Physiology Mammary gland

1 physiology

1.1 hormonal control
1.2 pregnancy
1.3 weaning

physiology
hormonal control

lactiferous duct development occurs in females in response circulating hormones. first development seen during pre- , postnatal stages, , later during puberty. estrogen promotes branching differentiation, whereas in males testosterone inhibits it. mature duct tree reaching limit of fat pad of mammary gland comes being bifurcation of duct terminal end buds (teb), secondary branches sprouting primary ducts , proper duct lumen formation. these processes tightly modulated components of mammary epithelial ecm interacting systemic hormones , local secreting factors. however, each mechanism epithelial cells niche can delicately unique different membrane receptor profiles , basement membrane thickness specific branching area area, regulate cell growth or differentiation sub-locally. important players include beta-1 integrin, epidermal growth factor receptor (egfr), laminin-1/5, collagen-iv, matrix metalloproteinase(mmps), heparan sulfate proteoglycans, , others. elevated circulating level of growth hormone , estrogen multipotent cap cells on teb tips through thin, leaky layer of basement membrane. these hormones promote specific gene expression. hence cap cells can differentiate myoepithelial , luminal (duct) epithelial cells, , increased amount of activated mmps can degrade surrounding ecm helping duct buds reach further in fat pads. on other hand, basement membrane along mature mammary ducts thicker, strong adhesion epithelial cells via binding integrin , non-integrin receptors. when side branches develop, more “pushing-forward” working process including extending through myoepithelial cells, degrading basement membrane , invading periductal layer of fibrous stromal tissue. degraded basement membrane fragments (laminin-5) roles lead way of mammary epithelial cells migration. whereas, laminin-1 interacts non-integrin receptor dystroglycan negatively regulates side branching process in case of cancer. these complex yin-yang balancing crosstalks between mammary ecm , epithelial cells instruct healthy mammary gland development until adult.

there preliminary evidence soybean intake mildly stimulates breast glands in pre- , postmenopausal women.

pregnancy

secretory alveoli develop in pregnancy, when rising levels of prolactin, estrogen, , progesterone cause further branching, increase in adipose tissue , richer blood flow. in gestation, serum progesterone remains @ stably high concentration signaling through receptor continuously activated. 1 of transcribed genes, wnts secreted mammary epithelial cells act paracrinely induce more neighboring cells branching. when lactiferous duct tree ready, leaves alveoli differentiated luminal epithelial cells , added @ end of each branch. in late pregnancy , first few days after giving birth, colostrum secreted. milk secretion (lactation) begins few days later due reduction in circulating progesterone , presence of important hormone prolactin, mediates further alveologenesis, milk protein production, , regulates osmotic balance , tight junction function. laminin , collagen in myoepithelial basement membrane interacting beta-1 integrin on epithelial surface again, essential in process. binding ensures correct placement of prolactin receptors on basal lateral side of alveoli cells , directional secretion of milk lactiferous ducts. suckling of baby causes release of hormone oxytocin, stimulates contraction of myoepithelial cells. in combined control ecm , systemic hormones, milk secretion can reciprocally amplified provide enough nutrition baby.

weaning

during weaning, decreased prolactin, missing mechanical stimulation (baby suckling), , changes in osmotic balance caused milk stasis , leaking of tight junctions cause cessation of milk production. (passive) process of child or animal ceasing dependent on mother nourishment. in species there complete or partial involution of alveolar structures after weaning, in humans there partial involution , level of involution in humans appears highly individual. glands in breast secrete fluid in nonlactating women. in other species (such cows), alveoli , secretory duct structures collapse programmed cell death (apoptosis) , autophagy lack of growth promoting factors either ecm or circulating hormones. @ same time, apoptosis of blood capillary endothelial cells speeds regression of lactation ductal beds. shrinkage of mammary duct tree , ecm remodeling various proteinase under control of somatostatin , other growth inhibiting hormones , local factors. major structural change leads loose fat tissue fill empty space afterward. functional lactiferous duct tree can formed again when female pregnant again.