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Published on: August 20, 2016
Selective estrogen receptor modulators suppress mesangial cell collagen synthesis
J Neugarten1, A Acharya, J Lei
1Nephrology Division, Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York 10467, USA.
American Journal of Physiology. Renal Physiology
|August 5, 2000
Summary
Selective estrogen receptor modulators (SERMs) like LY-117018 and tamoxifen effectively suppress collagen synthesis in mesangial cells. This suggests potential for treating progressive renal disease without estrogen
Area of Science:
- Nephrology
- Endocrinology
- Pharmacology
Background:
- Selective estrogen receptor modulators (SERMs) exhibit tissue-specific estrogenic or anti-estrogenic effects.
- Estrogen receptor signaling plays a role in kidney physiology and disease.
- Matrix accumulation in glomerulosclerosis contributes to progressive renal disease.
Purpose of the Study:
- To investigate the impact of SERMs LY-117018 and tamoxifen on mesangial cell collagen synthesis.
- To determine the role of estrogen receptor-beta in mediating these effects.
Main Methods:
- Mesangial cells were treated with LY-117018, tamoxifen, estradiol, and genistein.
- Collagen type I and type IV gene transcription and protein synthesis were measured.
- Dose-dependent effects and relative potencies were analyzed.
Main Results:
- LY-117018 and tamoxifen suppressed type IV collagen synthesis and gene transcription in a dose-dependent manner, similar to estradiol.
- LY-117018 suppressed type I collagen synthesis dose-dependently, with potency similar to estradiol and greater than tamoxifen.
- Genistein also suppressed both collagen types, implicating estrogen receptor-beta.
Conclusions:
- Second-generation SERMs, such as LY-117018, can inhibit mesangial cell collagen synthesis.
- Estrogen receptor-beta appears to mediate the suppressive effects of estrogen on collagen production.
- SERMs may offer a therapeutic strategy for progressive renal diseases like glomerulosclerosis, potentially avoiding estrogen's reproductive side effects.
