Rabbit Corneal Endothelial Cells

Cat.No.: CSC-C5252S

Species: Rabbit

Source: Cornea; Eye

Cell Type: Endothelial Cell

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Cat.No.
CSC-C5252S
Description
The corneal endothelium is a single layer of flat hexagonal cells forming a boundary between the corneal stroma and the anterior chamber. This layer of cells functions as a pump to regulate stromal hydration.
Rabbit corneal endothelial cells from Creative Bioarray are isolated from the rabbit eye tissue. The method we use to isolate corneal endothelial cells was developed based on a combination of established and our proprietary methods. The rabbit corneal endothelial cells are characterized by immunofluorescence with antibodies specific to pan-cytokeratin (PCK). Each vial contains 0.5x10^6 cells per ml and is delivered frozen.
Species
Rabbit
Source
Cornea; Eye
Cell Type
Endothelial Cell
Disease
Normal
Quality Control
Rabbit Corneal Endothelial Cells are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast and fungi.
Storage and Shipping
Creative Bioarray ships frozen cells on dry ice. On receipt, immediately transfer frozen cells to liquid nitrogen (-180 °C) until ready for experimental use. Never can cells be kept at -20 °C.
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

Rabbit corneal endothelial cells (RCECs) form the single layer of neuroectoderm-derived cells lining the posterior corneal surface. A principal strength of RCECs is their ability to establish highly reproducible, contact-inhibited monolayers exhibiting the classic polygonal, predominantly hexagonal morphology. These cells develop well-organized apicolateral tight junctions, demarcated by continuous ZO-1 localization, and uniformly express the defining endothelial markers Na⁺/K⁺-ATPase, aquaporin-1, and N-cadherin, while retaining robust transendothelial electrical resistance. Crucially, unlike primary human corneal endothelial cells, which are notoriously post-mitotic and challenging to expand, RCECs—especially those derived from young rabbits—retain a marked intrinsic proliferative capacity. This permits transient expansion without immediate loss of phenotype, enabling mechanistic studies of cell cycle re-entry and regenerative repair that are difficult in human cells.

The rabbit origin confers substantial practical and translational benefits. The large eye size simplifies endothelial isolation, yielding abundant, highly pure cells free from stromal contamination. The controlled age and genetic uniformity of laboratory rabbits minimize donor variability, ensuring experimental consistency. Furthermore, the direct alignment with established rabbit models of corneal endothelial injury, cryoinjury, and Descemet membrane transplantation enables seamless in vitro–in vivo correlation. Together, these features establish primary RCECs as a cost-effective, ethically accessible, and physiologically faithful platform for investigating endothelial pathophysiology, drug toxicity, and tissue-engineering strategies.

IGFBP4 Suppresses EndMT by Inhibiting the Wnt2/β-Catenin Signaling Pathway in Rabbit Corneal Endothelial Cells

Endothelial-mesenchymal transition (EndMT) represents a major limiting factor in the in vitro expansion of corneal endothelial cells (CECs). This study aims to identify the key genes and signaling pathways driving EndMT in rabbit CECs (RCECs) and to explore targeted interventions to preserve cellular phenotype, ultimately improving in vitro culture protocols.

During serial passaging, primary RCECs underwent significant EndMT, characterized by progressive cellular enlargement and the acquisition of a fibroblast-like morphology. Comparative transcriptome analysis via high-throughput RNA sequencing of passage 0 (P0) and passage 3 (P3) RCECs revealed significant differential expression of EndMT-associated genes. Specifically, bioinformatic analyses (GO/KEGG) highlighted the downregulation of IGFBP4 and the upregulation of WNT components, implicating Wnt pathway activation in the EndMT process. Functionally, overexpressing IGFBP4 or knocking down WNT2 in RCECs substantially decreased the expression of EndMT markers (α-SMA and vimentin) as well as core components of the Wnt2/β-catenin pathway (Frizzled, Dvl, p-β-catenin, and p-TCF-4). Conversely, opposite genetic manipulations yielded elevated expression levels. Collectively, these findings demonstrate that IGFBP4 effectively suppresses EndMT and maintains the functional CEC phenotype by inhibiting the Wnt2/β-catenin signaling pathway.

RCECs tend to undergo EndMT during in vitro culture.
Fig. 1. RCECs tend to undergo EndMT during in vitro culture (Ke, Hongqin, et al., 2026).
IGFBP4 inhibits Wnt/β-catenin signaling in RCECs.
Fig. 2. IGFBP4 inhibits Wnt/β-catenin signaling in RCECs (Ke, Hongqin, et al., 2026).

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