Zhang Jingxue

iPSC-Derived Trabecular Meshwork Cells Stimulate Endogenous TM Cell Division Through Gap Junction in a Mouse Model of Glaucoma.

Our findings reveal a crucial role of gap junction, especially Cx43, in iPSC-based TM regeneration, and provides insights to enhance the regenerative effect of iPSCs in glaucoma therapy.

Xeno- and Feeder-Free Differentiation of Human iPSCs to Trabecular Meshwork-Like Cells by Recombinant Cytokines.

We successfully generated a xeno- and feeder-free differentiation protocol with recombinant cytokines to generate the TM progenitor and TM-like cells from human iPSCs.

Pigment Dispersion Contributes to Ocular Immune Privilege in a DBA/2J Mouse Model of Pigmentary Glaucoma.

Dispersion of pigment particles in the anterior chamber of the eye enhances the state of ocular immune privilege by influencing the immunosuppressive microenvironment and inducing more Treg cells to reestablish ACAID.

AAV-DJ-Mediated MYOC Silencing as a Gene Therapy Approach for Myocilin-Associated Glaucoma.

AAV-DJ-mediated MYOC silencing effectively alleviated glaucomatous pathology in Tg-MYOCP370L mice, highlighting its potential as a gene therapy strategy for myocilin-associated glaucoma.

Dynein, kinesin and morphological changes in optic nerve axons in a rat model with cerebrospinal fluid pressure reduction: the Beijing Intracranial and Intraocular Pressure (iCOP) study.

Experimental models with an acute IOP rise or with an acute CSFP reduction showed similar morphologic changes in the retinal ganglion cell axons and similar immunohistochemical changes in the axonal motor proteins kinesin HC and dynein IC.

Glaucoma and the Role of Cerebrospinal Fluid Dynamics.

Axonal Transport in the Rat Optic Nerve Following Short-Term Reduction in Cerebrospinal Fluid Pressure or Elevation in Intraocular Pressure.

Both short-term lowering of CSFP and short-term rise in IOP were associated with a disturbance of both the orthograde and retrograde axonal transport.