Education

07/2014-12/2015, Visiting scholar• Pharmacology • School of Medicine• Emory University• US.

09/2009-07/2014, Ph. D • Pharmacology in Chinese and Western medicine • School of Medicine •Guangzhou University of Chinese Medicine.

09/2005-07/2009，B.S.• Chinese Medicine •School of Medicine • Hubei Ethnic College.

Work

03/2023- The Great Bay Area Center For Brain Research, South Medical University, Guangzhou, China.

06/2021-10/2022, Senior research fellow •Neuroscience• School of medicine• Mayo Clinic• Rochester.

01/2015-06/2021, Postdoctoral scholar/Project Scientist • Neuroscience • School of medicine• University of California, Davis.

Research interest

1. TDP-43 mutant aggregation appear in most ALS and FTD patients, but how it causes neurodegeneration remains not fully understood. To study the mechanism of TDP-43 related neurodegeneration disease, we found myelination is disrupted during neuronal pathology progress by using TDP-43 mutant transgenic mice model. The oligodendrocyte precursor cells, major cell type leading to remyelination, discern proliferation, activation, and inflammation, whereas its function and relationship with neurodegeneration was elusive. To demonstrate significant changes and function during disease development and explore the new function of OPCs regulating inflammation and neurodegeneration, we will apply the cut-edges technologies such as 2-Phtoton microscopy, single cell sequencing, and high-resolution electronic microscopy in future study.

2. OPCs occupy 5% of all CNS lifelong cells, well-known for its function for generation of myelinating oligodendrocytes. However, there are a large population of OPCs exists in the area without myelination, suggesting OPCs affect CNS apart from being the cellular source of new myelin. How to distinguish the population of OPCs which not differentiation into oligodendrocytes with the ones compromised into myelinated oligodendrocytes remains unknown. And what factor and molecule determine the OPCs differentiation fate remains unclear.

3. OPCs differentiation is inhibited in demyelinated disease such as multiple sclerosis and Periventricular leukomalacia. Microglia, the immune cells in CNS, activation is required for myelin debris remove and further remyelination. But how microglia modulate OPCs proliferation, differentiation and oligodendrocytes regeneration remains elusive. We will use new tools (AAV virus or transgenic model) to manipulate microglia, evaluate the OPC-microglia cross talk and test the new target for remyelination.

Representative publications

1. Zhang S*, Kim BK*, et al., and Guo FZ. (2020) Glial cell specific regulation of CNS angiogenesis by Hifα-activated different signaling pathways. Nature Communications,11, 2027, DOI:10.1038/s41467-020-15656-4. [PMID: 32332719]

2. Zhang S*, Wang Y*, et al., and Guo FZ. (2021) The Wnt effector TCF7l2 promotes oligodendroglial differentiation by repressing autocrine BMP4-mediated signaling, J Neurosci, 2021;41(8):1650-1664. [PMID: 33452226]

3. Zhang S, Wang Y, et al., and Guo FZ. (2021) HIFα regulates developmental myelination independent of autocrine Wnt signaling. J Neurosci, 2021;41(2):251-268. [PMID: 33208471]

4. Zhang S*, Zhu XQ*, et al., and Guo FZ. (2018) Sox2 is essential for oligodendroglial proliferation and differentiation during postnatal brain myelination and CNS remyelination. J Neurosci,14;38(7)1291-17. [PMID: 29335358]

5. Zhang S, et al., and Guo FZ. (2018) The Stem Cell Factor Sox2 Is a Positive Timer of Oligodendrocyte Development in the Postnatal Murine Spinal Cord. Molecular Neurobiology, 55(12):9001-9015. [PMID: 29623612]

6. Wang Y*, Zhang S*, Zhaohui Lan* et al., and Guo FZ. (2022) Sox2 is essential for astrocyte maturation and its deletion leads to hyperactive behavior in mice. Cell Reports, 20;41(12):111842. [PMID:36543123]

7. Wang Y, Zhang YH, Zhang S, et al., and Guo FZ. (2021）PARP1-mediated PARylation activity is essential for oligodendroglial differentiation and CNS myelination. Cell Reports, 37(1):109695. [PMID:34610310]