Description: Rationale: Efficient clearance of apoptotic cells (efferocytosis) is a prerequisite for inflammation resolution and tissue repair. After myocardial infarction, phagocytes are recruited to the heart and promote clearance of dying cardiomyocytes. The molecular mechanisms of efferocytosis of cardiomyocytes and in the myocardium are unknown. The injured heart provides a unique model to examine relationships between efferocytosis and subsequent inflammation resolution, tissue remodeling, and organ function. Objective: We set out to identify mechanisms of dying cardiomyocyte engulfment by phagocytes and, for the first time, to assess the causal significance of disrupting efferocytosis during myocardial infarction. Methods and Results: In contrast to other apoptotic cell receptors, macrophage myeloid-epithelial-reproductive tyrosine kinase was necessary and sufficient for efferocytosis of cardiomyocytes ex vivo. In mice, Mertk was specifically induced in Ly6c LO myocardial phagocytes after experimental coronary occlusion. Mertk deficiency led to an accumulation of apoptotic cardiomyocytes, independently of changes in noncardiomyocytes, and a reduced index of in vivo efferocytosis. Importantly, suppressed efferocytosis preceded increases in myocardial infarct size and led to delayed inflammation resolution and reduced systolic performance. Reduced cardiac function was reproduced in chimeric mice deficient in bone marrow Mertk ; reciprocal transplantation of Mertk +/+ marrow into Mertk –/– mice corrected systolic dysfunction. Interestingly, an inactivated form of myeloid-epithelial-reproductive tyrosine kinase, known as solMER, was identified in infarcted myocardium, implicating a natural mechanism of myeloid-epithelial-reproductive tyrosine kinase inactivation after myocardial infarction. Conclusions: These data collectively and directly link efferocytosis to wound healing in the heart and identify Mertk as a significant link between acute inflammation resolution and organ function.

Description: : Gum Hollow Delta is a small microtidal, aggradational to slightly progradational, hyperpycnal, tropical-cyclone-dominated delta in Nueces Bay (Texas). The delta formed over the past 80 years following anthropogenically diverted, high sediment-laden stream runoff through Gum Hollow Creek into Nueces Bay. Gum Hollow Delta formed episodically due to high runoff and increased discharge in Gum Hollow Creek and temporarily elevated sea level during Gulf of Mexico tropical cyclones. The delta is 600 m long, 1000 m wide, and 1.6 m thick. Fifty-one vibracores were taken along four dip transects and two strike transects to delineate the internal sedimentology, architecture, and geochronology of the delta. The delta consists of nine bedsets (tempestites) representing deltaic growth events. Internal stratigraphic correlations were constrained by the identification of significant widespread flooding surfaces and by 137 Cs geochronology. Flooding surfaces formed as storm surges produced short-term base-level rises in Nueces Bay, which were followed by rapid hyperpycnal sedimentation events. Tropical cyclones such as the 1933 Hurricane (Hurricane Eleven), 1945 Hurricane (Hurricane Five), and the 1949 Hurricane (Hurricane Ten) and named hurricanes Alice (1954), Carla (1961), Beulah (1967), Celia (1970), Allen (1980), and Bret (1999) produced significant base-level rises and deltaic depositional events. Distributary-channel avulsions are also associated with the landfall of these tropical cyclones. Comparison of the timing of the deposition of these hyperpycnal tempestites, constrained by 137 Cs geochronology, historical aerial photographs, and the historical record of Gulf of Mexico tropical cyclones indicate that the Gum Hollow Delta preserves an 80-year record of storminess.