Dr Xiangjian Zheng

Associate Faculty, Centenary Institute
Conjoint Senior Lecturer, Sydney Medical School,

Telephone 61 2 9565 6235

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Biographical details

Dr. Zheng is the head of Lab of Cardiovascular Signaling at Centenary Institute and a member of Faculty of Medicine. His current research focuses on molecular mechanisms of cardiovascular development and diseases. He obtained his Ph.D in Molecular Medicine from Medical College of Georgia, where he studies lipid signaling in skin biology and endocrine control of blood pressure control. Zheng continued on his research in lipid signaling as a research fellow in Department of Pharmacology at Vanderbilt University School of Medicine. He used the combination of zebrafish model and lipidomics approaches to investigated lipid-mediated signaling in angiogenesis and cancer biology. After joined Penn Cardiovascular Institute at Perelman School of Medicine at University of Pennsylvania, Zheng’s research became more focused on human vascular diseases.

Research interests

The Zheng Lab is interested in understanding:i)basic signaling mechanisms underlying cardiovascular development and diseases; and ii) the role of endothelium in organ development and regeneration.

The precisely regulated development and function of cardiovascular system is essential for the normal function of every other organ. The endothelium is also believed to provide instructive roles for organ development and regeneration. The understanding of how blood vessels form and maintain, and how endothelial cells interact with other cell types within organ systems is critical for designing treatments of many diseases, eg. from cardiovascular diseases, diabetes, cancer to dementia.

One of currently focused vascular diseases in Zheng Lab is cerebral cavernous malformation (CCM). CCMs are sporadic or inherited vascular malformations in the brain, which can lead to stroke. CCMs affects 0.1~0.5% people in the human population, yet the effective drug treatment is lacking. Mutations in three genes, CCM1, CCM2 and CCM3, have been identified as causing human CCM disease. The lab is currently using genetically engineered mouse model to mimic these human mutations and investigates how these genes control blood vessel formation and how their loss of function leads to vessel malformation. This research should lead to the identification of therapeutic targets for CCM and related vascular diseases.

Current projects

1.Endothelial cell heterogeneity and CCM signaling in blood vessel formation.

2. Matrix homeostasis in CCM pathogenesis

3. CCM signaling in heart development.

Selected Publications:

1. Zhou Z, RawnsleyD, Goddard L, Pan W, Cao X, Jakus Z, Zheng H, Yang J, Arthur S, WhiteheadKJ, LiD, Zhou B, Garcia BA, Zheng X* and Kahn ML*. The cerebral cavernous malformation pathway controls cardiac development via regulation of endocardial MEKK3 signaling and KLF expression. Dev Cell 32(2): 168-180 (2015)(* co-corresponding author).

2. Zheng X, Riant F, Bergametti F, Myers CD, Tang AT, KleavelandB, Pan W, Yang J, Tounier-Reserve E and Kahn ML. Cerebral cavernous malformations arise independent of heart-of-glass receptor. Stroke 45(5): 1505-09(2014).

3. Zheng X, Xu C, Smith AO, Stratman AN, ZouZ, KleavelandB, YuanL, Didiku C, Skuli N, ZaslavskyA, ChenM, Cheng L, DavisGE, and Kahn ML. Dynamic regulation of cerebral cavernous malformation pathway controls cardiovascular stability and growth. Dev cell 23 (2): 342-355 (2012).

4. Qin H,Zheng X, Zhong X, Shetty AK, EliasPM and BollagWB. Aquaporin-3 in keratinocytes and skin: its role and interaction with phospholipase D2. Arch BiochemBiophys.508(2): 138-43 (2011).

5. Zheng X, Xu C, Di Lorenzo A, Kleaveland B, Zou Z, Seiler C, Chen M, Cheng L, XiaoJ, He J, Pack MA, Sessa WC and Kahn ML. CCM3 signaling through sterile 20-like kinases plays an essential role during zebrafish cardiovascular development and in human cerebral cavernous malformations. J Clin Invest. 120 (8): 2795-804 (2010).

6. Zeng XX*, ZhengX*, Xiang Y, Cho HP, Jessen JR, Zhong TP, Solnica-Krezel L and Brown HA. Phospholipase D1 is required for angiogenesis of intersegmental blood vessels In zebrafish. Dev Biol. 328(2): 363-76 (2009). * equal contribution

7. Kleaveland B, Zheng X, Liu JJ, Blum Y, Tung JJ, Zou Z, Chen M, Guo L, Lu M, Zhou D, Kitajewski J, Affolter M, Ginsberg MH and Kahn M. Regulation of cardiovascular development and integrity by the heart of glass-cerebral cavernous malformation protein pathway. Nature Medicine, 15(2): 169-76 (2009).

