Dysfunctional or death of retinal photoreceptors is an irreversible phenomenon that is closely associated with a broad range of retinal degenerative diseases, such as retinitis pigmentosa and age-related macular degeneration (AMD), resulting in successive loss of visual function and blindness. In search for viable treatment for retinal degenerative diseases, mesenchymal stem cells (MSCs) has demonstrated promising therapeutic capabilities to repair and replace damaged photoreceptor cells in both in vitro and in vivo conditions. Nevertheless, the dearth of MSC differentiation capacity into photoreceptors has limited its use in cell replacement therapy. Erythropoietin (EPO) has vital role in early neural retinal cell differentiation and demonstrated rescue potential on dying photoreceptor cells. Hence, we aimed to evaluate the differentiation capacity of MSCs into photoreceptor cells in the presence of human EPO protein. We derived the MSC from human Wharton's jelly of umbilical cord and transduced the cells with lentivirus particles encoding EPO and green fluorescent protein (GFP) as reporter gene. The transduced cells were selectively cultured and induced to differentiate into photoreceptors by exposing to photoreceptor differentiation cocktail. Our preliminary results showed that transduced cells exposed to induction medium had an enhanced differentiation capacity when compared to non-transduced cells. Our results demonstrated a novel strategy to increase the yield of in vitro photoreceptor differentiation and may be potentially useful in improving the efficiency of stem cell transplantation for ocular disorders.
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http://dx.doi.org/10.1016/j.jphotobiol.2019.04.008 | DOI Listing |
Neurobiol Dis
December 2024
Department of Physiology & Neuroscience, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. Electronic address:
Huntington's disease (HD) is caused by the expansion of a CAG repeat, encoding a string of glutamines (polyQ) in the first exon of the huntingtin gene (HTTex1). This mutant huntingtin protein (mHTT) with extended polyQ forms aggregates in cortical and striatal neurons, causing cell damage and death. The retina is part of the central nervous system (CNS), and visual deficits and structural abnormalities in the retina of HD patients have been observed.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
December 2024
Halberg Chronobiology Center, University of Minnesota, Minneapolis, MN 55455, USA.
This review explores the intricate relationship between glaucoma and circadian rhythm disturbances. As a principal organ for photic signal reception and transduction, the eye plays a pivotal role in coordinating the body's circadian rhythms through specialized retinal ganglion cells (RGCs), particularly intrinsically photosensitive RGCs (ipRGCs). These cells are critical in transmitting light signals to the suprachiasmatic nucleus (SCN), the central circadian clock that synchronizes physiological processes to the 24-hour light-dark cycle.
View Article and Find Full Text PDFPhotodiagnosis Photodyn Ther
December 2024
Department of Ophthalmology, Tianjin Medical University General Hospital, Tianjin, China, Ministry of Education International Joint Laboratory of Ocular Diseases, Tianjin, China, Tianjin Key Laboratory of Ocular Trauma, Tianjin, China, Tianjin Institute of Eye Health and Eye Diseases, Tianjin, China, China-UK "Belt and Road" Ophthalmology. Electronic address:
Background: This study investigated the association between photoreceptor structural restoration and visual function outcomes in patients undergoing surgery for closed macular holes (MHs). Using adaptive optics scanning laser ophthalmoscopy (AOSLO) and microperimetry, we aimed to provide a more detailed understanding of photoreceptor recovery and visual improvement in closed MHs.
Methods: We conducted a retrospective observational study of 31 eyes of 28 patients who underwent vitrectomy with internal limiting membrane (ILM) peeling to treat idiopathic MHs.
Sci Rep
December 2024
INCI-UPR3212-CNRS, 8 Allée du Général Rouvillois, 67000, Strasbourg, France.
Mutations in the gene ABCA4 coding for photoreceptor-specific ATP-binding cassette subfamily A member 4, are responsible for Stargardts Disease type 1 (STGD1), the most common form of inherited macular degeneration. STGD1 typically declares early in life and leads to severe visual handicap. Abca4 gene-deletion mouse models of STGD1 accumulate lipofuscin, a hallmark of the disease, but unlike the human disease show no or only moderate structural changes and no functional decline.
View Article and Find Full Text PDFStem Cells Transl Med
December 2024
NEI/OSCTRS/OGVFB, Bethesda, MD, United States.
Retinal pigment epithelium (RPE) atrophy is a significant cause of human blindness worldwide, occurring in polygenic diseases such as age-related macular degeneration (AMD) and monogenic diseases such as Stargardt diseases (STGD1) and late-onset retinal degeneration (L-ORD). The patient-induced pluripotent stem cells (iPSCs)-derived RPE (iRPE) model exhibits many advantages in understanding the cellular basis of pathological mechanisms of RPE atrophy. The iRPE model is based on iPSC-derived functionally mature and polarized RPE cells that reproduce several features of native RPE cells, such as phagocytosis of photoreceptor outer segments (POS) and replenishment of visual pigment.
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