Expression and single nucleotide polymorphisms of vitamin D receptor gene in cows with puerperal metritis in Egypt

The aim of this work is to study the expression profile of the vitamin D receptor (VDR), 1-alpha hydroxylase enzyme, and chemokine regulated on activation normal T-cell expressed and secreted genes (RANTES) genes in dairy cows with puerperal metritis, as well as to study the association between polymorphisms in the VDR gene and occurrence of such disease condition, which is considered a key to advances in the preventive medicine for such a problem in the future. Blood samples were collected from 60 dairy cows; from which 48 dairy cows proved to suffer puerperal metritis and other 12 apparently healthy recent parturient dairy cows were selected randomly for assessment the fold change variation in the expression profiles of the studied genes. Depending on the clinical examination, the normal cut-off point of the serum calcium, phosphorus, glucose, magnesium, potassium, sodium, and chloride, and the normal reference values of parathyroid hormone (PTH), 18 out of 48 dairy cows suffered puerperal metritis with a normal metabolic profile, which underwent further molecular analysis. In the studied dairy cows that suffered puerperal metritis with a normal metabolic profile, the expression pattern of the VDR and RANTES genes showed a significant up-regulation (P < 0.05), whereas the expression pattern of 1 alpha-hydroxylase enzyme gene showed a significant down-regulation (P < 0.05) in comparison with those of healthy recent parturient dairy cows. The sequenced regions of the VDR gene (exon 7, partial intron 6, partial intron 7) didn't exhibit polymorphisms in their nucleotide sequence, and consecutively their amino acid sequence when compared to the published sequence on the gene bank. The results propose that the VDR gene (exon 7, partial intron 6, partial intron 7) polymorphisms do not play a role in the pathogenesis of puerperal metritis in dairy cows, excluding a role of the vitamin Din puerperal metritis. (C) 2022 Elsevier Inc. All rights reserved.