Changes in the Rumen Papillae During the Periparturient Transition in Holstein Dairy Cows are Accompanied by Changes in Abundance of Proteins Involved in Intracellular pH Regulation, But not SCFA Transport

摘要

The objective of this study was to examine changes in SCFA transport capacity in the rumen epithelium during the parturition transition period. Twelve pregnant, cannulated primiparous and multiparous cows were fed a standard Total Mixed Ration (TMR)for the duration of the dry period; after calving, all cows were switched to an early lactation TMR. Rumen pH, fluid and biopsies were taken 3 weeks before anticipated calving (PRE), 1 week after actual calving (PERI) and 6 weeks after calving (POST). Rumen biopsies were analyzed for transport protein abundance using immunofluorescence. Immunofluorescence analysis showed no significant changes in the abundance of monocarboxylate co-transporter, isoform 1 among the PRE, PERI and POST periods (16878±1555A.U., 15613±1508 A.U. and 16886±1555 A.U. respectively; MCT1). Also, sodium/proton exchanger, isoform 3 (NHE3) was not significantly different among the PRE, PERI and POST periods (10467±1066 A.U., 9465±1066 A.U., 8552±1109 A.U., respectively). Sodium/Bicarbonate Co-transporter, isoform 1 (NBC1) was likewise unaffected by time, with the protein abundance among PRE, PERI and POST parturition periods changing from 16467±1274 A.U., 13983±1318 A.U. and 15047± 1324 A.U., respectively. Abundance of Carbonic Anhydrase, isoform 2 (CA2) decreased from 12332±1580 A.U (PRE) to 7235±1580 (PERI) and 8121±1643 (POST) and this decrease was significant (p = 0.01 PRE v. PERI). The observed changes in protein abundance suggest that long-term adaptation of the rumen epithelium occurs to increase transport capacity. Decreased CA2 abundance suggests that intracellular acidification is occurring as part of epithelial remodelling. Taken together, this implies that, during the periparturient transition, a decrease in rumen pH leads to a decrease in intracellular pH in the rumen epithelium, promoting epithelial remodelling that result in increased SCFA transport capacity.