Sarah Coughlan
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Sarah Coughlan has a total of 24 co-authors. Here are the top co-authors by number of shared publications:
- Abey Martin
Department of BioMedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA
1 shared publication - Arturo Bravo-Nuevo
Department of BioMedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA
1 shared publication - Brian Heist
Department of BioMedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA
1 shared publication - Carlos Font
Department of BioMedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA
1 shared publication - Christopher K. Sutera
Department of BioMedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA
1 shared publication - Courtney Helm
Department of BioMedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA
1 shared publication
Latest Publications
- Open Access
- 14 May 2025
- Published by MDPI AG in Applied Sciences
- Vol. 15 (10) , 5486
Increased Myo/Nog Cell Presence and Phagocytic Activity in Retinal Degeneration: Insights from a Mouse Model
Myo/Nog cells play a pivotal role in ocular development and demonstrate a rapid response to stress and injury. This study investigates their behavior and distribution in a murine model of retinitis pigmentosa, specifically in C3H/HeJ mice, which exhibit photoreceptor degeneration due to a homozygous mutation in the Pde6brd1 gene. Retinal samples from C3H/HeJ and C57BL/6J mice were analyzed at postnatal weeks 2.5 to 6 using hematoxylin and eosin staining, immunofluorescence for brain-specific angiogenesis inhibitor 1 (BAI1) expressed in Myo/Nog cells, and TUNEL labeling for apoptotic cell detection. The results demonstrated a progressive thinning of the outer nuclear layer (ONL) in C3H mice, accompanied by a significant increase in Myo/Nog cell numbers. In normal retinas, Myo/Nog cells were primarily located in the inner nuclear and outer plexiform layers. However, in C3H/HeJ mice, they accumulated in the ONL near apoptotic photoreceptors and within the choroid. Notably, in these degenerative regions, Myo/Nog cells exhibited features of phagocytosis, suggesting a role in apoptotic cell clearance. Additionally, parallels between Myo/Nog cell responses in retinitis pigmentosa and models of oxygen-induced retinopathy, ocular hypertension, and light damage suggest that these cells may be leveraged for therapeutic purposes.
- 14 May 2025
- Published by MDPI AG in Applied Sciences
- Vol. 15 (10) , 5486
Open AccessIncreased Myo/Nog Cell Presence and Phagocytic Activity in Retinal Degeneration: Insights from a Mouse Model
Myo/Nog cells play a pivotal role in ocular development and demonstrate a rapid response to stress and injury. This study investigates their behavior and distribution in a murine model of retinitis pigmentosa, specifically in C3H/HeJ mice, which exhibit photoreceptor degeneration due to a homozygous mutation in the Pde6brd1 gene. Retinal samples from C3H/HeJ and C57BL/6J mice were analyzed at postnatal weeks 2.5 to 6 using hematoxylin and eosin staining, immunofluorescence for brain-specific angiogenesis inhibitor 1 (BAI1) expressed in Myo/Nog cells, and TUNEL labeling for apoptotic cell detection. The results demonstrated a progressive thinning of the outer nuclear layer (ONL) in C3H mice, accompanied by a significant increase in Myo/Nog cell numbers. In normal retinas, Myo/Nog cells were primarily located in the inner nuclear and outer plexiform layers. However, in C3H/HeJ mice, they accumulated in the ONL near apoptotic photoreceptors and within the choroid. Notably, in these degenerative regions, Myo/Nog cells exhibited features of phagocytosis, suggesting a role in apoptotic cell clearance. Additionally, parallels between Myo/Nog cell responses in retinitis pigmentosa and models of oxygen-induced retinopathy, ocular hypertension, and light damage suggest that these cells may be leveraged for therapeutic purposes.