Publications by authors named "J PAPILLON"

Article Synopsis
  • Calcium-independent phospholipase A2γ (iPLA2γ) plays a role in kidney health, with its deletion in mice leading to mitochondrial issues and heightened autophagy in kidney cells, yet not causing albuminuria directly.
  • In a study involving diabetic models, iPLA2γ knockout (KO) mice did not show the expected increase in albuminuria compared to control mice, even with similar hyperglycemia levels.
  • The findings suggest that the absence of iPLA2γ offers protection against chronic kidney damage during diabetes, linked to enhanced autophagy in the glomeruli.
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Protein misfolding in the endoplasmic reticulum (ER) of podocytes contributes to the pathogenesis of glomerular diseases. Protein misfolding activates the unfolded protein response (UPR), a compensatory signaling network. We address the role of the UPR and the UPR transducer, inositol-requiring enzyme 1α (IRE1α), in streptozotocin-induced diabetic nephropathy in mice.

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Corneal epithelial barrier represents one of the major limitations to ocular drug delivery and can be explored non-invasively through the evaluation of its electrical properties. Human corneas stored in active storage machine (ASM) could represent an interesting physiological model to explore transcorneal drug penetration. We designed a new system adapted to human corneas preserved in ASM to explore corneal epithelial barrier function ex-vivo.

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Uveal melanoma (UM) is the most common primary intraocular malignancy in the adult eye. Despite the aggressive local management of primary UM, the development of metastases is common with no effective treatment options for metastatic disease. Genetic analysis of UM samples reveals the presence of mutually exclusive activating mutations in the Gq alpha subunits GNAQ and GNA11.

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SLK controls the cytoskeleton, cell adhesion, and migration. Podocyte-specific deletion of SLK in mice leads to podocyte injury as mice age and exacerbates injury in experimental focal segment glomerulosclerosis (FSGS; adriamycin nephrosis). We hypothesized that adhesion proteins may be substrates of SLK.

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