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Proteomic changes in anterior capsule of diabetic, age-related and post-vitrectomy cataract.

ABSTRACT: The focus of our research centers on exploring the proteome changes and corresponding signaling pathways involved in the development of diabetic cataract, age-related cataract and post-vitrectomy cataract, investigating aqueous humor, anterior capsule and lens human samples. Outstanding proteomic profiles of the three sample types have been generated using DIA proteomics. We have observed substantial differences in the regulation of several pathways between our groups and samples types, and we have particularly highlighted the involvement of non-canonical Wnt receptor signaling pathway, glycosaminoglycan and glycosphingolipid pathways, and oxidation reduction pathway in the formation of different cataract forms.

INSTRUMENT(S): Q Exactive HF-X

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Lens Epithelium

DISEASE(S): Cataract

SUBMITTER: Martina Samiotaki

LAB HEAD: Christina Karakosta

PROVIDER: PXD045547 | Pride | 2025-05-06

REPOSITORIES: Pride

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Project description:We developed a human cerebral organoid model derived from induced pluripotent stem cells (iPSCs) with targeted genome editing to abolish protein expression of the Contactin Associated Protein-like 2 (CNTNAP2) autism spectrum disorder (ASD) risk gene, mimicking loss-of-function mutations seen in patients. CNTNAP2-/- cerebral organoids displayed accelerated cell cycle, ventricular zone disorganisation and increased cortical folding. Proteomic analysis revealed disruptions in glutamatergic/GABAergic synaptic pathways and neurodevelopment, highlighting increased protein expression of corticogenesis and neurodevelopment-related genes such as Forkhead box protein G1 (FOXG1) and Paired box 6 (PAX6). Transcriptomic analysis revealed differentially expressed genes (DEG) belonging to inhibitory neuron-related gene networks. Interestingly, there was a weak correlation between the transcriptomic and proteomic data, suggesting nuanced translational control mechanisms. Along these lines we find upregulated Protein Kinase B (Akt)/mechanistic target of rapamycin (mTOR) signalling in CNTNAP2-/- organoids. Spatial transcriptomics analysis of CNTNAP2-/- ventricular zones demonstrated pervasive changes in gene expression, particularly in PAX6- cells, implicating upregulation of cell cycle regulation pathways, synaptic and glutamatergic/GABAergic pathways. We noted a significant overlap of all omics datasets with idiopathic ASD (macrocephaly) iPSC-derived telencephalic organoids DEG, where FOXG1 was upregulated, along with aberrant expression of Glutamate decarboxylase 1 (GAD1) and T-Box Brain Transcription Factor 1 (TBR1), suggesting altered GABAergic/glutamatergic neuron development. These findings potentially highlight a shared mechanism in the early cortical development of various forms of ASD, further elucidate the role of CNTNAP2 in ASD pathophysiology and cortical development and pave the way for targeted therapies using cerebral organoids as preclinical models.

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Proteomic changes in anterior capsule of diabetic, age-related and post-vitrectomy cataract.

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