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Moderate hyperoxia inhibits glomus cell proliferation in the carotid body of neonatal rats
Author(s) -
Broge Thomas A,
Dmitrieff Elizabeth F,
Piro Samantha E,
Bavis Ryan W
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.961.2
Subject(s) - hyperoxia , carotid body , glomus cell , tunel assay , apoptosis , andrology , endocrinology , medicine , lung , biology , immunohistochemistry , carotid arteries , biochemistry
Rats exposed to hyperoxia during the perinatal period exhibit smaller carotid bodies with fewer O 2 ‐sensitive glomus cells as adults (Erickson et al., 1998, J. Physiol. 509: 519‐26). To study the time course and mechanisms underlying these changes, rats were exposed to 60% O 2 or room air from birth and their carotid bodies were harvested at various postnatal ages (P1‐P7, P14) for histological analysis (n=6 per age per treatment). The carotid bodies of hyperoxia‐treated rats were significantly smaller than those of age‐matched controls beginning at P4. Additional pups were injected with BrdU at P1, P3 and P5 and assayed for cumulative cell division 24 hours later (i.e., at P2, P4 and P6). The proportion of glomus cells that were BrdU‐positive was significantly reduced by hyperoxia at P4 (9±1% (SEM) vs. 28±3%; P <0.001); a similar trend was observed at P2 but not at P6. TUNEL staining was used to assess cell death at P2, P4 and P6. The proportion of glomus cells that were TUNEL‐positive was low at all ages but somewhat greater in hyperoxia‐treated rats (0.9±0.1% vs. 0.3±0.1% across ages; P <0.01). These data indicate that hyperoxia attenuates postnatal growth of the carotid body by inhibiting glomus cell proliferation during the first few days of exposure, although hyperoxia‐induced apoptosis may also contribute to the smaller carotid body size. Supported by NIH grant P20 RR‐016463 (Maine INBRE).