Transforming growth factor β1 and its receptor soluble endoglin are altered in polycystic ovary syndrome during controlled ovarian stimulation

Capsule:
Increased transforming growth factor-b1 and decreased levels of its receptor, soluble endoglin are found in women with polycystic ovarian syndrome (PCOS) and may be implicated in PCOS pathogenesis and its increased risk for ovarian hyperstimulation.

Authors:
Reshef Tal, M.D., Ph.D., David B. Seifer, M.D., Aya Shohat-Tal, Ph.D., Richard V. Grazi, M.D., Henry E. Malter, Ph.D.

Volume 100, Issue 2, Pages 538-543, August 2013

Abstract:

Objective:
To evaluate the relationship between transforming growth factor (TGF)-β1 and its receptor, soluble endoglin (sENG), in the serum and follicular fluid of women with polycystic ovarian syndrome (PCOS)
compared with that of non-PCOS normal ovulating women during controlled ovarian stimulation (COS).

Design:
Prospective case-control study.

Setting:
Academic-affiliated assisted reproductive technology unit.

Patient(s):
Fourteen PCOS and 14 matched non-PCOS control women undergoing COS.

Intervention(s):
Serum was collected on day 3 (baseline), day of hCG, and day of retrieval. Follicular fluid (FF) was collected on day of oocyte retrieval. ELISA was performed to determine TGF-β1 and sENG protein levels.

Main Outcome Measure(s):
Serum and FF levels of TGF-β1 and sENG.

Result(s):
Serum TGF-β1 did not change significantly during COS but was increased in PCOS compared with non-PCOS women on day 3 and days of hCG administration and oocyte retrieval. Serum sENG increased after hCG administration only in the non-PCOS control group. In addition, serum sENG was decreased in PCOS compared with non-PCOS control women on the days of hCG and retrieval. Accordingly, the bioavailability of TGF-β1 (TGF-β1/sENG ratio) was increased in women with PCOS compared with non-PCOS controls at all three time points. No differences in either factor were noted in FF between groups.

Conclusion(s):
The increased TGF-β1 bioavailability in PCOS is not only due to increased TGF-β1 levels but also to decreased levels of its receptor, sENG. These data suggest that increased TGF-β1 bioavailability may contribute to the pathogenesis of PCOS and its increased risk for ovarian hyperstimulation.

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