Down-regulation of milk synthesis through PA-PG-PL system: an adaptation mechanism during heat stress

Dairy farming plays an important role in strengthening the rural economy. It provides supplementary employment, an additional source of income to many small and marginal farmers, household nutrition security. However, heat is a major constraint on animal productivity in the tropical belt and arid areas. The negative effects of global warming will be manifest in animal agriculture of both developed and developing countries. According to IPCC predictions, the global average surface temperature may increase between 1.8 and 4°C by year 2100. Under such circumstances, milk production is impaired as a result of the drastic changes in biological functions under heat stress. Heat stress in dairy cows as all temperature-related forces encourage changes or adjustments which may occur from the cellular to the total animal level to help the cows stay away from physiological disorders and then to better adapt to an adverse thermal environment. Such adaptation involves activation of the hypothalamus-pituitary-adrenocortical axis by external stress, liberating cortisol into blood plasma, which in turn induces the liberation of plasminogen activator (PA) from the mammary epithelial cells into the mammary cistern, where it activates the plasminogen-plasmin (PG-PL) system. Thus this PA-PG-PL system is a milk-borne factor which down regulates the milk secretion during the heat stress. This negative feedback system specifically forms β-casein (CN) fragment (f) (1–28) from β-CN, which acts as the negative control signal by closing potassium channels on the apical membrane of the epithelial cells of mammary gland. Along with that, this caseinophosphopeptides through their phospho-serine residues can bind 20 to 40 moles of Ca2+ which is essential for maintaining the tight junction integrity of the mammary secretory epithelium. As a result, disruption of the integrity of mammary epithelial cell tight junction depresses milk yield. Determination of such adaptation of animals to thermal stress opens new opportunities as means of improving thermal tolerance. Further research is needed, to determine the nature of the interaction of β-CN f (1–28) with regulatory elements in the apical membrane of mammary gland epithelial cells, and to identify these channels and the components of the inward signal transduction. However, continued research evaluating methods to improve productive performance of thermally stress animals is warranted.