8. Zheng X and Bollag WB. Aquaporin 3 is collocated with phospholipase D2 in caveolin rich membrane microdomains and down regulated upon keratinocyte differentiation. JInvest Dermatol.121:1487-1495 (2003).

9. Zheng X and Chen X. Aquaporin 3, a glycerol and water transporter, is regulated by p73 of the p53 family. FEBS letters, 489:4-7 (2000).

International links

United States

(University of Pennsylvania) Collaborating in CCM pathogenesis research

Selected grants

2017

  • Coupling the mechanical, signalling and transcriptional mechanisms that initiate pathogenesis of Cerebral Cavernous Malformation; Hogan B, Zheng X; National Health and Medical Research Council (NHMRC)/Project Grants.

2015

  • Novel therapy approaches for diabetes and its liver and heart complications; Gorrell M, Keane F, Tu T, Shackel N, Bowen D, Bertolino P, Seth D, Chen J, Cook A, Liu R, Zheng X, Gamble J, McCaughan G; Rebecca L Cooper Medical Research Foundation/Research Support.

2014

  • The role of Heg-CCM2L signaling in angiogenesis; Zheng X; National Health and Medical Research Council (NHMRC)/Project Grants.

Selected publications

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Journals

  • Pi, J., Tao, T., Zhuang, T., Sun, H., Chen, X., Liu, J., Cheng, Y., Yu, Z., Zhu, H., Zheng, X., et al (2017). A microRNA302-367-Erk1/2-Klf2-S1pr1 Pathway Prevents Tumor Growth via Restricting Angiogenesis and Improving Vascular Stability. Circulation Research, 120(1), 85-98. [More Information]
  • Tang, A., Choi, J., Kotzin, J., Yang, Y., Hong, C., Hobson, N., Girard, R., Zeineddine, H., Lightle, R., Zheng, X., et al (2017). Endothelial TLR4 and the microbiome drive cerebral cavernous malformations. Nature, 545(7654), 305-310. [More Information]
  • Choi, J., Yang, X., Foley, M., Wang, X., Zheng, X. (2017). Induction and micro-CT imaging of cerebral cavernous malformations in mouse model. Journal of Visualized Experiments, 2017 (127), 1-5. [More Information]
  • Zhou, Z., Tang, A., Wong, W., Bamezai, S., Goddard, L., Shenkar, R., Zhou, S., Yang, J., Wright, A., Foley, M., Zheng, X., et al (2016). Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling. Nature, 532(7597), 122-126. [More Information]
  • Choi, J., Foley, M., Zhou, Z., Wong, W., Gokoolparsadh, N., Arthur, J., Li, D., Zheng, X. (2016). Micro-CT imaging reveals Mekk3 heterozygosity prevents cerebral cavernous malformations in Ccm2-deficient mice. PloS One, 11(8), 1-14. [More Information]

2017

  • Pi, J., Tao, T., Zhuang, T., Sun, H., Chen, X., Liu, J., Cheng, Y., Yu, Z., Zhu, H., Zheng, X., et al (2017). A microRNA302-367-Erk1/2-Klf2-S1pr1 Pathway Prevents Tumor Growth via Restricting Angiogenesis and Improving Vascular Stability. Circulation Research, 120(1), 85-98. [More Information]
  • Tang, A., Choi, J., Kotzin, J., Yang, Y., Hong, C., Hobson, N., Girard, R., Zeineddine, H., Lightle, R., Zheng, X., et al (2017). Endothelial TLR4 and the microbiome drive cerebral cavernous malformations. Nature, 545(7654), 305-310. [More Information]
  • Choi, J., Yang, X., Foley, M., Wang, X., Zheng, X. (2017). Induction and micro-CT imaging of cerebral cavernous malformations in mouse model. Journal of Visualized Experiments, 2017 (127), 1-5. [More Information]

2016

  • Zhou, Z., Tang, A., Wong, W., Bamezai, S., Goddard, L., Shenkar, R., Zhou, S., Yang, J., Wright, A., Foley, M., Zheng, X., et al (2016). Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling. Nature, 532(7597), 122-126. [More Information]
  • Choi, J., Foley, M., Zhou, Z., Wong, W., Gokoolparsadh, N., Arthur, J., Li, D., Zheng, X. (2016). Micro-CT imaging reveals Mekk3 heterozygosity prevents cerebral cavernous malformations in Ccm2-deficient mice. PloS One, 11(8), 1-14. [More Information]

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