期刊
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
卷 309, 期 11, 页码 E936-E948出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00329.2015
关键词
beta-thalassemia; bone histomorphometry; bone mineral density; osteoporosis
资金
- Mahidol University
- Thailand Research Fund (TRF)-Mahidol University through the TRF Senior Research Scholar Grant [RTA5780001]
- Thailand Research Fund-Mahidol University through the Royal Golden Jubilee Ph.D. Program [PHD/0352/2550]
- Faculty of Science, Mahidol University
- National Science and Technology Development Agency, Thailand
beta-Thalassemia, a hereditary anemic disorder, is often associated with skeletal complications that can be found in both males and females. The present study aimed to investigate the age-and sex-dependent changes in bone mineral density (BMD) and trabecular microstructure in beta(IVSII-654) knockin thalassemic mice. Dual-energy X-ray absorptiometry and computer-assisted bone histomorphometry were employed to investigate temporal changes in BMD and histomorphometric parameters in male and female mice of a beta(IVSII-654) knockin mouse model of human beta-thalassemia, in which impaired splicing of beta-globin transcript was caused by hemizygous C -> T mutation at nucleotide 654 of intron 2. Young, growing beta(IVSII-654) mice (1 mo old) manifested shorter bone length and lower BMD than their wild-type littermates, indicating possible growth retardation and osteopenia, the latter of which persisted until 8 mo of age (adult mice). Interestingly, two-way analysis of variance suggested an interaction between sex and beta(IVSII-654) genotype, i.e., more severe osteopenia in adult female mice. Bone histomorphometry further suggested that low trabecular bone volume in male beta(IVSII-654) mice, particularly during a growing period (1-2 mo), was primarily due to suppression of bone formation, whereas both a low bone formation rate and a marked increase in osteoclast surface were observed in female beta(IVSII-654) mice. In conclusion, osteopenia and trabecular microstructural defects were present in both male and female beta(IVSII-654) knockin thalassemic mice, but the severity, disease progression, and cellular mechanism differed between the sexes.
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