PMID- 8895364
OWN - NLM
STAT- MEDLINE
DCOM- 19961217
LR  - 20071114
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 137
IP  - 11
DP  - 1996 Nov
TI  - Tumor necrosis factor-alpha: a multifunctional regulator of mammary gland 
      development.
PG  - 4915-24
AB  - To determine whether tumor necrosis factor-alpha (TNF alpha) plays a 
      physiological role in normal mammary gland development, TNF alpha and TNF 
      receptor expression were measured in epithelial cells (MEC) isolated from mammary 
      glands of virgin, pregnant, lactating, and postlactational (day 7 of involution) 
      rats. TNF alpha messenger RNA (mRNA) increased significantly during pregnancy, 
      then decreased during lactation and involution. The 26-kDa transmembrane form of 
      TNF alpha protein, undetectable in MEC from virgin rats, increased throughout 
      pregnancy and lactation, and disappeared during involution. In contrast, p55 TNF 
      receptor (TNFR) mRNA levels peaked in early lactation and declined thereafter, 
      whereas p75 TNFR mRNA levels rose steadily through lactation. Using agonistic 
      antibodies specific to either TNFR, the individual roles of each TNFR were 
      investigated in MEC in primary culture. The p55 TNFR was found to be the sole 
      mediator of TNF alpha-induced proliferation. Intriguingly, the two receptors were 
      found to have opposing effects on functional differentiation (casein 
      accumulation), with inhibition occurring through the p55 receptor and stimulation 
      through the p75 receptor. Taken together, these results suggest that TNF alpha 
      plays a role in the growth and development of the mammary gland. In addition, 
      both TNF receptors are important for TNF alpha function and may mediate different 
      effects.
FAU - Varela, L M
AU  - Varela LM
AD  - Grace Cancer Drug Center, Roswell Park Cancer Institute, Buffalo, New York 14263, 
      USA.
FAU - Ip, M M
AU  - Ip MM
LA  - eng
GR  - CA-09072/CA/NCI NIH HHS/United States
GR  - CA-16056/CA/NCI NIH HHS/United States
GR  - CA-57317/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Antibodies)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 62229-50-9 (Epidermal Growth Factor)
SB  - IM
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Epidermal Growth Factor/pharmacology
MH  - Epithelial Cells
MH  - Epithelium/metabolism
MH  - Female
MH  - Lactation/physiology
MH  - Mammary Glands, Animal/cytology/metabolism/*physiology
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Organoids/metabolism
MH  - Postpartum Period
MH  - Pregnancy
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Tumor Necrosis Factor/*biosynthesis
MH  - *Transcription, Genetic/drug effects
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/pharmacology
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
AID - 10.1210/endo.137.11.8895364 [doi]
PST - ppublish
SO  - Endocrinology. 1996 Nov;137(11):4915-24. doi: 10.1210/endo.137.11.8895364.