A Cardiovascular Disease-Linked Gut Microbial Metabolite Acts via Adrenergic Receptors

Using untargeted metabolomics (n = 1,162 subjects), the plasma metabolite (m/z = 265.1188) phenylacetylglutamine (PAGln) was discovered and then shown in an independent cohort (n = 4,000 subjects) to be associated with cardiovascular disease (CVD) and incident major adverse cardiovascular events (my...

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Vydáno v:Cell Ročník 180; číslo 5; s. 862
Hlavní autoři: Nemet, Ina, Saha, Prasenjit Prasad, Gupta, Nilaksh, Zhu, Weifei, Romano, Kymberleigh A, Skye, Sarah M, Cajka, Tomas, Mohan, Maradumane L, Li, Lin, Wu, Yuping, Funabashi, Masanori, Ramer-Tait, Amanda E, Naga Prasad, Sathyamangla Venkata, Fiehn, Oliver, Rey, Federico E, Tang, W H Wilson, Fischbach, Michael A, DiDonato, Joseph A, Hazen, Stanley L
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 05.03.2020
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ISSN:1097-4172, 1097-4172
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Abstract Using untargeted metabolomics (n = 1,162 subjects), the plasma metabolite (m/z = 265.1188) phenylacetylglutamine (PAGln) was discovered and then shown in an independent cohort (n = 4,000 subjects) to be associated with cardiovascular disease (CVD) and incident major adverse cardiovascular events (myocardial infarction, stroke, or death). A gut microbiota-derived metabolite, PAGln, was shown to enhance platelet activation-related phenotypes and thrombosis potential in whole blood, isolated platelets, and animal models of arterial injury. Functional and genetic engineering studies with human commensals, coupled with microbial colonization of germ-free mice, showed the microbial porA gene facilitates dietary phenylalanine conversion into phenylacetic acid, with subsequent host generation of PAGln and phenylacetylglycine (PAGly) fostering platelet responsiveness and thrombosis potential. Both gain- and loss-of-function studies employing genetic and pharmacological tools reveal PAGln mediates cellular events through G-protein coupled receptors, including α2A, α2B, and β2-adrenergic receptors. PAGln thus represents a new CVD-promoting gut microbiota-dependent metabolite that signals via adrenergic receptors.
AbstractList Using untargeted metabolomics (n = 1,162 subjects), the plasma metabolite (m/z = 265.1188) phenylacetylglutamine (PAGln) was discovered and then shown in an independent cohort (n = 4,000 subjects) to be associated with cardiovascular disease (CVD) and incident major adverse cardiovascular events (myocardial infarction, stroke, or death). A gut microbiota-derived metabolite, PAGln, was shown to enhance platelet activation-related phenotypes and thrombosis potential in whole blood, isolated platelets, and animal models of arterial injury. Functional and genetic engineering studies with human commensals, coupled with microbial colonization of germ-free mice, showed the microbial porA gene facilitates dietary phenylalanine conversion into phenylacetic acid, with subsequent host generation of PAGln and phenylacetylglycine (PAGly) fostering platelet responsiveness and thrombosis potential. Both gain- and loss-of-function studies employing genetic and pharmacological tools reveal PAGln mediates cellular events through G-protein coupled receptors, including α2A, α2B, and β2-adrenergic receptors. PAGln thus represents a new CVD-promoting gut microbiota-dependent metabolite that signals via adrenergic receptors.
Using untargeted metabolomics (n = 1,162 subjects), the plasma metabolite (m/z = 265.1188) phenylacetylglutamine (PAGln) was discovered and then shown in an independent cohort (n = 4,000 subjects) to be associated with cardiovascular disease (CVD) and incident major adverse cardiovascular events (myocardial infarction, stroke, or death). A gut microbiota-derived metabolite, PAGln, was shown to enhance platelet activation-related phenotypes and thrombosis potential in whole blood, isolated platelets, and animal models of arterial injury. Functional and genetic engineering studies with human commensals, coupled with microbial colonization of germ-free mice, showed the microbial porA gene facilitates dietary phenylalanine conversion into phenylacetic acid, with subsequent host generation of PAGln and phenylacetylglycine (PAGly) fostering platelet responsiveness and thrombosis potential. Both gain- and loss-of-function studies employing genetic and pharmacological tools reveal PAGln mediates cellular events through G-protein coupled receptors, including α2A, α2B, and β2-adrenergic receptors. PAGln thus represents a new CVD-promoting gut microbiota-dependent metabolite that signals via adrenergic receptors.Using untargeted metabolomics (n = 1,162 subjects), the plasma metabolite (m/z = 265.1188) phenylacetylglutamine (PAGln) was discovered and then shown in an independent cohort (n = 4,000 subjects) to be associated with cardiovascular disease (CVD) and incident major adverse cardiovascular events (myocardial infarction, stroke, or death). A gut microbiota-derived metabolite, PAGln, was shown to enhance platelet activation-related phenotypes and thrombosis potential in whole blood, isolated platelets, and animal models of arterial injury. Functional and genetic engineering studies with human commensals, coupled with microbial colonization of germ-free mice, showed the microbial porA gene facilitates dietary phenylalanine conversion into phenylacetic acid, with subsequent host generation of PAGln and phenylacetylglycine (PAGly) fostering platelet responsiveness and thrombosis potential. Both gain- and loss-of-function studies employing genetic and pharmacological tools reveal PAGln mediates cellular events through G-protein coupled receptors, including α2A, α2B, and β2-adrenergic receptors. PAGln thus represents a new CVD-promoting gut microbiota-dependent metabolite that signals via adrenergic receptors.
