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Dr. Keqing Wang

Keqing Wang

Keqing moved to England from Beijing in 1997, joining the University of Birmingham as a post-graduate student. In 1998 she was award a Masters in Immunology with Distinction and a University-funded PhD, which she was awarded in 2002. 

Keqing has extensive postdoctoral research experience in immunology, inflammation and the vascular biology of pregnancy. For the last four years, she has focused on pregnancy-associated complications, funded through a MRC programme grant. Her pregnancy studies identified hydrogen sulphide (H2S) as an important regulator of the placental vasculature development and showed that a deficiency in its production induces preeclampsia-like features. This research provided the first direct evidence that a decrease in placenta growth factor in first trimester, which is associated with poor pregnancy outcome, may stem from H2S/CSE dysregulation. Furthermore, this study identified H2S as a potential new target for therapeutic intervention against preeclampsia and intrauterine fetal growth restriction. This work was published in the June edition of the prestigious journal Circulation (N.B. Add links to paper). Wang is also listed as a co-inventor on a recent patent application filed by the University.

As part of the Vascular Medicine Unit at Aston, Keqing is developing a key strand of our overall strategy, which is to evaluate a new pathway in preeclampsia and intrauterine growth restriction. Her recent study demonstrated that levels of hydrogen sulfide (H2S), one of the gaseous transmitters, is reduced in the maternal circulation of women with preeclampsia and is associated with reduced H2S producing enzyme expression in placenta. This discovery provides the first direct evidence that decreases in placenta growth factor in the first trimester, which is associated with poor pregnancy outcome, may stem from H2S/CSE dysregulation.  Furthermore, it shows that inhibition of H2S production leads to abnormal placental vascularization and fetal growth restriction in pregnant animals and that a H2S donor can restore these features. In combination with the previous findings of the Vascular Research group, this latest study has built the foundation for our working hypothesis: Dysregulation of gaseous transmitters/enzymes pathways alters the angiogenic balance in favour of anti-angiogenic factors (sFlt-1 & sEng) in pregnancy to induce abnormal placentation and maternal hypertension, and that supplementation of these gaseous transmitters can restore the balance and be used as a potential new target for therapeutic intervention against preeclampsia and intrauterine fetal growth restriction. 
Keqing’s personal research interest is in inflammation and neutrophil biology. Over the last four years she has collaborated with Prof Stuart Egginton from the University of Leeds to investigate the role of monocytes/neutrophils in Angiopoietin-1 mediated atherosclerosis. She has also been collaborating with Dr. David Thicket, Clinical Senior Lecturer at the University of Birmingham, a lung physician responsible for running the lung injury and fibrosis treatment (LIFT) research programme. Their collaborative research has demonstrated the role of neutrophil-induced soluble endoglin in acute lung injury. These collaborative studies have generated data for grant applications and two manuscripts are currently being prepared for submission.