Trauma-Induced Spinal Cord Endothelial Cell Response Governed by Epigenetic Kdm6a-CNN1 Interaction

In a recent study, researchers have made significant strides in understanding the cellular mechanisms that contribute to the debilitating effects of Spinal Cord Injury (SCI). The study, which focused on the microvascular endothelial cells (SCMECs) within the spinal cord, revealed that an increase in UTX, a lysine demethylase, following SCI leads to the senescence of these crucial cells. This process subsequently promotes the secretion of pro-inflammatory factors that create an unfavorable environment for spinal cord repair.

SCI, a form of central nervous system trauma, often results in paralysis and sensory loss. The pathophysiological changes post-SCI have been scrutinized, revealing increased cellular senescence as a key factor impeding regeneration. The study pinpointed the upregulated presence of UTX in SCMECs after SCI, which corresponded with amplified inflammation through the senescence-associated secretory phenotype (SASP). Furthermore, deletion of UTX in endothelial cells provided protection against SCMECs senescence and moderated SASP secretion, fostering a more conducive environment for neurological recovery.

The research, conducted in a controlled laboratory setting, utilized a contusion SCI model in mice to investigate the relationship between UTX upregulation and SCMECs senescence. Experimental findings suggest that targeting the UTX-CNN1 axis—the pathway that includes UTX and calponin 1, a protein associated with muscle contraction—could represent a novel therapeutic approach to improve outcomes

Source: Nature.com

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