{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen SY"],"funding":["NEI NIH HHS","National Eye Institute, National Institutes of Health, Bethesda, MD"],"pagination":["280-295"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7986837"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(3)"],"pubmed_abstract":["Quiescence and self-renewal of human corneal epithelial progenitor/stem cells (LEPC) are regulated by the limbal niche, presumably through close interaction with limbal (stromal) niche cells (LNC). Paired box homeotic gene 6 (Pax6), a conserved transcription factor essential for eye development, is essential for proper differentiation of limbal and corneal epithelial stem cells. Pax6 haploinsufficiency causes limbal stem cell deficiency, which leads to subsequent corneal blindness. We previously reported that serial passage of nuclear Pax6+ LNC resulted in the gradual loss of nuclear Pax6+ and neural crest progenitor status, the latter of which was reverted upon recovery of Pax6. These findings suggest Pax6 plays a pivotal role in supporting the self-renewal of LEPC in limbal niche. Herein"],"journal":["Stem cells (Dayton, Ohio)"],"pubmed_title":["HC-HA/PTX3 from amniotic membrane reverts senescent limbal niche cells to Pax6+ neural crest progenitors to support limbal epithelial progenitors."],"pmcid":["PMC7986837"],"funding_grant_id":["R01 EY006819","RO1 EY06819"],"pubmed_authors":["Hsu D","Chen SY","Zhu Y","Zhang Y","Tseng SCG"],"additional_accession":[]},"is_claimable":false,"name":"HC-HA/PTX3 from amniotic membrane reverts senescent limbal niche cells to Pax6+ neural crest progenitors to support limbal epithelial progenitors.","description":"Quiescence and self-renewal of human corneal epithelial progenitor/stem cells (LEPC) are regulated by the limbal niche, presumably through close interaction with limbal (stromal) niche cells (LNC). Paired box homeotic gene 6 (Pax6), a conserved transcription factor essential for eye development, is essential for proper differentiation of limbal and corneal epithelial stem cells. Pax6 haploinsufficiency causes limbal stem cell deficiency, which leads to subsequent corneal blindness. We previously reported that serial passage of nuclear Pax6+ LNC resulted in the gradual loss of nuclear Pax6+ and neural crest progenitor status, the latter of which was reverted upon recovery of Pax6. These findings suggest Pax6 plays a pivotal role in supporting the self-renewal of LEPC in limbal niche. Herein","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2025-04-22T02:05:44.932Z","creation":"2025-04-05T20:15:03.938Z"},"accession":"S-EPMC7986837","cross_references":{"pubmed":["33373496"],"doi":["10.1002/stem.3323"]}}