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• W2123451036 abstract "Apnea associated with infection and inflammation is a major medical concern in preterm infants. Prostaglandin E2 (PGE2) serves as a critical mediator between infection and apnea. We hypothesize that alteration of the microsomal PGE synthase-1 (mPGES-1) PGE2 pathway influences respiratory control and response to hypoxia. Nine-d-old wild-type (WT) mice, mPGES-1 heterozygote (mPGES-1+/–), and mPGES-1 knockout (mPGES-1–/–) mice were used. Respiration was investigated in mice using flow plethysmography after the mice received either interleukin-1β (IL-1β) (10 µg/kg) or saline. Mice were subjected to a period of normoxia, subsequent exposure to hyperoxia, and finally either moderate (5 min) or severe hypoxia (until 1 min after last gasp). IL-1β worsened survival in WT mice but not in mice with reduced or no mPGES-1. Reduced expression of mPGES-1 prolonged gasping duration and increased the number of gasps during hypoxia. Response to intracerebroventricular PGE2 was not dependent on mPGES-1 expression. Activation of mPGES-1 is involved in the rapid and vital response to severe hypoxia as well as inflammation. Attenuation of mPGES-1 appears to have no detrimental effects, yet prolongs autoresuscitation efforts and improves survival. Consequently, inhibition of the mPGES-1 pathway may serve as a potential therapeutic target for the treatment of apnea and respiratory disorders." @default.
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• W2123451036 date "2012-08-27" @default.
• W2123451036 modified "2023-10-17" @default.
• W2123451036 title "mPGES-1 and prostaglandin E2: vital role in inflammation, hypoxic response, and survival" @default.
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• W2123451036 doi "https://doi.org/10.1038/pr.2012.119" @default.
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