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Neonatal respiratory distress syndrome and underlying mechanisms in cloned cattle
Author(s) -
Rao Yifan,
Sun Xiuzhu,
Yang Na,
Zhang Fanyi,
Jiang Xiaojing,
Huang Linhua,
Guo Xiaogai,
Du Weihua,
Hao Haisheng,
Zhao Xueming,
Jiang Qiuling,
Liu Yan
Publication year - 2018
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.22956
Subject(s) - biology , respiratory distress , homeostasis , pathogenesis , neonatal respiratory distress syndrome , transcription factor , immunology , andrology , endocrinology , medicine , genetics , gene , pregnancy , gestational age , anesthesia
Neonatal respiratory distress is a major mortality factor in cloned animals, but the pathogenesis of this disease is rarely investigated. In this study, four neonatal cloned cattle, born after full‐term gestation, exhibited symptoms of neonatal respiratory distress syndrome (NRDS), which included symptoms of hyaline membrane disease as well as disordered surfactant homeostasis in their collapsed lungs. No differences in DNA methylation or histone modifications correlated with the suppressed SPB and SPC transcription observed in the cloned cattle group ( p > 0.05), whereas TTF‐1 occupancy at SPB and SPC promoter regions in cloned cattle was significantly reduced to 24% and 20% that of normal lungs, respectively ( SPB , p < 0.05; SPC , p < 0.01). Decreased TTF1 expression, dysregulation of SPB and SPC transcription by TTF‐1, and disordered proteolytic processing of Surfactant protein B precursor together potentially contribute to the disruption of surfactant homeostasis and NRDS in bovine clones. Elucidation of the associated mechanisms should facilitate the development of novel preventive or therapeutic strategies to reduce the mortality rate of cloned animals and to improve the efficiency of SCNT technology.