{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T09:23:26Z","timestamp":1762161806707,"version":"3.41.2"},"reference-count":140,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,10,23]],"date-time":"2023-10-23T00:00:00Z","timestamp":1698019200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100006955","name":"Office of Extramural Research, National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006955","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:p>Clinical frailty affects \u223c10% of people over age 65 and is studied in a chronically inflamed (Interleukin-10 knockout; \u201cIL10-KO\u201d) mouse model. Frailty phenotypes overlap the spectrum of diseases (\u201claminopathies\u201d) caused by mutations in <jats:italic>LMNA<\/jats:italic>. <jats:italic>LMNA<\/jats:italic> encodes nuclear intermediate filament proteins lamin A and lamin C (\u201clamin A\/C\u201d), important for tissue-specific signaling, metabolism and chromatin regulation. We hypothesized that wildtype lamin A\/C associations with tissue-specific partners are perturbed by chronic inflammation, potentially contributing to dysfunction in frailty. To test this idea we immunoprecipitated native lamin A\/C and associated proteins from skeletal muscle, hearts and brains of old (21\u201322\u00a0months) IL10-KO versus control C57Bl\/6 female mice, and labeled with Tandem Mass Tags for identification and quantitation by mass spectrometry. We identified 502 candidate lamin-binding proteins from skeletal muscle, and 340 from heart, including 62 proteins identified in both tissues. Candidates included frailty phenotype-relevant proteins Perm1 and Fam210a, and nuclear membrane protein Tmem38a, required for muscle-specific genome organization. These and most other candidates were unaffected by IL10-KO, but still important as potential lamin A\/C-binding proteins in native heart or muscle. A subset of candidates (21 in skeletal muscle, 30 in heart) showed significantly different lamin A\/C-association in an IL10-KO tissue (<jats:italic>p<\/jats:italic> &amp;lt; 0.05), including AldoA and Gins3 affected in heart, and Lmcd1 and Fabp4 affected in skeletal muscle. To screen for binding, eleven candidates plus prelamin A and emerin controls were arrayed as synthetic 20-mer peptides (7-residue stagger) and incubated with recombinant purified lamin A \u201ctail\u201d residues 385\u2013646 under relatively stringent conditions. We detected strong lamin A binding to peptides solvent exposed in Lmcd1, AldoA, Perm1, and Tmem38a, and plausible binding to Csrp3 (muscle LIM protein). These results validated both proteomes as sources for native lamin A\/C-binding proteins in heart and muscle, identified four candidate genes for Emery-Dreifuss muscular dystrophy (CSRP3, LMCD1, ALDOA, and PERM1), support a lamin A-interactive molecular role for Tmem38A, and supported the hypothesis that lamin A\/C interactions with at least two partners (AldoA in heart, transcription factor Lmcd1 in muscle) are altered in the IL10-KO model of frailty.<\/jats:p>","DOI":"10.3389\/fcell.2023.1240285","type":"journal-article","created":{"date-parts":[[2023,10,23]],"date-time":"2023-10-23T11:28:15Z","timestamp":1698060495000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["Native lamin A\/C proteomes and novel partners from heart and skeletal muscle in a mouse chronic inflammation model of human frailty"],"prefix":"10.3389","volume":"11","author":[{"given":"Fatima D.","family":"Elzamzami","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arushi","family":"Samal","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adith S.","family":"Arun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tejas","family":"Dharmaraj","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Neeti R.","family":"Prasad","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alex","family":"Rendon-Jonguitud","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lauren","family":"DeVine","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeremy D.","family":"Walston","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert N.","family":"Cole","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katherine L.","family":"Wilson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2023,10,23]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"H1451","DOI":"10.1152\/ajpheart.01194.2006","article-title":"Age-related changes in lamin A\/C expression in cardiomyocytes","volume":"293","author":"Afilalo","year":"2007","journal-title":"Am. 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