Bik promotes proteasomal degradation to control low-grade inflammation

Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage to organ systems and thereby contribute to age-related disorders, such as respiratory disorders, heart disease, metabolic disorders, autoimmu...

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Published in:The Journal of clinical investigation Vol. 134; no. 4
Main Authors: Mebratu, Yohannes A., Jones, Jane T., Liu, Congjian, Negasi, Zerihun H., Rahman, Mizanur, Rojas-Quintero, Joselyn, O’Connor, George T., Gao, Wei, Dupuis, Josée, Cho, Michael H., Litonjua, Augusto A., Randell, Scott, Tesfaigzi, Yohannes
Format: Journal Article
Language:English
Published: United States American Society for Clinical Investigation 15.02.2024
Subjects:
Allergic reaction
Allergy
Animals
Apoptosis
Apoptosis Regulatory Proteins
Apoptotic proteins
Autoimmunity
Development and progression
Diseases
Emphysema
Emphysema, Pulmonary
Female
Genetic aspects
Genetic engineering
Health aspects
Heart diseases
Hexosyltransferases
Humans
Inflammation
Inflammation - genetics
Male
Massachusetts
Mice
Mitochondrial Proteins
New Mexico
Nuclear Proteins
Physiological aspects
Proteasome Endopeptidase Complex - genetics
Proteins
Proteolysis
Proto-Oncogene Proteins c-bcl-2
Single nucleotide polymorphisms
Tetracycline
Tetracyclines
United States
New Mexico
Massachusetts
Inflammation
NF-kappaB
Peptides
Apoptosis
ISSN:1558-8238, 0021-9738, 1558-8238
Online Access:Get full text
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Abstract Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage to organ systems and thereby contribute to age-related disorders, such as respiratory disorders, heart disease, metabolic disorders, autoimmunity, and cancer. However, the molecular mechanisms governing low-level inflammation are largely unknown. We discovered that Bcl-2-interacting killer (Bik) deficiency causes low-level inflammation even at baseline and the development of spontaneous emphysema in female but not male mice. Similarly, a single nucleotide polymorphism that reduced Bik levels was associated with increased inflammation and enhanced decline in lung function in humans. Transgenic expression of Bik in the airways of Bik-deficient mice inhibited allergen- or LPS-induced lung inflammation and reversed emphysema in female mice. Bik deficiency increased nuclear but not cytosolic p65 levels because Bik, by modifying the BH4 domain of Bcl-2, interacted with regulatory particle non-ATPase 1 (RPN1) and RPN2 and enhanced proteasomal degradation of nuclear proteins. Bik deficiency increased inflammation primarily in females because Bcl-2 and Bik levels were reduced in lung tissues and airway cells of female compared with male mice. Therefore, controlling low-grade inflammation by modifying the unappreciated role of Bik and Bcl-2 in facilitating proteasomal degradation of nuclear proteins may be crucial in treating chronic age-related diseases.
AbstractList Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage to organ systems and thereby contribute to age-related disorders, such as respiratory disorders, heart disease, metabolic disorders, autoimmunity, and cancer. However, the molecular mechanisms governing low-level inflammation are largely unknown. We discovered that Bcl-2-interacting killer (Bik) deficiency causes low-level inflammation even at baseline and the development of spontaneous emphysema in female but not male mice. Similarly, a single nucleotide polymorphism that reduced Bik levels was associated with increased inflammation and enhanced decline in lung function in humans. Transgenic expression of Bik in the airways of Bik-deficient mice inhibited allergen- or LPS-induced lung inflammation and reversed emphysema in female mice. Bik deficiency increased nuclear but not cytosolic p65 levels because Bik, by modifying the BH4 domain of Bcl-2, interacted with regulatory particle non-ATPase 1 (RPN1) and RPN2 and enhanced proteasomal degradation of nuclear proteins. Bik deficiency increased inflammation primarily in females because Bcl-2 and Bik levels were reduced in lung tissues and airway cells of female compared with male mice. Therefore, controlling low-grade inflammation by modifying the unappreciated role of Bik and Bcl-2 in facilitating proteasomal degradation of nuclear proteins may be crucial in treating chronic age-related diseases.
Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage to organ systems and thereby contribute to age-related disorders, such as respiratory disorders, heart disease, metabolic disorders, autoimmunity, and cancer. However, the molecular mechanisms governing low-level inflammation are largely unknown. We discovered that Bcl-2-interacting killer (Bik) deficiency causes low- level inflammation even at baseline and the development of spontaneous emphysema in female but not male mice. Similarly, a single nucleotide polymorphism that reduced Bik levels was associated with increased inflammation and enhanced decline in lung function in humans. Transgenic expression of Bik in the airways of B/'/c- deficient mice inhibited allergen- or LPS- induced lung inflammation and reversed emphysema in female mice. Bik deficiency increased nuclear but not cytosolic p65 levels because Bik, by modifying the BH4 domain of Bcl-2, interacted with regulatory particle non-ATPase 1 (RPN1) and RPN2 and enhanced proteasomal degradation of nuclear proteins. Bik deficiency increased inflammation primarily in females because Bcl-2 and Bik levels were reduced in lung tissues and airway cells of female compared with male mice. Therefore, controlling low-grade inflammation by modifying the unappreciated role of Bik and Bcl-2 in facilitating proteasomal degradation of nuclear proteins may be crucial in treating chronic age-related diseases.
Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage to organ systems and thereby contribute to age-related disorders, such as respiratory disorders, heart disease, metabolic disorders, autoimmunity, and cancer. However, the molecular mechanisms governing low-level inflammation are largely unknown. We discovered that Bcl-2-interacting killer (Bik) deficiency causes low-level inflammation even at baseline and the development of spontaneous emphysema in female but not male mice. Similarly, a single nucleotide polymorphism that reduced Bik levels was associated with increased inflammation and enhanced decline in lung function in humans. Transgenic expression of Bik in the airways of Bik-deficient mice inhibited allergen- or LPS-induced lung inflammation and reversed emphysema in female mice. Bik deficiency increased nuclear but not cytosolic p65 levels because Bik, by modifying the BH4 domain of Bcl-2, interacted with regulatory particle non-ATPase 1 (RPN1) and RPN2 and enhanced proteasomal degradation of nuclear proteins. Bik deficiency increased inflammation primarily in females because Bcl-2 and Bik levels were reduced in lung tissues and airway cells of female compared with male mice. Therefore, controlling low-grade inflammation by modifying the unappreciated role of Bik and Bcl-2 in facilitating proteasomal degradation of nuclear proteins may be crucial in treating chronic age-related diseases.Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage to organ systems and thereby contribute to age-related disorders, such as respiratory disorders, heart disease, metabolic disorders, autoimmunity, and cancer. However, the molecular mechanisms governing low-level inflammation are largely unknown. We discovered that Bcl-2-interacting killer (Bik) deficiency causes low-level inflammation even at baseline and the development of spontaneous emphysema in female but not male mice. Similarly, a single nucleotide polymorphism that reduced Bik levels was associated with increased inflammation and enhanced decline in lung function in humans. Transgenic expression of Bik in the airways of Bik-deficient mice inhibited allergen- or LPS-induced lung inflammation and reversed emphysema in female mice. Bik deficiency increased nuclear but not cytosolic p65 levels because Bik, by modifying the BH4 domain of Bcl-2, interacted with regulatory particle non-ATPase 1 (RPN1) and RPN2 and enhanced proteasomal degradation of nuclear proteins. Bik deficiency increased inflammation primarily in females because Bcl-2 and Bik levels were reduced in lung tissues and airway cells of female compared with male mice. Therefore, controlling low-grade inflammation by modifying the unappreciated role of Bik and Bcl-2 in facilitating proteasomal degradation of nuclear proteins may be crucial in treating chronic age-related diseases.
Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage to organ systems and thereby contribute to age-related disorders, such as respiratory disorders, heart disease, metabolic disorders, autoimmunity, and cancer. However, the molecular mechanisms governing low-level inflammation are largely unknown. We discovered that Bcl-2–interacting killer (Bik) deficiency causes low-level inflammation even at baseline and the development of spontaneous emphysema in female but not male mice. Similarly, a single nucleotide polymorphism that reduced Bik levels was associated with increased inflammation and enhanced decline in lung function in humans. Transgenic expression of Bik in the airways of Bik-deficient mice inhibited allergen- or LPS-induced lung inflammation and reversed emphysema in female mice. Bik deficiency increased nuclear but not cytosolic p65 levels because Bik, by modifying the BH4 domain of Bcl-2, interacted with regulatory particle non-ATPase 1 (RPN1) and RPN2 and enhanced proteasomal degradation of nuclear proteins. Bik deficiency increased inflammation primarily in females because Bcl-2 and Bik levels were reduced in lung tissues and airway cells of female compared with male mice. Therefore, controlling low-grade inflammation by modifying the unappreciated role of Bik and Bcl-2 in facilitating proteasomal degradation of nuclear proteins may be crucial in treating chronic age-related diseases. The cell death regulatory Bik binds to nuclear Bcl-2 to modify protein stability and inflammation.
Audience Academic
Author O’Connor, George T.
Rojas-Quintero, Joselyn
Tesfaigzi, Yohannes
Gao, Wei
Negasi, Zerihun H.
Mebratu, Yohannes A.
Jones, Jane T.
Rahman, Mizanur
Randell, Scott
Liu, Congjian
Dupuis, Josée
Cho, Michael H.
Litonjua, Augusto A.
AuthorAffiliation 2 University Geisel School of Medicine, Department of Microbiology and Immunology, Dartmouth, Hanover, New Hampshire, USA
8 Division of Pediatric Pulmonary Medicine, University of Rochester Medical Center, Rochester, New York, USA
1 Brigham and Women’s Hospital, Division of Pulmonary and Critical Medicine, Harvard Medical School, Boston, Massachusetts, USA
4 National Heart, Lung, and Blood Institute’s (NHLBI’s) Framingham Heart Study, Framingham, Massachusetts, USA
3 Pulmonary Center, Boston University School of Medicine, Boston, Massachusetts, USA
6 Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, Canada
7 Channing Division of Network Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA
9 Marsico Lung Institute, UNC School of Medicine, Chapel Hill, North Carolina, USA
5 Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts, USA
AuthorAffiliation_xml – name: 7 Channing Division of Network Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA
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– name: 3 Pulmonary Center, Boston University School of Medicine, Boston, Massachusetts, USA
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– name: 4 National Heart, Lung, and Blood Institute’s (NHLBI’s) Framingham Heart Study, Framingham, Massachusetts, USA
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Issue 4
Keywords Inflammation
NF-kappaB
Peptides
Apoptosis
Language English
License http://creativecommons.org/licenses/by/4.0
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Authorship note: YAM and JTJ contributed equally to this work.
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Snippet Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage...
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SubjectTerms Allergic reaction
Allergy
Animals
Apoptosis
Apoptosis Regulatory Proteins
Apoptotic proteins
Autoimmunity
Development and progression
Diseases
Emphysema
Emphysema, Pulmonary
Female
Genetic aspects
Genetic engineering
Health aspects
Heart diseases
Hexosyltransferases
Humans
Inflammation
Inflammation - genetics
Male
Massachusetts
Mice
Mitochondrial Proteins
New Mexico
Nuclear Proteins
Physiological aspects
Proteasome Endopeptidase Complex - genetics
Proteins
Proteolysis
Proto-Oncogene Proteins c-bcl-2
Single nucleotide polymorphisms
Tetracycline
Tetracyclines
Title Bik promotes proteasomal degradation to control low-grade inflammation
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