What question did this study set out to answer?

Investigate how glucocorticoids regulate lipocalin-type prostaglandin D synthase (L-PGDS) and examine the role of L-PGDS-derived PGD2 in protecting hearts against ischemia/reperfusion injury.

May 19, 2009Journal of Clinical InvestigationOpen Access

Glucocorticoid protects rodent hearts from ischemia/reperfusion injury by activating lipocalin-type prostaglandin D synthase–derived PGD2 biosynthesis

View Full Paper

Ask AI

Bookmark

Authors

STSatori TokudomeJikei University School of Medicine MSMotoaki SanoHeart Failure & Transplant KSKen ShinmuraKeio University

Discussion

Member takes

Implication

Experimental study demonstrates that glucocorticoids alleviate ischemia/reperfusion injury in rodent hearts via L-PGDS activation, highlighting an unexpected survival pathway in cardiomyocytes.

Key Points

Investigate how glucocorticoids regulate lipocalin-type prostaglandin D synthase (L-PGDS) and examine the role of L-PGDS-derived PGD2 in protecting hearts against ischemia/reperfusion injury.
Treated cultured rat cardiomyocytes and mice with glucocorticoid receptor agonists to measure changes in L-PGDS, cPLA2, and COX2 expression as well as PGD2 synthesis.
Tested cardioprotective effects of dexamethasone using Langendorff-perfused isolated hearts and in vivo mouse models of ischemia/reperfusion in wild-type, COX2-inhibited, and L-PGDS-deficient mice.
Assessed cardiomyocyte survival and downstream signaling pathways under anoxia/reoxygenation stress following PGD2 administration in vitro.
Glucocorticoid receptor activation upregulated L-PGDS, COX2, and cPLA2, establishing PGD2 as the predominant prostaglandin induced in rat cardiomyocytes and mouse hearts.
Dexamethasone treatment reduced myocardial infarct size and improved functional recovery following ischemia/reperfusion in wild-type mice, but these cardioprotective effects were completely abolished by COX2 inhibition or L-PGDS gene knockout.
Exogenous PGD2 protected cultured cardiomyocytes against anoxia/reoxygenation-induced cell death through the D-type prostanoid receptor and downstream ERK1/2 pathway signaling.

Cite This Study

Tokudome et al. (2009) studied this question.

synapsesocial.com/papers/6a8799415c5abb51fa3434eb https://doi.org/10.1172/jci37413

View Full Paper

Ask AI

Bookmark

Implication

Experimental study demonstrates that glucocorticoids alleviate ischemia/reperfusion injury in rodent hearts via L-PGDS activation, highlighting an unexpected survival pathway in cardiomyocytes.

Glucocorticoid protects rodent hearts from ischemia/reperfusion injury by activating lipocalin-type prostaglandin D synthase–derived PGD2 biosynthesis

Discussion

Member takes

Implication

Key Points

Cite This Study

Glucocorticoid protects rodent hearts from ischemia/reperfusion injury by activating lipocalin-type prostaglandin D synthase–derived PGD2 biosynthesis

Discussion

Member takes

Implication

Key Points

Cite This Study

Also Consider

Also Consider