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Tariq, S.

Publications and source records attributed to Tariq, S..

2 recordsLinked to original sources

Intravital Cholesterol Depletion Reduces Membrane Dynamics and Increases Mechanosensitivity in Osteocytes In Vivo

Osteocytes detect mechanical forces within bone through signaling processes organized at the plasma membrane. Membrane cholesterol regulates membrane organization, dynamics, and mechanical properties, yet its role in osteocyte mechanotransduction in vivo remains unknown. Here, we developed an intravital multiphoton imaging approach to quantify membrane-associated uptake, retention, and clearance alongside load-induced Ca2+ signaling in osteocytes within the intact metatarsal. Using fluorescent nanoparticles and a membrane-labeling probe, we tracked these processes before and after pharmacological cholesterol depletion. Cholesterol depletion reduced osteocyte membrane uptake and retention and altered clearance in both sexes, while affecting load-induced Ca2+ signaling in a sex-dependent manner. In females, cholesterol depletion increased both the proportion of osteocytes responding to mechanical loading and the magnitude of their responses, whereas neither outcome changed in males. These findings identify plasma membrane cholesterol as a regulator of osteocyte membrane dynamics and mechanical responsiveness in vivo. More broadly, this work establishes an approach for directly examining how membrane composition and turnover regulate mechanotransduction in cells embedded within their native tissue environment.

cell biology↗

Embryonic motor neuron programming factors reactivate immature gene expression and suppress ALS pathologies in postnatal motor neurons

Aging is a major risk factor in amyotrophic lateral sclerosis (ALS) and other adult-onset neurodegenerative disorders. Whereas young neurons are capable of buffering disease-causing stresses, mature neurons lose this ability and degenerate over time. We hypothesized that the resilience of young motor neurons could be restored by re-expression of the embryonic motor neuron selector transcription factors ISL1 and LHX3. We found that viral re-expression of ISL1 and LHX3 reactivates aspects of the youthful gene expression program in mature motor neurons and alleviates key disease-relevant phenotypes in the SOD1G93A mouse model of ALS. Our results suggest that redeployment of lineage-specific neuronal selector transcription factors can be an effective strategy to attenuate age-dependent phenotypes in neurodegenerative disease.

neuroscience↗