Assistant Professor of Medicine
Ph.D., Neuroscience Program, Case Western Reserve University School of Medicine Research
General field of research:
Extracellular signaling in embryogenesis and regeneration.
Affiliations other than medicine:
Evans Center for Interdisciplinary Biomedical Research
Pulmonary Center, Department of Medicine
Phone: (617)-414 3291
Other research websites:
Research group information:
Thanh Tran, Postdoc, email@example.com
Kelsi Radzikinas, Research Assistant, firstname.lastname@example.org
Cell signaling; Muscle stem cells; Neurogenesis; Extracellular matrix; Aging
Summary of research interest:
• Regulation of stem cell function and aging by heparan sulfate and Sulfs;
• Role of neurotrophins in pulmonary neurogenesis and disease;
Environmental signals play crucial roles in self-renewal of stem cells, tissue regeneration and aging. A variety of these signals not only interact with heparan sulfate in the extracellular matrix, their signaling activities also are controlled by heparan sulfate. One major goal of the Ai lab is to investigate heparan sulfate-dependent mechanisms that regulate extracellular signaling during stem cell maintenance and tissue regeneration. Our study is focused on two heparan sulfate-modifying enzymes called Sulfs. We have established unique enzymatic activities of Sulfs and their differential regulation of several extracellular signals, including Wnts, FGFs and GDNF. Ongoing studies are investigating functions of Sulfs in age-impaired regeneration of the skeletal muscle.
Another major project is to investigate neurogenesis in the respiratory tract by both intrinsic and extrinsic neurons. Specifically, we are studying neurotrophin signaling during coordinated lung morphogenesis and innervation.
Ambasta R., Ai, X., and Emerson C.P. Jr. 2007. “QSulf1 function requires asparagine-linked glycosylation.” J. Biol. Chem.; 282(47):34492-98.
Ai X, Kitazawa T, Do AT, Kusche-Gullberg M, Labosky PA, Emerson CP Jr. 2007. SULF1 and SULF2 regulate heparan sulfate-mediated GDNF signaling for esophageal innervation. Development; 134(18):3327-38.
Lansdoff A., Do A.T., Kusche-Gullberg M., Emerson C.P. Jr., and Ai X. (corresponding author) 2007. “Sulfs are regulators of growth factor signaling for satellite cell differentiation and muscle regeneration.” Developmental Biology; 311: 464-77.
Ai X. (corresponding author), Kitazawa T., Do A.T., Kusche-Gullberg M., Labosky P.A., and Emerson, C.P. 2007. “Extracellular heparan sulfate 6-O-endosulfatases, MSulf1 and MSulf2, co-regulate GDNF signaling for esophageal innervation.” Development; 134(18): 3327-38.
Danesin C., Agius E., Escalas N., Ai X., Emerson C.P., and Soula C. 2006. “Ventral neural progenitors switch toward an oligodendroglial fate in response to increased Sonic hedgehog (Shh) activity: involvement of Sulfatase 1 in modulating Shh signaling in the ventral spinal cord.” J Neurosci. 26(19):5037-48.
Riobó N.A., Lu K., Ai X., Haines G.M., and Emerson C.P. Jr. 2006. “PI3 Kinase and Akt are essential for Sonic Hedgehog Signaling.” Proc. Natl. Acad. Sci. U.S.A.; 103(12):4505-4510.
Ai X., Do A.T., Kusche-Gullberg M., Lu K., Lindahl U., and Emerson C.P. Jr. 2006. “Conserved domain structures and enzymatic activities of quail heparan sulfate 6-O endosulfatases.” J. Biol. Chem.; 281(8):4969-4976.
Wang S., Ai X. (co-first author), Freeman S.D., Pownall M.E., Lu Q., Kessler D.S., and Emerson C.P. Jr. 2004. “QSulf1, a heparan sulfate 6-O-endosulfatase, inhibits fibroblast growth factor signaling in mesoderm induction and angiogenesis.” Proc. Natl. Acad. Sci . U.S.A.; 101:4833-4838.
Ai X., Do A.T., Lozynska O., Kusche-Gullberg M., Lindahl U., and Emerson C.P. Jr. 2003. “QSulf1 remodels the 6-O sulfation states of cell surface heparan sulfate proteoglycans to promote Wnt signaling.” J Cell Biol.; 162(2):341-51.
Dhoot G.K., Gustafsson M.K., Ai X., Sun W., Standiford D.M., and Emerson C.P. Jr. 2001. “Regulation of Wnt signaling and embryo patterning by an extracellular sulfatase.” Science; 293(5535):1663-6.
Technologies available for sharing upon request:
Animal models of skeletal muscle regeneration; Immunohistochemistry