Yingzi Yang
Harvard University, MA·Genetics
Bone and the tissues that anchor teeth do not regrow easily once badly damaged, and both repairs depend on stem cells that sit in specialized local environments, or niches. Two projects ask the same basic question in two places — the tissue that holds a tooth in its socket, and the flat bones of the skull — namely how injury changes the niche, and how the altered niche tells resident stem cells to multiply, move to the wound, and become the right kind of cell.
- Fields
Genetics
Biology
Medicine & Clinical Research
- Topics
periodontal regeneration
periodontal disease
periodontitis
- Grants
- 2 known grants, through Mar 2030
What they work on
- Characterize periodontal crestal stem cells, including Gli1+ cells that report Hedgehog signaling activity, and determine how they are activated by injury in the upper rim of the tooth socket where bone, ligament and gum meet.
- Identify the signaling pathways that control periodontal crestal stem cell activation and their differentiation into alveolar bone, periodontal ligament and gingival lineages during tissue repair in mice.
- Test whether the niche factors Cxcl12, a cell-guiding chemokine, and Sonic Hedgehog drive periodontal regeneration in a mouse periodontitis model with severe inflammation, where tissue defects are more pronounced.
- Define suture stem cells in the fibrous joints between skull bones and test how Cxcl12 and Gαi/Gαs G-protein signaling, including the Cxcl12 receptor Cxcr4, direct their migration to a calvarial injury site.
- Determine how Gαi/Gαs signaling and Sonic Hedgehog control suture stem cell expansion and their differentiation into osteoblasts, the bone-forming cells needed to bridge skull defects.
- Determine how the Cxcl12 and Shh pathways interact during calvarial bone regeneration, building on the finding that loss of Gαs raises Shh expression and promotes osteoblast differentiation.
More about the research
In both, the signals Cxcl12 (a chemokine, a protein that guides cell migration) and Sonic Hedgehog (Shh, a developmental signaling protein) are proposed to be the key injury-induced niche factors. The goal is to learn enough about these natural repair circuits to coax tissue to rebuild itself rather than relying on grafts or implants.
Why it matters
Periodontal disease is a major cause of tooth loss and a global public health burden, and large skull defects frequently fail to heal with bone, carrying high morbidity. Identifying the injury-induced niche signals, chiefly Cxcl12 and Hedgehog, that mobilize resident stem cells could point to treatments that harness the body's own repair capacity for more predictable periodontal regeneration and for craniofacial defects and other skeletal diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
J Fenno
University of Michigan, MI·Microbiology & Immunology
Characterize how dentilisin, a protease complex built on the PrtP lipoprotein, and the oligomeric Msp protein are assembled in the Treponema denticola outer membrane, using purified native and recombinant proteins.
Shaoping Zhang
University of Iowa, IA·Microbiology & Immunology
Define how a type I interferon (IFN-I)–IL-27 pathway controls the inflammatory IL-17–neutrophil axis in a mouse model of periodontitis, a gum disease that destroys tooth-supporting bone.
Dong Zhou
University of Connecticut, CT·Physiology
Determine the mechanistic role of extracellular matrix protein 1 (ECM1), a secreted matrix protein switched on within hours of injury, in forming the kidney microenvironment after acute kidney injury, using ex vivo approaches.
The school
Harvard University: 42 labs on PI Pages, $1.5B a year on research, 712 research doctorates a year.
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