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However, co-translational regulatory mechanisms remain poorly characterized in intact mammalian systems. As a proof-of-concept, we developed a multi-omics approach to investigate endothelial-specific, co-translational regulation by modifying the translating ribosome affinity purification (TRAP) in vivo. We simultaneously co-immunoprecipitated (IP) polysome-associated mRNAs and proteins from the hearts of hemagglutinin-tagged ribosomal protein L22 mice (RiboTag) crossed with inducible endothelial-specific\n                    <jats:italic>Cdh5CreERT2<\/jats:italic>\n                    mice (\n                    <jats:italic>RiboTag<\/jats:italic>\n                    <jats:sub>\n                      <jats:italic>EC<\/jats:italic>\n                    <\/jats:sub>\n                    ). To perturb endothelial function, female mice were injected with E.\n                    <jats:italic>coli<\/jats:italic>\n                    lipopolysaccharide (LPS) (6\u00a0mg\/Kg, i.p., 12\u00a0h). Hearts were homogenized, with ~\u200910% used for input RNA-Seq and proteomics controls, and the remainder for IP of ribosome-bound polyadenylated mRNA and proteins. Endothelial cell transcripts (\n                    <jats:italic>pecam1<\/jats:italic>\n                    ,\n                    <jats:italic>cdh5<\/jats:italic>\n                    ) were enriched\u2009&gt;\u20095-fold, while markers characteristic of other cell types were significantly depleted (&lt;\u20090.05 q-value). We aligned transcriptomic and proteomic datasets (&gt;\u20091250 overlapping terms) to identify pathways associated with concordant and discordant co-translational regulation. LPS was identified as the upstream regulator of the co-translational dataset that was concordantly regulated. Upregulated mRNAs but not proteins related to glycolysis were discordantly regulated. These findings validate our proof-of-concept multi-omics approach as a predictive platform for identifying disease-relevant pathways regulated at the co-translational level\n                    <jats:italic>in vivo.<\/jats:italic>\n                  <\/jats:p>","DOI":"10.1007\/s11010-026-05551-9","type":"journal-article","created":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T10:50:27Z","timestamp":1777373427000},"page":"2381-2398","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Co-translational profiling in the cardiac endothelium in response to LPS-induced inflammation in female mice in vivo: a proof-of-concept approach"],"prefix":"10.1007","volume":"481","author":[{"given":"Chad M.","family":"Warren","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bhairavi","family":"Swaminathan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paulina","family":"Langa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephanie R.","family":"Villa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Walter C.","family":"Thompson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magdalena","family":"Chrzanowska","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan K.","family":"Kitajewski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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