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Chary, P.

Publications and source records attributed to Chary, P..

2 recordsLinked to original sources

Hemodynamic and electrophysiological progression of the Rose Bengal photothrombotic stroke model in mice: vasoactive properties of Rose Bengal, tissue heating, wavelength optimization, and sex differences in lesion volume

The photothrombotic stroke model is gaining popularity due to its relative simplicity, minimal invasiveness, and clinical relevance. Photothrombosis involves the delivery of an intravascular photosensitizer (Rose Bengal) followed by its photoactivation, resulting in vessel occlusion and ischemia. Using a combination of complementary optical and non-optical techniques, we characterized the physiological changes in mice undergoing photothrombosis. We report that Rose Bengal acts as a rapid vasoconstrictor, inducing hypoemia both in the brain and periphery even in the absence of its photoactivation. Conversely, we find that light, when used at photothrombosis-appropriate intensities and durations, induces large amounts of tissue heating and hyperemia even in the distal non-illuminated hemisphere. Furthermore, we show that use of the optimal photothrombotic wavelength based on the Rose Bengal absorption spectrum (yellow-561nm) produces a more consistent and pronounced drop in blood flow, and a shorter latency to the initial spreading depolarization (SD), ultimately resulting in a larger stroke. Similarly, when yellow light is used to induce a stroke in ChR2-expressing mice, the electrophysiological and hemodynamic confounds from green light cross activation of ChR2 are eliminated. Finally, we observe across cohorts that male mice have larger strokes than females. Altogether, we extensively describe important caveats and confounds concerning photothrombosis and provide a detailed characterization of its early ischemic events. Significance statementPhotothrombosis is a powerful model of ischemic stroke which uses light to photoactivate an intravascular dye (Rose Bengal). However, little is known about the independent effects of both the Rose Bengal and the light used to activate it. We show that both manipulations introduce separate confounds relevant to stroke outcomes, something which should be considered and accounted for when using this technique. In addition, we demonstrate that by using the optimal Rose Bengal excitation wavelength, the blood flow drop is more pronounced and consistent, resulting in larger strokes and perhaps better modelling human injury. Furthermore, we show that precautions can be taken to avoid spectral overlap when integrating photothrombosis in optogenetic experiments. Finally, we explore sex differences in lesion volume.

neuroscience↗

Rescue of blood coagulation Factor VIII exon-16 mis-splicing by antisense oligonucleotides

The human Factor VIII (F8) protein is essential for the blood coagulation cascade and specific F8 mutations cause the rare bleeding disorder Hemophilia A (HA). Here, we investigated the impact of HA-causing single-nucleotide mutations on F8 pre-mRNA splicing. We found that 14/97 ([~]14.4%) coding sequence mutations tested in our study induced exon skipping. Splicing patterns of 4/11 ([~]36.4%) F8 exons tested were especially sensitive to the presence of common disease-causing mutations. RNA-chemical probing analyses revealed a three-way junction structure at the 3' end of intron 15 (TWJ-3-15). TWJ-3-15 sequesters the polypyrimidine tract, a key determinant of 3' splice site strength. Using exon-16 of the F8 gene as a model, we designed specific antisense oligonucleotides (ASOs) that target TWJ-3-15 and identified three that promote the splicing of F8 exon-16. Interaction of TWJ-3-15 with ASOs increases accessibility of the polypyrimidine tract and inhibits the binding of hnRNPA1-dependent splicing silencing factors. Moreover, ASOs targeting TWJ-3-15 rescue diverse splicing-sensitive HA-causing mutations, most of which are distal to the 3 splice site being impacted. The TWJ-3-15 structure and its effect on mRNA splicing provide a model for HA etiology in patients harboring specific F8 mutations and provide a framework for precision RNA-based HA therapies.

molecular biology↗