TY - JOUR
T1 - Effects of sex steroids on the proliferation of thymic epithelial cells in a culture model
T2 - A role of protein kinase C
AU - SAKABE, KOU
AU - KAWASHIMA, ISSEI
AU - URANO, RIE
AU - SEIKI, KANJI
AU - Itoh, Tsunetoshi
PY - 1994/1/1
Y1 - 1994/1/1
N2 - Using a rat thymic epithelial cell line (TEC; IT‐45R1), the present study attempted to elucidate the mechanism of action of sex steroid hormones (SH) on the proliferation of TEC The findings were as follows: (a) the proliferation of TEC in response to SH was mediated through protein kinase C activity introduced as a result of interaction between SH and plasma‐borne inhibitors; (b) the strong inhibitory effect of SH on TEC proliferation might be mediated through the SH receptor pathway because the proliferative response was triggered by progesterone (P) and androgen (A), whereas the inhibitory response was triggered by P, A and oestrogen. These results clearly suggest that the control of TEC proliferation is a ‘shut‐off’ mechanism triggered by high plasma levels of SH. This further refers to the speculation that the development of the normal thymus may be due to a lack of this ‘shut‐off’ mechanism so that development occurs at the adequate plasma SH levels that are often observed before puberty. However, this development is inhibited at the high plasma SH levels after puberty and/or during pregnancy.
AB - Using a rat thymic epithelial cell line (TEC; IT‐45R1), the present study attempted to elucidate the mechanism of action of sex steroid hormones (SH) on the proliferation of TEC The findings were as follows: (a) the proliferation of TEC in response to SH was mediated through protein kinase C activity introduced as a result of interaction between SH and plasma‐borne inhibitors; (b) the strong inhibitory effect of SH on TEC proliferation might be mediated through the SH receptor pathway because the proliferative response was triggered by progesterone (P) and androgen (A), whereas the inhibitory response was triggered by P, A and oestrogen. These results clearly suggest that the control of TEC proliferation is a ‘shut‐off’ mechanism triggered by high plasma levels of SH. This further refers to the speculation that the development of the normal thymus may be due to a lack of this ‘shut‐off’ mechanism so that development occurs at the adequate plasma SH levels that are often observed before puberty. However, this development is inhibited at the high plasma SH levels after puberty and/or during pregnancy.
KW - plasma‐borne inhibitor
KW - proliferation
KW - protein kinase C
KW - sex hormones
KW - thymic epithelial cells (TEC)
UR - http://www.scopus.com/inward/record.url?scp=0028322234&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028322234&partnerID=8YFLogxK
U2 - 10.1111/j.1440-1711.1994.tb03777.x
DO - 10.1111/j.1440-1711.1994.tb03777.x
M3 - Article
C2 - 8088858
AN - SCOPUS:0028322234
VL - 72
SP - 193
EP - 199
JO - Immunology and Cell Biology
JF - Immunology and Cell Biology
SN - 0818-9641
IS - 3
ER -