Abstract
Hoxa1 mutation adversely affect fetal pig development, but whether all-trans retinoic acid (ATRA) administration to Hoxa1+/− pregnant sows can improve Hoxa1−/− fetal pig development defects has not been reported. A total of 24 healthy Hoxa1+/− sows were mated with a healthy Hoxa1+/− boar and randomly assigned to one control group and nine experiment groups. ATRA was orally administered to pregnant sows at the doses of 0, 4, 5, or 6 mg/kg maternal body weight on 12, 13, and 14 days post coitum (dpc), respectively, and a total of 146 live piglets were delivered including 37 Hoxa1−/− piglets and 109 non-Hoxa1−/− piglets. Results indicated that Hoxa1−/− piglets delivered by sows in control group had bilateral microtia, canal atresia and ear's internal defects, and had lower birth liveweight and external ear score than non-Hoxa1−/− neonatal piglets (P < 0.05). Maternal administration with ATRA can effectively correct the development defects of Hoxa1−/− fetal pigs, Hoxa1−/− neonatal piglets delivered by sows administered ATRA at a dose of 4 mg/kg body weight on 14 dpc had higher birth liveweight (P > 0.05) and higher scores of external ear (P < 0.05) compared to Hoxa1−/− neonatal piglets from the control group, but had no significantly difference in terms of birth liveweight and external ear integrity than non-Hoxa1−/− piglets from the control group (P > 0.05). The time of ATRA administration significantly affected Hoxa1−/− fetal development (P < 0.05). Administration of ATRA to Hoxa1+/− pregnant sows at 4 mg/kg body weight on 14 dpc can effectively improve the birth liveweight and ear defects of Hoxa1−/− piglets.
Highlights
Gene mutations, nutrition imbalance or adverse maternal environments may lead to abnormal development or death of fetuses [1,2,3]
While there was no significant difference in average birth weight of Hoxa1−/− piglets among control group and experimental
Groups (P > 0.05) with an exception of group 2 (G2), Hoxa1−/− piglets delivered by sows of G2 had a significant lower average birth liveweight than Hoxa1−/− piglets from group 7 (G7) and group 9 (G9), respectively (P < 0.05) but had no significant lower average birth liveweight compared to Hoxa1−/− piglets from other groups (P > 0.05)
Summary
Nutrition imbalance or adverse maternal environments may lead to abnormal development or death of fetuses [1,2,3]. Hox cluster genes regulate the migration and differentiation of cranial neural crest cells (CNCC) and embryonic patterning, thereby vitally impacting fetal organogenesis during embryonic development [4, 5]. Mutations of hox family genes may cause abnormal CNCC migration and in turn result in abnormal development of fetus [6,7,8]. Hoxa mutations can lead to auricle loss and external auditory canal damage [10, 11] and to cardio-cerebrovascular abnormalities [12, 13]. G>TC results in abnormal auricle and external auditory canal, dyspnea, and even death in newborn piglets [15] Qiao et al [15] firstly reported that the Hoxa mutation of g.50111251 G>TC results in abnormal auricle and external auditory canal, dyspnea, and even death in newborn piglets [15]
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