- Postdoctoral Associate
- Baylor College of Medicine
- Houston, TX, US
- Assistant researcher
- Institute of Biochemistry and Cell Biology, SIBS, CAS
- Shanghai, China
- PhD from Institute of Biochemistry and Cell Biology, SIBS, CAS
- BS from Nanjing Agriculture University
My current goal is to expand my training in endocrinology to unravel the complex central mechanisms controlling the sex dimorphism of energy homeostasis.
- TAp63 contributes to the sexual dimorphism in POMC neuron functions and energy homeostasis
- Obesity is a major risk factor for cardiovascular diseases, due to its high prevalence and strong association with hypertension, coronary heart disease, and stroke. Female animals are more resistant to obesity than males, but the mechanisms for this sexual dimorphism remain elusive. In our previous studies, we first screened body weight-regulatory neural populations and found that pro-opiomelanocortin (POMC) neurons in female mice firing more rapidly than male POMC neurons. Further characterization showed that female mouse brains have more POMC neurons and express higher levels of POMC transcripts (per neuron). Further, these sex differences in POMC neurons were associated with higher expression levels of TAp63 (a transcription factor) or SRC1 (steroid receptor coactivator-1, a transcriptional coactivator) in female POMC neurons than in male counterparts. Importantly, our pilot studies showed that TAp63 and SRC1 can activate POMC gene expression in POMC neurons and the deletion of TAp63 or SRC1 only in POMC neurons regulates body weight in a sexually dimorphic fashion. Together, we developed a hypothesis that TAp63 and/or SRC1 contribute to the sexual dimorphism in POMC neuron functions and energy homeostasis. We will generate mice that lack TAp63 or SRC1 in adult POMC neurons, and characterize the energy homeostasis and POMC neuron characteristics (activity, population, projection, and gene expression profile) among male mice, female mice without or with intact ovary (Sham and OVX-V), and female without intact ovary but with estrogen supplement (OVX-E). In this way, we will determine whether TAp63 or SRC1 are the critical drivers for the sex difference of POMC neurons on body weight control, and whether the sexual dimorphic function of TAp63 or SRC1 is mediated by estrogen signals. In addition, we will identify more sexual dimorphic candidate genes that are important for energy homeostasis, which will set the foundation for further exploration of mechanisms for this sexual dimorphism of obesity. Our work will advance our understanding about the fundamental biology for sex differences in body weight control, which may facilitate the development of gender-specific therapeutic strategies for obesity and associated cardiovascular diseases.