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Dr. Timothy Blenkinsop, Icahn School of Medicine, Mount Sinai Hospital, “The Good, the Bad, and the Ugly of Human Retinal Pigment Epithelium Plasticity”

November 3 @ 12:00 pm - 1:00 pm

SCRMC Seminar Lab Series, ONLINE Tuesday, Nov. 3rd @ 12PM CT; Dr. Timothy A Blenkinsop, PhD; Assistant Professor | Cell, Developmental & Regenerative Biology; Black Family Stem Cell Institute, Ophthalmology; Icahn School of Medicine at Mount Sinai; presents, "The Good, the Bad, and the Ugly of Human Retinal Pigment Epithelium Plasticity"

CONNECTION INFO
The UW Stem Cell & Regenerative Medicine Center will continue to offer its weekly seminar online in a live (synchronously) format, so that you, as all can continue to participate in the Q & A session in real time. 

To connect and join our live Tuesday Stem Cell Seminar Series (now online), please click on this public link: https://us.bbcollab.com/guest/9947d7dba7714d818e48a01ae3600b56

We do encourage you all to review the instructions, linked below, in order to orient yourselves to this online platform environment. You are also welcome to jump into the room and test your ability to connect, including turning on your audio and video, prior to the scheduled event time. Our center’s Administrator, Hollie, will be in the room starting at 10:30 AM CT  the day of and can offer assistance as time allows.

Guest Access Instructional Overview: https://go.wisc.edu/ftti09

If you have any questions, please contact Hollie: hjthomps@medicine.wisc.edu

**STUDENTS: If you are a current student, please join via the BBCollaborate option in your Canvas course portal.

 


TOPIC
The Good, the Bad, and the Ugly of Human Retinal Pigment Epithelium Plasticity

SPEAKER

Dr. Timothy Blenkinsop, PhD
Assistant Professor | Cell, Developmental & Regenerative Biology; Black Family Stem Cell Institute, Ophthalmology; Icahn School of Medicine at Mount Sinai

 

ABSTRACT

Retinal Pigment Epithelium (RPE) plasticity has been demonstrated to foster regenerative healing when the retina is damaged, which is good, but also can lead to vision loss when wound healing goes awry, which is bad. Understanding the transcriptional machinery behind this plasticity is helpful in shifting the RPE towards a regenerative instead of pathological response upon injury. The RPE performs many functions necessary for vision. As such, disruption in any of these roles will lead to vision loss and is why there are so many RPE related diseases. In order to better understand how RPE dysfunction leads to vision loss, we examine post-mortem RPE and develop in vitro models using primary human RPE and stem cell-based organoid models. From this, we have characterized a subpopulation of RPE which exhibits stem cell-like characteristics and multipotentiality. Moreover, we have uncovered molecular machinery responsible for driving RPE towards a pathological wound healing response that leads to Proliferative Vitreoretinopathy (PVR) where the RPE form myocontractile fibrotic membranes inducing retinal detachments and vision loss. We suspect this inclination towards a contractile phenotype may be due to the fact that in development, the RPE shares the same lineage as the iris muscle. Iris muscle is the only known muscle which derives from the neuroectoderm and therefore epigenetically, the cells which give rise to RPE must also enable iris muscle specification at the optic cup tip.  This muscle program becomes activated when RPE cells lose their cell contacts and are stimulated with cytokines associated with PVR. This plasticity may also explain why PVR membranes form after pluripotent stem cell-derived RPE are transplanted in patients with AMD, which is ugly.

Details

Date:
November 3
Time:
12:00 pm - 1:00 pm
Event Category: