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Biology subjects

Forghani, R.

Publications and source records attributed to Forghani, R..

2 recordsLinked to original sources

Enabled primarily controls filopodial morphology, not actin organization, in the TSM1 growth cone in Drosophila

Ena/VASP proteins are processive actin polymerases that are required throughout animal phylogeny for many morphogenetic processes, including axon growth and guidance. Here we use live imaging of morphology and actin organization in the TSM1 axon of the Drosophila wing to dissect the mechanism of Ena action. We find that altering Ena activity has a substantial impact on filopodial morphology in this growth cone, but exerts only modest effects on actin organization. This is in contrast to the main regulator of Ena, Abl tyrosine kinase, which has profound effects on actin and only mild effects on TSM1 growth cone morphology. These data suggest that the primary role of Ena in this axon may be to link actin to morphogenetic processes of the plasma membrane, rather than regulating actin organization itself. These data also suggest that a key role of Ena, acting downstream of Abl, may be to maintain a constant filopodial organization of the growth cone, even as Abl activity varies in response to guidance cues in the environment. Summary statementWe dissect the function of the actin polymerase, Enabled, in axon growth by live-imaging of actin dynamics and axon morphology of the TSM1 neuron in its native environment in vivo.

neuroscience↗

Neurotrophic Factor-Laden Acellular Chondroitin Sulfate Scaffolds Promote Chronic Functional Recovery After Severe Traumatic Brain Injury

Severe traumatic brain injury (sTBI) survivors experience permanent functional disabilities due to significant volume loss and the brains poor capacity to regenerate. Chondroitin sulfate glycosaminoglycans (CS-GAGs) are key regulators of growth factor signaling and neural stem cell homeostasis in the brain. However, the efficacy of engineered CS (eCS) matrices in mediating structural and functional recovery after sTBI has not been investigated. We report that neurotrophic factor functionalized acellular eCS matrices implanted into the rat M1 region acutely post-sTBI, significantly enhanced cellular repair and gross motor function recovery when compared to controls, 20 weeks post-sTBI. Animals subjected to M2 region injuries followed by eCS matrix implantations, demonstrated the significant recovery of reach-to-grasp function. This was attributed to enhanced volumetric vascularization, activity-regulated cytoskeleton (Arc) protein expression, and perilesional sensorimotor connectivity. These findings indicate that eCS matrices implanted acutely post-sTBI can support complex cellular, vascular, and neuronal circuit repair, chronically after sTBI.

bioengineering↗