AI Article Synopsis

  • The study analyzed immune response and gene expression changes at the fetal-maternal interface in sheep pregnancies created by somatic cell nuclear transfer (SCNT), comparing them to natural breeding controls.
  • At term, significant alterations in gene expression related to apoptosis, growth factors, and immune response were found in the placental and endometrial tissues of SCNT pregnancies, indicating potential placental dysfunction.
  • By Day 45, only minor changes were observed, primarily in apoptosis and growth factor-related genes, while early endometrial gene expression was largely similar to controls.

Article Abstract

The hypothesis of this study was that the leukocyte populations and expression levels of genes related to immune response, growth factors and apoptosis would be altered at the fetal-maternal interface in somatic cell nuclear transfer (SCNT)-generated sheep pregnancies. Placental and endometrial samples from sheep pregnancies established by SCNT and natural breeding (control) were collected at 45 days and at term. Expression of genes related to growth factors, apoptosis and immune response was examined using quantitative reverse transcription polymerase chain reaction. Endometrial leukocyte populations and major histocompatibility class I (MHC-I) protein expression were examined by immunohistochemistry. At term we observed altered expression of genes related to apoptosis, growth factors and immune response in placental and endometrial tissue of SCNT pregnancies. In Day-45 pregnancies there was less-pronounced abnormal expression and only genes related to apoptosis and growth factors were abnormal in the placenta. Endometrial gene expression profiles were similar to age-matched controls. Placental MHC-I protein expression was similar in SCNT and controls at 45 days but increased in the SCNT at term. The altered gene expression at the fetal-maternal interface likely contributes to the placental dysfunction and overgrowth observed in sheep SCNT pregnancies.

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http://dx.doi.org/10.1071/RD17224DOI Listing

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