Integrated proteomic and transcriptomic landscape of human placenta in small for gestational age infants
Heyue Jin,
Xianyan Wang,
Lingyu Li,
Chen Rui,
Hong Gan,
Qunan Wang,
Fangbiao Tao,
Yumin Zhu
Affiliations
Heyue Jin
Department of Maternal & Child and Adolescent Health, School of Public Health, MOE Key Laboratory of Population Health Across Life Cycle, Anhui Provincial Key Laboratory of Population Health and Aristogenics, Anhui Medical University, Hefei, Anhui 230032, China; Medical School, Nanjing University, Nanjing, Jiangsu 210093, China
Xianyan Wang
Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, Anhui 230032, China
Lingyu Li
Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, Anhui 230032, China
Chen Rui
Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, Anhui 230032, China
Hong Gan
Department of Maternal & Child and Adolescent Health, School of Public Health, MOE Key Laboratory of Population Health Across Life Cycle, Anhui Provincial Key Laboratory of Population Health and Aristogenics, Anhui Medical University, Hefei, Anhui 230032, China
Qunan Wang
Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, Anhui 230032, China; Corresponding author
Fangbiao Tao
Department of Maternal & Child and Adolescent Health, School of Public Health, MOE Key Laboratory of Population Health Across Life Cycle, Anhui Provincial Key Laboratory of Population Health and Aristogenics, Anhui Medical University, Hefei, Anhui 230032, China; Corresponding author
Yumin Zhu
Medical School, Nanjing University, Nanjing, Jiangsu 210093, China; Corresponding author
Summary: Small for gestational age (SGA) infants affected by placental insufficiency are exposed to the risk of stillbirth and long-term complications. Based on RNA-seq and mass spectrometry, we identified dysregulated RNAs and proteins from the comparisons of SGA placental tissues and controls. We revealed two SGA-relevant co-expression modules (SRMs) that also significantly distinguished SGA from controls. Then we performed an integrated analysis of transcriptomic and proteomic profiles to trace their links to SGA as well as their significant correlations. For the core functional molecules we screened, we revealed their potential upstream regulators and validated them experimentally in an independent cohort. Overall, we pointed out insights into different molecular pathways for the pathological mechanisms of SGA and indicated potential target molecules that may be drivers of placental aberrations in the SGA infants.
