Download full-text PDF

Source
http://dx.doi.org/10.1016/0022-4731(81)90203-xDOI Listing

Publication Analysis

Top Keywords

inhibition estrogen-induced
4
estrogen-induced proliferation
4
proliferation cultured
4
cultured rabbit
4
rabbit uterine
4
uterine epithelial
4
epithelial cells
4
cells cell
4
cell density-dependent
4
density-dependent factor
4

Similar Publications

Venous thrombosis is a well-known complication of sex hormone therapy, with onset typically within weeks to months after initiation. Worldwide, more than 100 million pre-menopausal women use combined oral contraceptives, with tens to hundreds of thousands developing thrombosis annually, resulting in significant morbidity and mortality. Although it is known that estrogens can alter expression of coagulation factors, the pathways and mechanisms that connect the two systems, as well as the proteins involved in progression to thrombosis, are poorly understood.

View Article and Find Full Text PDF

During early pregnancy in mice, the establishment of uterine receptivity and endometrial decidualization require the extensive proliferation and differentiation of endometrial epithelial cells or stromal cells. Pin1 has been suggested to act as a molecular 'timer' of the cell cycle and is involved in the regulation of cellular proliferation and differentiation by binding many cell-cycle regulatory proteins. However, its physiological role during early pregnancy is still not fully understood.

View Article and Find Full Text PDF

Estrogen is thought to have a role in slowing down aging and protecting cardiovascular and cognitive function. However, high doses of estrogen are still positively associated with autoimmune diseases and tumors with systemic inflammation. First, we administered exogenous estrogen to female mice for three consecutive months and found that the aorta of mice on estrogen develops inflammatory manifestations similar to Takayasu arteritis (TAK).

View Article and Find Full Text PDF
Article Synopsis
  • * Treatment with E2 enhances matrix mineralization but is inhibited by certain antagonists of estrogen receptors, indicating a complex interaction at play.
  • * The study reveals that E2 activates the p38 MAPK pathway through estrogen receptors, potentially leading to the release of signaling molecules that could provide targets for osteoporosis treatments.
View Article and Find Full Text PDF

Estrogen Induces LCAT to Maintain Cholesterol Homeostasis and Suppress Hepatocellular Carcinoma Development.

Cancer Res

August 2024

Hubei Key Laboratory of Cell Homeostasis, Department of Hepatobiliary and Pancreatic Surgery, College of Life Sciences, Zhongnan Hospital of Wuhan University, Wuhan, China.

Hepatocellular carcinoma (HCC) is an aggressive disease that occurs predominantly in men. Estrogen elicits protective effects against HCC development. Elucidation of the estrogen-regulated biological processes that suppress HCC could lead to improved prevention and treatment strategies.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!