Secreted phosphoprotein 1 is a determinant of lung function development in mice.

Publisher: American Thoracic Society Country of Publication: United States NLM ID: 8917225 Publication Model: Print Cited Medium: Internet ISSN: 1535-4989 (Electronic) Linking ISSN: 10441549 NLM ISO Abbreviation: Am J Respir Cell Mol Biol Subsets: MEDLINE

Publication: 2000- : New York, NY : American Thoracic Society
Original Publication: [New York, NY : The Association, [c1989-

Gene Expression Regulation, Developmental*; Osteopontin/*genetics ; Pulmonary Alveoli/*growth & development ; Pulmonary Alveoli/*physiology ; Pulmonary Disease, Chronic Obstructive/*genetics; Alveolar Epithelial Cells/physiology ; Animals ; Animals, Newborn ; Core Binding Factor Alpha 1 Subunit/genetics ; Female ; Lung Compliance/genetics ; Male ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; Promoter Regions, Genetic/genetics ; Pulmonary Alveoli/cytology ; Receptor, Notch1/genetics

Secreted phosphoprotein 1 (Spp1) is located within quantitative trait loci associated with lung function that was previously identified by contrasting C3H/HeJ and JF1/Msf mouse strains that have extremely divergent lung function. JF1/Msf mice with diminished lung function had reduced lung SPP1 transcript and protein during the peak stage of alveologenesis (postnatal day [P]14-P28) as compared with C3H/HeJ mice. In addition to a previously identified genetic variant that altered runt-related transcription factor 2 (RUNX2) binding in the Spp1 promoter, we identified another promoter variant in a putative RUNX2 binding site that increased the DNA protein binding. SPP1 induced dose-dependent mouse lung epithelial-15 cell proliferation. Spp1((-/-)) mice have decreased specific total lung capacity/body weight, higher specific compliance, and increased mean airspace chord length (Lm) compared with Spp1((+/+)) mice. Microarray analysis revealed enriched gene ontogeny categories, with numerous genes associated with lung development and/or respiratory disease. Insulin-like growth factor 1, Hedgehog-interacting protein, wingless-related mouse mammary tumor virus integration site 5A, and NOTCH1 transcripts decreased in the lung of P14 Spp1((-/-)) mice as determined by quantitative RT-PCR analysis. SPP1 promotes pneumocyte growth, and mice lacking SPP1 have smaller, more compliant lungs with enlarged airspace (i.e., increased Lm). Microarray analysis suggests a dysregulation of key lung developmental transcripts in gene-targeted Spp1((-/-)) mice, particularly during the peak phase of alveologenesis. In addition to its known roles in lung disease, this study supports SPP1 as a determinant of lung development in mice.

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R01 HL085655 United States HL NHLBI NIH HHS; HL084932 United States HL NHLBI NIH HHS; HL085655 United States HL NHLBI NIH HHS; R01 HL077763 United States HL NHLBI NIH HHS; HL077763 United States HL NHLBI NIH HHS; R01 HL095397 United States HL NHLBI NIH HHS; HL095397 United States HL NHLBI NIH HHS; P50 HL084932 United States HL NHLBI NIH HHS; U01 ES015675 United States ES NIEHS NIH HHS; ES015675 United States ES NIEHS NIH HHS

Keywords: asthma; chronic obstructive pulmonary disease; emphysema; osteopontin; pulmonary fibrosis

0 (Core Binding Factor Alpha 1 Subunit)
0 (Notch1 protein, mouse)
0 (Receptor, Notch1)
0 (Runx2 protein, mouse)
0 (Spp1 protein, mouse)
106441-73-0 (Osteopontin)

Date Created: 20140513 Date Completed: 20150102 Latest Revision: 20211021

20231215

PMC4224082

10.1165/rcmb.2013-0471OC

24816281