The laboratory for reproductive health mainly focus on the effect of metabolism disease and cardiovascular disease onphysiological function of male and female gonad organ(testis and ovary), fertilization, gestation and health of offspring and postpartum mothers, try to find out the novel target to improve reproductive function, aim to develop rapid and accurate diagnostic reagents or detected methods, explore the specific targeting agents and programs, hope to give some contribution to human reproductive health.
The research area include:
The latest indicators in 2016 show that the infertility rate in China has soared from 3 % to 12 % in the past 20 years. Currently, there are more than 40 million infertile patients in China. With the increasing pressure of life, women generally delay marriage and childbearing age, the older the age, the greater the impact on fertility, such as decreased ovarian function, the overall decline in reproductive functions can lead to infertility. According to the world health organization, in the 21st century, infertility will be second only to cancer and cardiovascular disease, become the third major disease harmful to female health.
Laboratory for Reproductive Health is committed to research on reproductive immune and endocrine diseases, contributing to the reproductive health and eugenics.
We first reported the expression of chemerin and its receptors in human and rat testis, we also found that chemerin could suppress hCG induced testosterone secretion. The paper “Expression of chemerin and its receptors in rat testes and its action on testosterone secretion” was published on the Journal of Endocrinology on 2014.
We next reported the expression of chemerin and its receptor GPR1 in mouse ovary, specifically on follicles and corpus luteum. Furtherly, we demonstrated its suppression on hCG induced progesterone secretion and regulatory effect on steroidogenesis during the development of follicle and corpus luteum and luteolysis. The paper “The role of GPR1 signaling in mice corpus luteum” was published on the Journal of Endocrinology on May 4, 2016.
At the same time, we also explored the role of chemerin/CMKLR1 pathway in follicle function and steroidogenesis. More important, we found that CMKLR1 deficiency partially ameliorated the negative effect of DHT on progesterone secretion, cycling, and anovulation in mice treated chronically with DHT. The paper “CMKLR1 deficiency maintains ovarian steroid production in mice treated chronically with dihydrotestosterone” was published on the Scientific Reports on Feb 19, 2016.
Figure 2 Modulation of progesterone and estradiol biosynthesis in follicles with DHT treatment.
Now we are working on the role of GPR1 in steroid synthesis in hyperandrogenism mice and have already achieved some results. From all of our results we can demonstrate that chemerin and it receptors play important roles in steroidogenesis and could be new therapeutic targets of endocrine disorders induced reproductive diseases and infertility.