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Understanding molecular mechanisms behind germinal matrix hemorrhage

Researchers have utilized a mouse model to determine the molecular mechanisms underlying germinal matrix hemorrhage. Nearly 12,000 premature infants born annually in the US are affected by neonatal brain hemorrhage which results in mortality and long-term morbidity. Unfortunately, no treatment exists for this condition, and the only preventive measure is steroids before birth, which has deleterious effects on brain development. The hemorrhage originates from the rupture of small brain vessels in a highly fragile region known as the germinal matrix.

However, the cellular and molecular mechanisms of this disorder remain poorly understood. In a recent study led by Drs. Jui Dave and Daniel Greif at Yale University found that mutant embryonic mice lacking the gene, Alk5 in pericytes (cells that support small brain vessels) develop germinal matrix hemorrhage. The condition arises due to enhanced proliferation of endothelial cells and upregulated protease activity which result in vessel rupture and hemorrhage. Furthermore, the study reveals that treating mutant mice with a recombinant protein, TIMP3 effectively attenuates the hemorrhage and reduces bleeding. The study is published in the journal Developmental Cell.

The findings from this study provide novel insights into the pathogenesis of germinal matrix hemorrhage and are likely to shed light on other brain disorders such as stroke and aneurysms as well. Although further research is needed to fully understand the beneficial effects of TIMP3, this study promises to broaden the scope of therapeutic intervention for this devastating disorder.

Citation: Dave, Jui M., Teodelinda Mirabella, Scott D. Weatherbee, and Daniel M. Greif. “Pericyte ALK5/TIMP3 Axis Contributes to Endothelial Morphogenesis in the Developing Brain.” Developmental Cell, 2018. doi:10.1016/j.devcel.2018.01.018.

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