Novel Role of Estrogen Receptor-α on Regulating Chondrocyte Phenotype and Response to Mechanical Loading

2021 ◽  
Author(s):  
Ning Wang ◽  
Xiurui Zhang ◽  
Benjamin B. Rothrauff ◽  
Madalyn R. Fritch ◽  
Alexander Chang ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mechanical Loading ◽  
Estrogen Receptor Α ◽  
Chondrocyte Phenotype

Membrane estrogen receptor α is essential for estrogen signaling in the male skeleton

2018 ◽  
Vol 239 (3) ◽  
pp. 303-312 ◽  
Author(s):  
H H Farman ◽  
K L Gustafsson ◽  
P Henning ◽  
L Grahnemo ◽  
V Lionikaite ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Estrogen Signaling ◽  
Areal Bone Mineral Density ◽  
Male Mice ◽  
Mineral Density ◽  
Intact Male ◽  
Trabecular Thickness ◽  
Total Body

The importance of estrogen receptor α (ERα) for the regulation of bone mass in males is well established. ERα mediates estrogenic effects both via nuclear and membrane-initiated ERα (mERα) signaling. The role of mERα signaling for the effects of estrogen on bone in male mice is unknown. To investigate the role of mERα signaling, we have used mice (Nuclear-Only-ER; NOER) with a point mutation (C451A), which results in inhibited trafficking of ERα to the plasma membrane. Gonadal-intact male NOER mice had a significantly decreased total body areal bone mineral density (aBMD) compared to WT littermates at 3, 6 and 9 months of age as measured by dual-energy X-ray absorptiometry (DEXA). High-resolution microcomputed tomography (µCT) analysis of tibia in 3-month-old males demonstrated a decrease in cortical and trabecular thickness in NOER mice compared to WT littermates. As expected, estradiol (E2) treatment of orchidectomized (ORX) WT mice increased total body aBMD, trabecular BV/TV and cortical thickness in tibia compared to placebo treatment. E2 treatment increased these skeletal parameters also in ORX NOER mice. However, the estrogenic responses were significantly decreased in ORX NOER mice compared with ORX WT mice. In conclusion, mERα is essential for normal estrogen signaling in both trabecular and cortical bone in male mice. Increased knowledge of estrogen signaling mechanisms in the regulation of the male skeleton may aid in the development of new treatment options for male osteoporosis.

scholarly journals Expression of Estrogen Receptor Alpha and Evaluation of Histological Degeneration Scores in Fibroblasts of Hypertrophied Ligamentum Flavum: A Qualitative Study

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1752
Author(s):  
Christina C. Westhoff ◽  
Christian-Dominik Peterlein ◽  
Hanna Daniel ◽  
Juergen R. Paletta ◽  
Roland Moll ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Ligamentum Flavum ◽  
Estrogen Receptor Α ◽  
Group Differences ◽  
Elastic Fibers ◽  
Disk Herniation ◽  
Spinal Decompression ◽  
Lumbar Spinal

The most common spinal disorder in elderly is lumbar spinal stenosis (LSS), resulting partly from ligamentum flavum (LF) hypertrophy. Its pathophysiology is not completely understood. The present study wants to elucidate the role of estrogen receptor α (ER α) in fibroblasts of hypertrophied LF. LF samples of 38 patients with LSS were obtained during spinal decompression. Twelve LF samples from patients with disk herniation served as controls. Hematoxylin & Eosin (H&E) and Elastica stains and immunohistochemistry for ER α were performed. The proportions of fibrosis, loss and/or degeneration of elastic fibers and proliferation of collagen fibers were assessed according to the scores of Sairyo and Okuda. Group differences in the ER α and Sairyo and Okuda scores between patients and controls, male and female sex and absence and presence of additional orthopedic diagnoses were assessed with the Mann–Whitney U test. There was a tendency towards higher expression of ER α in LF fibroblasts in the hypertrophy group (p = 0.065). The Sairyo and Okuda scores were more severe for the hypertrophy group but, in general, not statistically relevant. There was no statistically relevant correlation between the expression of ER α and sex (p = 0.326). ER α expression was higher in patients with osteochondrosis but not statistically significant (p = 0.113). In patients with scoliosis, ER α expression was significantly lower (p = 0.044). LF hypertrophy may be accompanied by a higher expression of ER α in fibroblasts. No difference in ER α expression was observed regarding sex. Further studies are needed to clarify the biological and clinical significance of these findings.

Role of the proteasome in the regulation of estrogen receptor α turnover and function in MCF-7 breast carcinoma cells

2005 ◽  
Vol 94 (4) ◽  
pp. 347-359 ◽  
Author(s):  
Ioanna Laïos ◽  
Fabrice Journé ◽  
Denis Nonclercq ◽  
Doris Salazar Vidal ◽  
Robert-Alain Toillon ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Breast Carcinoma ◽  
Estrogen Receptor Α ◽  
Carcinoma Cells ◽  
Breast Carcinoma Cells ◽  
And Function ◽  
Mcf 7

scholarly journals Expression and role of estrogen receptor α and β in medullary thyroid carcinoma: different roles in cancer growth and apoptosis

2007 ◽  
Vol 195 (2) ◽  
pp. 255-263 ◽  
Author(s):  
Mi Ae Cho ◽  
Mi Kyung Lee ◽  
Kee-Hyun Nam ◽  
Woung Youn Chung ◽  
Cheong Soo Park ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Thyroid Carcinoma ◽  
Medullary Thyroid Carcinoma ◽  
Tumor Staging ◽  
Estrogen Receptor Α ◽  
C Cells ◽  
Tissue Samples ◽  
Medullary Thyroid ◽  
Tt Cells

Medullary thyroid carcinoma (MTC) originates from parafollicular C cells. Estrogen receptor β(ERβ) expressionwas detected in normal parafollicular C cells and MTC tumor tissue, but ERα expression in MTC tumors still remains undetermined. The appearance and loss of ERα or ERβ expression has been known to play a role in the development and progression of many human cancers. We performed immunohistochemical studies of ERα, ERβ, and Ki67, a mitotic index, in 11 human MTC tissue samples. ERα was detected in 10 cases (91%), and ERβ expression was observed in 8 cases (72.7%). A majority (8/10) of ERα-positive tumors showing ERβ Ki67 expression was detected in three cases (27.3%). Neither clinical parameters nor tumor node metastasis (TNM) tumor staging was correlated with the positivity for ERs or Ki67. To investigate the biological role of each ER, we used ER-negative MTC TT cells and adenoviral vectors carrying ERα (Ad-ERα), ERβ (Ad-ERβ), estrogen response element (ERE)-Luc (Ad-ERE-Luc), and activator protein 1 (AP1)-Luc (Ad-AP1-Luc). Estrogen stimulated and anti-estrogen, ICI 182 780, suppressed ERE reporter activity in TT cells expressing ERα or ERβ, suggesting that both ERs use the same classical ERE-mediated pathway. Ad-ERα infection stimulated TT cell growth; in contrast, Ad-ERβ infection suppressed their growth. Apoptosis was detected in Ad-ERβ-infected TT cells. Estrogen and anti-estrogen suppressed AP1 activity in Ad-ERα-infected cells, whereas upon Ad-ERβ infection estrogen further stimulated AP1 activity which in turn is suppressed by anti-estrogen, suggesting that each ER acts differently through a non-ERE-mediated pathway. Our results suggest that ERα and ERβ may play different roles in MTC tumor growth and progression.

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