Development of Aging-Related Emphysematous and Lymphoma-Like Lesions is Enhanced by the Lack of Secretoglobin 3A2 in Mouse Lungs.


Journal

International journal of chronic obstructive pulmonary disease
ISSN: 1178-2005
Titre abrégé: Int J Chron Obstruct Pulmon Dis
Pays: New Zealand
ID NLM: 101273481

Informations de publication

Date de publication:
2022
Historique:
received: 23 07 2021
accepted: 30 04 2022
entrez: 2 6 2022
pubmed: 3 6 2022
medline: 7 6 2022
Statut: epublish

Résumé

Secretoglobin (SCGB) 3A2 is a novel bioactive molecule with anti-inflammatory and anti-fibrotic activities. SCGB3A2 also promotes the maturation of bronchial divergence and the lungs during embryonic development. However, much remains unknown concerning the roles of SCGB3A2 in diseases associated with aging. The lungs of The alveolar spaces of KO mice continuously expanded between 0.5 and 2 years of age, accompanied by increases of the mean linear intercept and destructive index. KO mouse lungs displayed inflammation associated with lymphocyte aggregate starting at 1 year of age, and the inflammation was worse than that of WT mouse lungs. A high number of lymphoma-like cells were presented in 2-year-old KO mouse lungs. White pulp fusion was detected in the spleens of both WT and KO mice older than 0.5 years; however, the fusion was more severe in KO mice than in WT mice. The expression of surfactant protein (SP)-A, SP-B, SP-C, and SP-D mRNAs in KO mouse lungs decreased with age, and after 1 year of age, the expression of most SPs was significantly lower in KO mice than in WT mice. RNAseq demonstrated that the expression of immune system-related genes was highly altered in KO mouse lungs. SCGB3A2 may be required for maintaining homeostasis and immune activity in the lungs during aging. SCGB3A2 deficiency might increase the risk of emphysema of the lung.

Sections du résumé

Background
Secretoglobin (SCGB) 3A2 is a novel bioactive molecule with anti-inflammatory and anti-fibrotic activities. SCGB3A2 also promotes the maturation of bronchial divergence and the lungs during embryonic development. However, much remains unknown concerning the roles of SCGB3A2 in diseases associated with aging.
Methods
The lungs of
Results
The alveolar spaces of KO mice continuously expanded between 0.5 and 2 years of age, accompanied by increases of the mean linear intercept and destructive index. KO mouse lungs displayed inflammation associated with lymphocyte aggregate starting at 1 year of age, and the inflammation was worse than that of WT mouse lungs. A high number of lymphoma-like cells were presented in 2-year-old KO mouse lungs. White pulp fusion was detected in the spleens of both WT and KO mice older than 0.5 years; however, the fusion was more severe in KO mice than in WT mice. The expression of surfactant protein (SP)-A, SP-B, SP-C, and SP-D mRNAs in KO mouse lungs decreased with age, and after 1 year of age, the expression of most SPs was significantly lower in KO mice than in WT mice. RNAseq demonstrated that the expression of immune system-related genes was highly altered in KO mouse lungs.
Conclusion
SCGB3A2 may be required for maintaining homeostasis and immune activity in the lungs during aging. SCGB3A2 deficiency might increase the risk of emphysema of the lung.

Identifiants

pubmed: 35651829
doi: 10.2147/COPD.S330170
pii: 330170
pmc: PMC9150920
doi:

Substances chimiques

RNA, Messenger 0
Scgb3a2 protein, mouse 0
Secretoglobins 0
Surface-Active Agents 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1247-1260

Subventions

Organisme : Intramural NIH HHS
ID : ZIA BC010449
Pays : United States

Informations de copyright

© 2022 Kurotani et al.

Déclaration de conflit d'intérêts

The authors declare that they have no conflict of interests.

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Auteurs

Reiko Kurotani (R)

Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University, Yonezawa, Yamagata, 992-8510, Japan.

Akira Kurumazuka (A)

Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University, Yonezawa, Yamagata, 992-8510, Japan.

Satoshi Sakahara (S)

Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University, Yonezawa, Yamagata, 992-8510, Japan.

Kei Takakura (K)

Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University, Yonezawa, Yamagata, 992-8510, Japan.

Yutaro Yokoyama (Y)

Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University, Yonezawa, Yamagata, 992-8510, Japan.

Lei Xu (L)

Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Jieqiong Dai (J)

Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Maxwell P Lee (MP)

Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Nobue Kumaki (N)

Department of Pathology, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.

Hiroyuki Abe (H)

Biochemical Engineering, Graduate School of Science and Engineering, Yamagata University, Yonezawa, Yamagata, 992-8510, Japan.

Shioko Kimura (S)

Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

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Classifications MeSH