title: Chronic hypoxia in pregnancy affects thymus development in Balb/c mouse offspring via IL2 Signaling.
abstract: Hypoxia during pregnancy can adversely affect development. This study, addressed the impact of prenatal hypoxia on thymus development in the rodent offspring. Pregnant Balb/c mice were exposed to hypoxia or normoxia during pregnancy, and the thymuses of their offspring were tested. Chronic hypoxia during pregnancy resulted in significantly decreased fetal body weight, with an increased thymus-to-body weight ratio. Histological analysis revealed a smaller cortical zone in the thymus of the offspring exposed to hypoxia. A reduction in the cortical T lymphocyte population corresponded to increased mRNA abundance of caspase 3 (Casp3) and decreased expression of the proliferation marker Ki-67 (Mki67). Differences in T lymphocyte sub-populations in the thymus further indicate that thymus development in offspring was retarded or stagnated by prenatal hypoxia. The abundance of IL2 and its receptor was reduced in the thymus following prenatal hypoxia. This was accompanied by an increase in thymus HIF1A and IKKβ and a decrease in phosphorylated NFKB, MAP2K1, and MAPK1/3 compared to control pregnancies. Together, these results implicate deficiencies in IL2-mediated signaling as one source of prenatal-hypoxia-impaired thymus development.
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Xiaopeng
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Xiuwen
authors.initials: X
authors.lastname: Zhou
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Lingjun
authors.initials: L
authors.lastname: Li
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Sun
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Qingqing
authors.initials: Q
authors.lastname: Gao
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Pengjie
authors.initials: P
authors.lastname: Zhang
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Jiaqi
authors.initials: J
authors.lastname: Tang
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: He
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.
authors.forename: Di
authors.initials: D
authors.lastname: Zhu
authors.affiliation: Institute for Fetology, First Hospital of Soochow University, Suzhou, China.|Center for Perinatal Biology, Loma Linda University, California.
authors.forename: Zhice
authors.initials: Z
authors.lastname: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis; D049109:Cell Proliferation; D005260:Female; D020567:Fetal Weight; D000860:Hypoxia / Q000150:complications* / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism*; D038041:Lymphopoiesis; D051379:Mice; D008807:Mice, Inbred BALB C; D009929:Organ Size; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism*; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000378:metabolism / Q000473:pathology; D013950:Thymus Gland / Q000196:embryology* / Q000473:pathology
chemical_list: D007376:Interleukin-2