Lactation persistency: Insights from mammary cell proliferation studies

A. V. Capuco*, S. E. Ellis§, S. A. Hale¶, E. Long†, R. A. Erdman¶, X. Zhao#, and M. J. Paape‡
*Gene Evaluation and Mapping Laboratory; †Germplasm and Gamete Physiology Laboratory; ‡Immunology and Disease Resistance Laboratory, Animal and Natural Resources Institute, USDA, ARS, Beltsville, MD 20705; §Animal and Veterinary Sciences Department, Clemson University, Clemson SC 29634; ¶Department of Animal and Avian Sciences, University of Maryland, College Park 20742; and #Department of Animal Science, McGill University, Ste. Anne de Bellevue, Quebec H9X 3V9 Canada

ABSTRACT A persistent lactation is dependent on maintaining the number and activity of milk secreting cells with advancing lactation. When dairy cows are milked twice daily, the increase in milk yield from parturition to peak lactation is due to increased secretory activity per cell rather than to accretion of additional epithelial cells. After peak lactation, declining milk yield is due to loss of mammary epithelial cells by apoptosis. During lactation, only 0.3% of mammary cells proliferate in a 24-h period. Yet this proliferative rate is sufficient to replace most mammary epithelial cells by the end of lactation. Management practices can influence lactation persistency. Administration of bovine somatotropin may enhance persistency by increasing cell proliferation and turnover, or by reducing the rate of apoptosis. Increased photoperiod may also increase persistency of lactation by mechanisms that are as yet undefined. Increased milking frequency during the first weeks of lactation increases milk yield, even after return to less frequent milking, with increases of approximately 8% over the entire lactation. A mammary cell proliferation response to frequent milking during early lactation appears to be involved. Conversely, advanced pregnancy, infrequent milking, and mastitis increase death of epithelial cells by apoptosis. Regulation of mammary cell renewal provides a key to increasing persistency. Investigations to characterize epithelial cells that serve as the proliferative population in the bovine mammary gland have been initiated. Epithelial cells that stain lightly in histological sections are evident through all phases of mammary development and secretion and account for nearly all proliferation in the prepubertal gland. Characterization of these cells may provide a means to regulate mammary cell proliferation and thus to enhance persistency, reduce the effects of mastitis, and decrease the necessity for a dry period.

Key Words: Apoptosis, Cell proliferation, Cell renewal, Lactation Efficiency, Ruminants

© 2003, by the American Society of Animal Science. All rights reserved.

J. Anim. Sci. 2003. 81(Suppl. 3):18-31

Implications

Increasing the mammary gland's ability to replace those cells that die during lactation is key to enhancing persistency. The proliferative population of mammary epithelial cells has been identified in histological sections as lightly staining cells. Epithelial cells with this staining characteristic are evident during all stages of mammary development and function. Development of markers for these cells and their further characterization may provide important keys to manipulating cell proliferation to enhance mammary development and lactational persistency. Because apoptosis is typically very low in the lactating gland, mechanisms to globally reduce mammary apoptosis will be difficult to evaluate and perhaps of minimal value. However, treatments to minimize apoptosis during mastitis may be of particular importance. The complexity of pathways for regulating mammary cell proliferation and apoptosis provides a challenge to comprehensive understanding, but also provides opportunities for developing novel regulatory strategies to reduce the length of the dry period and increase lactational persistency. Manipulation of these processes can be achieved through transgenic approaches, manipulation of hormonal and paracrine factors, and selection for naturally occurring genetic polymorphisms.


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