ArticlePloS one2026
Fatty acid-binding protein 5 (FABP5) modulates limbal epithelial cell homeostasis by regulating the expression of key genes under both normal and inflammatory conditions, in vitro.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital aniridia, a rare disorder caused by PAX6 haploinsufficiency, is characterized by progressive, vision-threatening aniridia-associated keratopathy (AAK) with limbal epithelial dysfunction and chronic inflammation. Downregulation of fatty acid binding protein 5 (FABP5) has been reported in conjunctival cells of congenital aniridia patients and in limbal epithelial cells (LECs) of the PAX6 siRNA knockdown model. We aimed to investigate the effects of FABP5 deficiency on LECs gene expression, without or with inflammatory stimuli. To achieve FABP5 knockdown, human primary LECs were transfected with FABP5 siRNA, using Lipofectamine 2000. Inflammation was induced 48 hours after transfection by incubating cells with 2 µg/mL lipopolysaccharides (LPS) or 1 ng/ml IL-1β. Thereafter, gene and protein levels were examined using qPCR, Western blot and ELISA. Significant downregulation of PAX6, KRT3 and MMP2 and upregulation of KRT12 mRNA level was observed upon FABP5 knockdown (p ≤ 0.022). Under inflammatory conditions (IL-1β or LPS treatment), FABP5 knockdown led to reduced PAX6, FOSL2, IL-6, PTGES2, KRT3, MAPK3 and MMP2 (p ≤ 0.048) and increased VEGFα and CRABP2 mRNA expression levels compared to control LECs (p ≤ 0.034). Following FABP5 knockdown, reduced PAX6, IL-6 and KRT3 protein levels were confirmed in absence of inflammatory stimuli and in cells treated with IL-1β (p ≤ 0.034). Our results suggest a novel role of FABP5 protein in AAK progression by controlling expression levels of genes and proteins involved in LEC differentiation. In addition, under inflammatory conditions, FABP5 deficiency affects key transcription factors (PAX6, FOSL2), genes regulating LEC migration, differentiation and cell maintenance (KRT3, VEGFα, MAPK3, CRABP2), and genes involved in inflammation (IL-6, PTGES2).
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.