Unknown

Dataset Information

0

Increased expression of pro-inflammatory cytokines at the fetal-maternal interface in bovine pregnancies produced by cloning.


ABSTRACT:

Problem

A significant rate of spontaneous abortion is observed in cattle pregnancies produced by somatic cell nuclear transfer (SCNT). Major histocompatibility complex class I (MHC-I) proteins are abnormally expressed on the surface of trophoblast cells from SCNT conceptuses.

Method of study

MHC-I homozygous compatible (n = 9), homozygous incompatible (n = 8), and heterozygous incompatible (n = 5) pregnancies were established by SCNT. Eight control pregnancies were established by artificial insemination. Uterine and trophoblast samples were collected on day 35 ±1 of pregnancy, the expression of immune-related genes was examined by qPCR, and the expression of trophoblast microRNAs was assessed by sequencing.

Results

Compared to the control group, trophoblast from MHC-I heterozygous incompatible pregnancies expressed increased levels of CD28, CTLA4, CXCL8, IFNG, IL1A, IL2, IL10, IL12B, TBX21, and TNF, while GNLY expression was downregulated. The MHC-I homozygous incompatible treatment group expressed increased levels of IFNG, IL1A, and IL2 while the MHC-I homozygous compatible group did not differentially express any genes compared to the control group. In the endometrium, relative to the control group, MHC-I heterozygous incompatible pregnancies expressed increased levels of CD28, CTLA4, CXCL8, IFNG, IL10, IL12B, and TNF, while GATA3 expression was downregulated. The MHC-I homozygous incompatible group expressed decreased amounts of CSF2 transcripts compared with the control group but did not have abnormal expression of any other immune-related genes. MHC-I incompatible pregnancies had 40 deregulated miRNAs compared to control pregnancies and 62 deregulated microRNAs compared to MHC-I compatible pregnancies.

Conclusions

MHC-I compatibility between the dam and fetus prevented an exacerbated maternal immune response from being mounted against fetal antigens.

SUBMITTER: Rutigliano HM 

PROVIDER: S-EPMC9285385 | biostudies-literature |

REPOSITORIES: biostudies-literature

Similar Datasets

| S-EPMC471570 | biostudies-literature
| S-EPMC7203721 | biostudies-literature
| S-EPMC9573150 | biostudies-literature
| S-EPMC3935001 | biostudies-literature
| S-EPMC8155594 | biostudies-literature
| S-EPMC11198379 | biostudies-literature
| S-EPMC4302218 | biostudies-literature
| S-EPMC7879580 | biostudies-literature
| S-EPMC7571453 | biostudies-literature
| S-EPMC5944101 | biostudies-literature