New Paper by VS Student Matangi Kumar

Investigating the regulation and role of Müller Glia in ocular hypertension induced retinal ganglion cell degeneration.

Congratulations to Matangi Kumar, Vision Science PhD candidate (Gronert and Flanagan Labs), on the publication of her first first-author paper, which was published in Investigative Ophthalmology & Visual Science (IOVS).

The study investigated the regulation and role of Müller Glia in ocular hypertension induced retinal ganglion cell degeneration. Müller Glia are essential for retinal health but can also drive pathogenesis when their mechanosensitive ion channel, TRPV4, gets activated by elevated intraocular pressure. Ocular hypertension amplifies the number of TRPV4 ion channels and chronic TRPV4 activation induces an inflammatory reactive Müller Glia phenotype. Matangi discovered that Müller Glia cells are a primary source of a neuroprotective lipid signal, LXB4 and that this pathway is also amplified in reactive Müller Glia cells to counter-regulate gliosis and aberrant activation of TRPV4. Therapeutic amplification of LXB4 inhibited gliosis and aberrant expression and signaling of TRPV4 in a mouse model of glaucoma. Matangi’s study supports targeting of the TRPV4–lipoxin pathway as a potential approach to protect against ocular hypertension–induced neurodegeneration in glaucoma.

Photo: Glial Fibrially Acid Protein and Vimentin Co-staining of Activated Primary Müller Glia.

Read the Paper Matangi's Profile