Ontogenic and nutritional regulation of steroid receptor and IGF-I transcript abundance in the prepubertal heifer mammary gland.
In prepubertal cattle, mammary development is characterized by the growth of an epithelial-rich parenchyma (PAR) into the mammary fat pad (MFP). This proliferation and accumulation of mammary epithelial cells require estrogen. Paradoxically, both epithelial cell proliferation and PAR accumulation rate decline with rising plasma estrogen as puberty approaches. The possibility that variation in abundance of estrogen receptors (ERs) in PAR or MFP accounts for a portion of these effects has not been examined in cattle. Additionally, we recently demonstrated that MFP is highly responsive to exogenous estrogen, suggesting that this tissue may play a role in coordinating estrogen's effects on PAR; however, the developing bovine MFP has yet to be studied in detail. To address these hypotheses, Holstein heifers were assigned to planes of nutrition supporting body growth rates of 950 (E) or 650 (R) g/day and harvested every 50 kg from 100 to 350 kg body weight (BW). Post-harvest, their mammary glands were dissected into PAR and MFP compartments. Transcript abundance of genes encoding members of the ER family (ERalpha, ERbeta, and estrogen-related receptor alpha-1 (ERRalpha)) and estrogen-responsive genes (IGF-I and progesterone receptor (PR)) were measured in both mammary compartments by quantitative real-time RT-PCR. Significant expression was detected for all genes in both compartments, with the exception of the ERbeta gene. Transcript abundance of both ERalpha and IGF-I decreased linearly with increasing BW within both compartments. ERRalpha and PR expressions decreased with increasing BW in PAR but not in MFP. Nutrition stimulated ERalpha and ERRalpha expression in the PAR but had no effect on IGF-I or PR in either PAR or MFP. Overall, ERalpha and IGF-I transcript abundance are consistent with the drop in mammary epithelial cell proliferation and PAR accretion observed over development, but do not support a negative effect of nutrition on PAR growth.
Meyer
M J
MJ
Department of Animal Science, Cornell University, 272 Morrison Hall, Ithaca, New York 14850, USA.
Rhoads
R P
RP
Capuco
A V
AV
Connor
E E
EE
Hummel
A
A
Boisclair
Y R
YR
Van Amburgh
M E
ME
D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001835:Body Weight; D002417:Cattle; D049109:Cell Proliferation; D004847:Epithelial Cells / Q000166:cytology / Q000378:metabolism; D047628:Estrogen Receptor alpha / Q000032:analysis / Q000235:genetics; D047629:Estrogen Receptor beta / Q000032:analysis / Q000235:genetics; D005260:Female; D015870:Gene Expression; D007150:Immunohistochemistry; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000235:genetics; D008321:Mammary Glands, Animal / Q000254:growth & development* / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000032:analysis* / Q000235:genetics; D011980:Receptors, Progesterone / Q000032:analysis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D012741:Sexual Maturation; D000097983:ERRalpha Estrogen-Related Receptor
D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D007334:Insulin-Like Growth Factor I; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D000097983:ERRalpha Estrogen-Related Receptor