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Community resilience increases a place-based community’s capacity to respond and adapt to life-changing environmental dynamics like climate change and natural disasters. Timely access to environmental data is an important factor for community resilience. Most Earth science information is created for a particular science community for a specific scientific purpose, without much thought to who else could benefit from it and how they might use it. New approaches are needed to facilitate better data production and integration for community use.In this session, we present the findings of a paper published by ESIP’s (Earth Science Information Partners) Community Resilience Cluster. As a convening space for over 150 member organizations across different sectors, ESIP’s biannual meetings, conference calls, and topic-driven clusters provided the infrastructure and expertise to support the Community Resilience cluster’s examination of the role of Earth science data for community resilience. This presentation highlights the challenges communities face when applying Earth science data to their efforts:• Inequity in the scientific process,• Gaps in data ethics and governance,• A mismatch of scale and focus, and• Lack of actionable information for communities.Recommendations are made as starting points to address the challenges, along with examples of good practices from across the Earth science community. Given ESIP’s data stewardship efforts with large organizations and across domains, the recommendations are applicable at scale. We offer actionable steps for the Earth science community to help them produce data to better support community resilience.

Elevated levels of reactive oxygen species and intracellular Ca2+ play a key role in endothelial barrier dysfunction in acute lung injury. We previously showed that H2O2-induced increases in intracellular calcium concentrations ([Ca2+]i) in lung microvascular endothelial cells (LMVECs) involve the membrane Ca2+ channel, transient receptor potential vanilloid-4 (TRPV4) and that inhibiting this channel attenuated H2O2-induced barrier disruption in vitro. We also showed that phosphorylation of TRPV4 by the Src family kinase, Fyn, contributes to H2O2-induced Ca2+ influx in LMVEC. In endothelial cells, Fyn is tethered to the cell membrane by CD36, a fatty acid transporter. In this study, we assessed the effect of genetic loss or pharmacological inhibition of CD36 on Ca2+ responses to H2O2. H2O2-induced Ca2+ influx was attenuated in LMVEC isolated from mice lacking CD36 ( CD36−/−). TRPV4 expression and function was unchanged in LMVEC isolated from wild-type (WT) and CD36−/− mice, as well as mice with deficiency for Fyn ( Fyn−/−). TRPV4 immunoprecipitated with Fyn, but this interaction was decreased in CD36−/− LMVEC. The amount of phosphorylated TRPV4 was decreased in LMVEC from CD36−/− mice compared with WT controls. Loss of CD36 altered subcellular localization of Fyn, while inhibition of CD36 fatty acid transport with succinimidyl oleate did not attenuate H2O2-induced Ca2+ influx. Lastly, we found that CD36−/− mice were protected from ischemia-reperfusion injury in vivo. In conclusion, our data suggest that CD36 plays an important role in H2O2-mediated lung injury and that the mechanism may involve CD36-dependent scaffolding of Fyn to the cell membrane to facilitate TRPV4 phosphorylation.