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Klopocki, E.

Publications and source records attributed to Klopocki, E..

2 recordsLinked to original sources

Small fibre neuropathy in Fabry disease: a human-derived neuronal in vitro disease model

Acral burning pain triggered by fever, thermal hyposensitivity, and skin denervation are hallmarks of small fibre neuropathy in Fabry disease, a life-threatening X-linked lysosomal storage disorder. Variants in the gene encoding alpha-galactosidase A may lead to impaired enzyme activity with cellular accumulation of globotriaosylceramide (Gb3). To study the underlying pathomechanism of Fabry-associated small fibre neuropathy, we generated a neuronal in vitro disease model using patient-derived induced pluripotent stem cells from three Fabry patients and one healthy control. We further generated an isogenic control line via CRISPR/Cas9 gene editing. We subjected iPSC to targeted peripheral neuronal differentiation and observed intra-lysosomal Gb3 accumulations in somas and neurites of Fabry sensory neurons using super-resolution microscopy. At functional level, patch-clamp analysis revealed a hyperpolarizing shift of voltage-gated sodium channel steady-state inactivation kinetics in Fabry cell lines as compared to the healthy control. Moreover, we demonstrate a drastic increase in Fabry sensory neuron Ca2+ levels at 39{degrees}C mimicking clinical fever (p < 0.001). This pathophysiological phenotype was accompanied by thinning of neurite calibres in sensory neurons obtained from Fabry patients compared to healthy control cells (p < 0.001). Linear-Nonlinear cascade models fit to spiking responses revealed that Fabry cell lines exhibit altered single neuron encoding properties relative to control. We further observed jam of mitochondrial trafficking at sphingolipid accumulations within Fabry sensory neurites utilizing a click-chemistry approach together with mitochondrial dysmorphism compared to healthy control cells. We pioneer insights into the cellular mechanisms contributing to pain, thermal hyposensitivity, and denervation in Fabry small fibre neuropathy, and pave the way for further mechanistic in vitro studies in Fabry disease and the development of novel treatment approaches.

neuroscience↗

Fndc3a (Fibronectin Domain Containing Protein 3A) influences median fin fold development and caudal fin regeneration in zebrafish by ECM alteration.

Summary statementWe investigated potential functions of Fndc3a during caudal fin development and regeneration in zebrafish. Reduced function interferes with correct epidermal cells structure and implies a role during vertebrate extremity development.\n\nAbstractInherited genetic alterations are often found to be disease-causing factors of patient phenotypes. To unravel the molecular consequences of newly identified factors functional investigations in vivo are eminent. We investigated molecular functions of FNDC3A (Fibronectin Domain Containing Protein 3A; HUGO), a novel candidate gene for split-hand/foot malformations (SHFM) in humans, by utilizing zebrafish (Danio rerio) as a vertebrate model. Patients with congenital SHFM display prominent limb malformations, which are caused by disturbance of limb development due to defects in apical ectodermal ridge (AER) establishment and maintenance. Initial gene expression and protein localization studies clarified the presence of fndc3a in developing and regenerating fins of zebrafish. For functional studies we established a hypomorphic fndc3a mutant line (fndc3awue1/wue1) via CRISPR/Cas9, exhibiting phenotypic malformations and changed gene expression patterns during early stages of median fin fold development. Furthermore, fndc3awue1/wue1 mutants display abnormal collagen localization, actinotrichia breakup and cellular defects in epidermal cells during caudal fin development. The observed effects are only temporary and later result in rather normal fin development in adults. In accordance with early fin development, proper caudal fin regeneration in adult fndc3awue1/wue1 mutants is hampered by interference with actinotrichia formation and epidermal cell abnormalities. Investigation of cellular matrix formation implied that loss of ECM structure is a common cause for both phenotypes. Our results thereby provide a molecular link between Fndc3a function during both developmental processes in zebrafish and foreshadow Fndc3a as a novel temporal regulator of epidermal cell properties during extremity development in vertebrates.

developmental biology↗