Pathological neovascularization in choroid, a leading cause of
blindness, is a characteristic of many fundus diseases, such as
diabetic retinopathy and
age-related macular degeneration. The present study aimed to elucidate the key signaling pathways in
choroidal neovascularization (CNV) by analyzing the
mRNA profiles of choroid and retina in tree shrews with CNV. We induced choroidal angiogenesis by
laser photocoagulation in 15 tree shrews and obtained
mRNA profiles of their choroids and retinas by high-throughput transcriptome sequencing. Hierarchical cluster analysis, weighted gene co-expression network analysis (WGCNA),
protein-
protein interaction (PPI) network analysis,
hematoxylin and
eosin (HE) staining, CD31 immunohistochemistry (IHC), and reverse transcription quantitative PCR (RT-qPCR) were performed. After
laser photocoagulation, we obtained a total of 350 differentially expressed genes (DEGs) in the choroid, including 59 genes in Module-FASN ("ME-FASN") module and 28 genes in Module-RPL ("ME-RPL") module. A total of 69 DEGs in retina, including 20 genes in Module-SLC ("ME-SLC") module. Bioinformatics analysis demonstrated that DEGs in choroid were mainly involved in membrane transport; DEGs in "ME-RPL" were prominent in pathways associated with
IgA production, antigen presentation, and
cell adhesion molecules (CAMs) signaling. DEGs in "ME-FASN" were involved in
fatty acid metabolism and
PPAR signaling pathway, while DEGs in "ME-SLC" were involved in GABAergic synapse, neuroactive life receptor interaction,
cholinergic synapse, and retrograde
endocannabinoid signaling pathway. PPI network analysis demonstrated that the
ribosomal protein family genes (
RPL31, RPL7, RPL26L1, and RPL19) are key factors of "ME-RPL,"
acyl-CoA superfamily genes (ACACA, ACAT1, ACAA2, and ACACB) and FASN are key factors of "ME-FASN" and superfamily of solid carrier genes (SLC17A6, SLC32A1, SLC12A5, and SLC6A1) and
complement genes (C4A, C3, and C2) are key factors of "ME-SLC." In conclusion, the present study discovered the important signal transductions (
fatty acid metabolic pathway and CAMs signaling) and genes (
ribosomal protein family and the
complement system) in tree shrew CNV. We consider that our findings hold implications in unraveling molecular mechanisms that underlie occurrence and development of CNV.