📖 ABSTRACT/OVERVIEW
Rumen epithelial cells are continuously exposed to mechanical distension from fermentation gas and fluid, osmotic fluctuations from feedstuff, and short-chain fatty acid concentrations that vary dynamically with diet composition. Mechanotransduction, the process by which mechanical stimuli are converted to cellular biochemical signals, is fundamental to rumen epithelial adaptation, including the regulation of volatile fatty acid absorption, tight junction integrity, and proliferative responses. In Nigerian cattle managed on diverse diets ranging from dry savannah grasses in the North to root crops and brewery waste in the South, rumen epithelial mechanotransduction may vary substantially. This study characterised mechanotransduction signalling pathways in primary rumen epithelial cells isolated from White Fulani, N'Dama, and Friesian crossbred cattle from farms in Kaduna, Edo, and Ogun states respectively, and exposed them to controlled osmotic stress of 400 mOsm versus 300 mOsm control, uniaxial cyclic mechanical stretch at 10 and 20 percent elongation, and increasing butyrate concentrations. Pathway analysis focused on integrin-focal adhesion kinase, mitogen-activated protein kinase, and mammalian target of rapamycin signalling axes by western blotting, immunofluorescence, and phosphoproteomics. White Fulani-derived cells showed significantly higher basal FAK phosphorylation and greater mTOR pathway activation under osmotic stress than Friesian crossbred cells. N'Dama cells demonstrated superior tight junction maintenance under mechanical stretch assessed by transepithelial electrical resistance. Butyrate-induced mTOR activation was breed-dependent. These mechanistic findings reveal breed-specific differences in rumen epithelial mechanotransduction with implications for dietary management recommendations, rumen acidosis susceptibility, and biotechnological manipulation of rumen physiology in Nigerian cattle systems. Keywords: mechanotransduction, rumen epithelium, mechanobiology, cattle breeds, mTOR.
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