Author Nemet, Ina
Saha, Prasenjit Prasad
Gupta, Nilaksh
Tang, W H Wilson
Li, Lin
DiDonato, Joseph A
Romano, Kymberleigh A
Fiehn, Oliver
Naga Prasad, Sathyamangla Venkata
Fischbach, Michael A
Hazen, Stanley L
Funabashi, Masanori
Rey, Federico E
Cajka, Tomas
Mohan, Maradumane L
Ramer-Tait, Amanda E
Skye, Sarah M
Wu, Yuping
Zhu, Weifei
Author_xml – sequence: 1
  givenname: Ina
  surname: Nemet
  fullname: Nemet, Ina
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 2
  givenname: Prasenjit Prasad
  surname: Saha
  fullname: Saha, Prasenjit Prasad
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 3
  givenname: Nilaksh
  surname: Gupta
  fullname: Gupta, Nilaksh
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 4
  givenname: Weifei
  surname: Zhu
  fullname: Zhu, Weifei
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 5
  givenname: Kymberleigh A
  surname: Romano
  fullname: Romano, Kymberleigh A
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 6
  givenname: Sarah M
  surname: Skye
  fullname: Skye, Sarah M
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 7
  givenname: Tomas
  surname: Cajka
  fullname: Cajka, Tomas
  organization: West Coast Metabolomics Center, University of California, Davis, Davis, CA 95616, USA
– sequence: 8
  givenname: Maradumane L
  surname: Mohan
  fullname: Mohan, Maradumane L
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 9
  givenname: Lin
  surname: Li
  fullname: Li, Lin
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 10
  givenname: Yuping
  surname: Wu
  fullname: Wu, Yuping
  organization: Department of Mathematics, Cleveland State University, Cleveland, OH 44115, USA
– sequence: 11
  givenname: Masanori
  surname: Funabashi
  fullname: Funabashi, Masanori
  organization: Department of Bioengineering and ChEM-H, Stanford University, Stanford, CA 94305, USA
– sequence: 12
  givenname: Amanda E
  surname: Ramer-Tait
  fullname: Ramer-Tait, Amanda E
  organization: Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, NE 68588, USA
– sequence: 13
  givenname: Sathyamangla Venkata
  surname: Naga Prasad
  fullname: Naga Prasad, Sathyamangla Venkata
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 14
  givenname: Oliver
  surname: Fiehn
  fullname: Fiehn, Oliver
  organization: West Coast Metabolomics Center, University of California, Davis, Davis, CA 95616, USA
– sequence: 15
  givenname: Federico E
  surname: Rey
  fullname: Rey, Federico E
  organization: Department of Bacteriology, University of Wisconsin-Madison, Madison, WI 53706, USA
– sequence: 16
  givenname: W H Wilson
  surname: Tang
  fullname: Tang, W H Wilson
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA; Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 17
  givenname: Michael A
  surname: Fischbach
  fullname: Fischbach, Michael A
  organization: Department of Bioengineering and ChEM-H, Stanford University, Stanford, CA 94305, USA
– sequence: 18
  givenname: Joseph A
  surname: DiDonato
  fullname: DiDonato, Joseph A
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA
– sequence: 19
  givenname: Stanley L
  surname: Hazen
  fullname: Hazen, Stanley L
  email: hazens@ccf.org
  organization: Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA; Center for Microbiome & Human Health, Cleveland Clinic, Cleveland, OH 44106, USA; Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH 44106, USA. Electronic address: hazens@ccf.org
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32142679$$D View this record in MEDLINE/PubMed
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Keywords cardiovascular disease
GPCR
thrombosis
gut microbe
metabolomics
adrenergic receptors
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References 32210404 - Nat Rev Cardiol. 2020 May;17(5):265
32348162 - Platelets. 2020 Jul 3;31(5):618-620
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Snippet Using untargeted metabolomics (n = 1,162 subjects), the plasma metabolite (m/z = 265.1188) phenylacetylglutamine (PAGln) was discovered and then shown in an...
Using untargeted metabolomics (n = 1,162 subjects), the plasma metabolite (m/z = 265.1188) phenylacetylglutamine (PAGln) was discovered and then shown in an...
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SubjectTerms Animals
Arteries - injuries
Arteries - metabolism
Arteries - microbiology
Bacterial Proteins - genetics
Bacterial Proteins - metabolism
Blood Platelets - metabolism
Blood Platelets - microbiology
Cardiovascular Diseases - blood
Cardiovascular Diseases - genetics
Cardiovascular Diseases - microbiology
Cardiovascular Diseases - pathology
Death, Sudden, Cardiac - pathology
Gastrointestinal Microbiome - genetics
Glutamine - analogs & derivatives
Glutamine - blood
Glutamine - genetics
Humans
Male
Metabolome - genetics
Metabolomics - methods
Mice
Myocardial Infarction - blood
Myocardial Infarction - microbiology
Platelet Activation - genetics
Receptors, Adrenergic, alpha - blood
Receptors, Adrenergic, alpha - genetics
Receptors, Adrenergic, beta - blood
Receptors, Adrenergic, beta - genetics
Risk Factors
Stroke - blood
Stroke - microbiology
Stroke - pathology
Thrombosis - genetics
Thrombosis - metabolism
Thrombosis - microbiology
Thrombosis - pathology
Title A Cardiovascular Disease-Linked Gut Microbial Metabolite Acts via Adrenergic Receptors
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