tract. Methods: Transgenic Gpr64mCherry reporter mice were histologically examined throughout the body and reporter protein expression in intestinal tuft Cells was confirmed by specific Cell ablation. The GPCR repertoire of intestinal Gpr64mCherry-positive tuft Cells was analyzed by quantitative RT-PCR analysis and in situ hybridization. The Gpr64mCherry was crossed into the general tuft Cell reporter Trpm5GFP to generate small intestinal organoids for time-lapse imaging. Intestinal tuft Cells were isolated from small Intestine, FACS-purified and transcriptionally compared using RNA-seq analysis. Results: Expression of the Gpr64mCherry reporter was identified in multiple organs and specifically in olfactory microvillous Cells, enteric nerves, and importantly in respiratory and GI tuft Cells. In the small Intestine, Cell ablation targeting Gpr64-expressing epithelial Cells eliminated tuft Cells. Transcriptional analysis of small intestinal Gpr64mCherry -positive tuft Cells confirmed expression of Gpr64 and the chemo-sensors Sucnr1, Gprc5c, Drd3, and Gpr41/Ffar3. Time-lapse studies of organoids from Trpm5GFP:Gpr64mCherry mice revealed sequential expression of initially Trpm5GFP and subsequently also Gpr64mCherry in maturing intestinal tuft Cells. RNA-seq analysis of small intestinal tuft Cells based on these two markers demonstrated a dynamic change in expression of transcription factors and GPCRs from young to mature tuft Cells. Conclusions: GPR64 is expressed in chemosensory epithelial Cells across a broad range of tissues; however, in the GI tract, GPR64 is remarkably selectively expressed in mature versus young immunoregulatory tuft Cells

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