The extracellular matrix modulates asynchronous concurrent lactation in tammar wallaby (Macropus eugenii)

The extracellular matrix modulates asynchronous concurrent lactation in tammar wallaby (Macropus eugenii) In contrast to eutherians, the reproductive cycle of the tammar wallaby (Macropus eugenii) consists of a short gestation (P1) leading to the birth of an altricial young and a long lactation. Tammar lactation has previously been divided into three post-parturition phases (2A, 2B and 3) characterised by progressive remodelling of the mammary gland and profound changes in milk composition. After milk stasis the mammary gland progresses to involution (INV) and reverts to resemble a pre-pregnancy state. During phases 2A and 2B the mammary gland is relatively small in size and produces small amounts of milk that is rich in carbohydrates but low in protein and lipids. Phase 3 is marked by an enlarged mammary gland secreting large volumes of milk that is rich in protein and lipid. Interestingly the wallaby is capable of asynchronous concurrent lactation (ACL) whereby the mother produces milk of different composition from adjacent mammary glands. This process may provide new insights into understanding local control of mammary epithelial cell function. Because of the key role that the extracellular matrix (ECM) plays in mammary structure and function, it may be hypothesized that differences in ECM composition between the adjacent glands provides the molecular mechanism regulating ACL. Wallaby mammary epithelial cells (WallMEC’s) extracted from P2A and P2B mammary tissues were cultured on ECM from P1, P2A, P2B, P3 and INV tissues and the expression of the phase specific markers tELP, tWAP, and tLLP-B genes representing phases 2A, 2B and 3 of tammar lactation respectively used to determine change in phenotype of the cells. WAllMEC’s extracted from phase 2B acquired phase 3 phenotype when grown on phase 3 ECM. Similarly P2A cells acquired P2B phenotype when cultured on P2B ECM. We also observed that the composition of ECM is lactation phase dependent. Intact, high molecular weight ECM proteins were observed in the earlier phases of lactation while the low molecular weight, monomeric or breakdown products of the major ECM proteins progressively increased from P1 through to INV. This study shows that progressive changes in ECM during lactation are most likely crucial for temporal, local regulation of milk protein expression and may modulate ACL.

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