{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T06:30:03Z","timestamp":1791095403024,"version":"4.1.0"},"reference-count":78,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2012,4,1]],"date-time":"2012-04-01T00:00:00Z","timestamp":1333238400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Marie Curie International Reintegration","award":["MIRG-CT-2006-044914"],"award-info":[{"award-number":["MIRG-CT-2006-044914"]}]},{"name":"Fondo de Investigaci\u00f3n Sanitaria","award":["PI06-1335"],"award-info":[{"award-number":["PI06-1335"]}]},{"name":"Department of Industry, Tourism and Trade of the Government of the Autonomous Community of the Basque Country","award":["2009\/2011"],"award-info":[{"award-number":["2009\/2011"]}]},{"name":"FPI","award":["BFI09-135"],"award-info":[{"award-number":["BFI09-135"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Lamin A (LMNA)-linked lipodystrophies may be either genetic (associated with LMNA mutations) or acquired (associated with the use of human immunodeficiency virus protease inhibitors [PIs]), and in both cases they share clinical features such as anomalous distribution of body fat or generalized loss of adipose tissue, metabolic alterations, and early cardiovascular complications. Both LMNA-linked lipodystrophies are characterized by the accumulation of the lamin A precursor prelamin A. The pathological mechanism by which prelamin A accumulation induces the lipodystrophy associated phenotypes remains unclear. Since the affected tissues in these disorders are of mesenchymal origin, we have generated an LMNA-linked experimental model using human mesenchymal stem cells treated with a PI, which recapitulates the phenotypes observed in patient biopsies. This model has been demonstrated to be a useful tool to unravel the pathological mechanism of the LMNA-linked lipodystrophies, providing an ideal system to identify potential targets to generate new therapies for drug discovery screening. We report for the first time that impaired adipogenesis is a consequence of the interaction between accumulated prelamin A and Sp1 transcription factor, sequestration of which results in altered extracellular matrix gene expression. In fact, our study shows a novel, essential, and finely tuned role for Sp1 in adipose lineage differentiation in human mesenchymal stem cells. These findings define a new physiological experimental model to elucidate the pathological mechanisms LMNA-linked lipodystrophies, creating new opportunities for research and treatment not only of LMNA-linked lipodystrophies but also of other adipogenesis-associated metabolic diseases.<\/jats:p>","DOI":"10.5966\/sctm.2011-0010","type":"journal-article","created":{"date-parts":[[2012,5,11]],"date-time":"2012-05-11T15:27:30Z","timestamp":1336750050000},"page":"309-321","source":"Crossref","is-referenced-by-count":36,"title":["Sp1 Transcription Factor Interaction with Accumulated Prelamin A Impairs Adipose Lineage Differentiation in Human Mesenchymal Stem Cells: Essential Role of Sp1 in the Integrity of Lipid Vesicles"],"prefix":"10.1093","volume":"1","author":[{"given":"Garbi\u00f1e","family":"Ruiz de Eguino","sequence":"first","affiliation":[{"name":"Stem Cells and Cell Therapy Laboratory, BioCruces, Hospital Universitario Cruces, Barakaldo, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arantza","family":"Infante","sequence":"additional","affiliation":[{"name":"Stem Cells and Cell Therapy Laboratory, BioCruces, Hospital Universitario Cruces, Barakaldo, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Schlangen","sequence":"additional","affiliation":[{"name":"Genome Analysis Platform, Center for Cooperative Research in Biosciences, CIC bioGUNE, Derio, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana M.","family":"Aransay","sequence":"additional","affiliation":[{"name":"Genome Analysis Platform, Center for Cooperative Research in Biosciences, CIC bioGUNE, Derio, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ane","family":"Fullaondo","sequence":"additional","affiliation":[{"name":"Genome Analysis Platform, Center for Cooperative Research in Biosciences, CIC bioGUNE, Derio, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mario","family":"Soriano","sequence":"additional","affiliation":[{"name":"Servicio Microscop\u00eda Electr\u00f3nica, Centro de Investigaci\u00f3n Pr\u00edncipe Felipe, Valencia, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e9 Manuel","family":"Garc\u00eda-Verdugo","sequence":"additional","affiliation":[{"name":"Laboratorio de Neurobiolog\u00eda Comparada, Instituto Cavanilles, Universitat de Valencia, Centro Investigaci\u00f3n Biom\u00e9dica en Red Enfermedades Neurodegenerativas, Valencia, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u00c1ngel G.","family":"Mart\u00edn","sequence":"additional","affiliation":[{"name":"Regulation of Cell Growth Laboratory, Fundaci\u00f3n Inbiomed, San Sebasti\u00e1n, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clara I.","family":"Rodr\u00edguez","sequence":"additional","affiliation":[{"name":"Stem 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