{"id":2150,"date":"2004-06-08T21:03:30","date_gmt":"2004-06-08T21:03:30","guid":{"rendered":"https:\/\/www.progeriaresearch.org\/?p=2150"},"modified":"2020-12-08T17:13:23","modified_gmt":"2020-12-08T22:13:23","slug":"gene-mutation-causes-progressive-changes-to-cell-structure-in-children-with-progeria","status":"publish","type":"post","link":"https:\/\/www.progeriaresearch.org\/it\/2004\/06\/08\/gene-mutation-causes-progressive-changes-to-cell-structure-in-children-with-progeria\/","title":{"rendered":"La mutazione genetica provoca cambiamenti progressivi nella struttura cellulare nei bambini con progeria"},"content":{"rendered":"

[et_pb_section fb_built=\u201d1\u2033 _builder_version=\u201d3.22\u2033][et_pb_row _builder_version=\u201d3.25\u2033 background_size=\u201diniziale\u201d background_position=\u201dtop_left\u201d background_repeat=\u201dripeti\u201d][et_pb_column type=\u201d4_4\u2033 _builder_version=\u201d3.25\u2033 custom_padding=\u201d|||\u201d custom_padding__hover=\u201d|||\u201d][et_pb_text _builder_version=\u201d4.6.5\u2033 background_size=\u201diniziale\u201d background_position=\u201dtop_left\u201d background_repeat=\u201dripeti\u201d]<\/p>\n

Nuovo studio promuove la ricerca di trattamenti e cure <\/em>per la malattia mortale dell'invecchiamento rapido<\/em><\/p>\n

[Boston, MA \u2013 8 giugno 2004] \u2013 I ricercatori hanno annunciato oggi che una mutazione del gene Lamin A provoca gradualmente effetti devastanti sulla struttura e la funzione cellulare nei bambini affetti da sindrome di Hutchinson-Gilford Progeria (HGPS o Progeria). Lo studio \u00e8 stato pubblicato nel numero di questa settimana Atti della National Academy of Sciences (PNAS).<\/em> La progeria \u00e8 una rara malattia genetica mortale caratterizzata dalla comparsa di un invecchiamento anticipato nei bambini.<\/p>\n

\"Robert<\/p>\n

Dott. Robert D. Goldman, Dottore di Ricerca
Universit\u00e0 del Nord-Ovest, Facolt\u00e0 di Medicina Feinberg<\/em><\/p>\n

"Sebbene sia una malattia rara, la Progeria \u00e8 da tempo considerata un modello per studiare i meccanismi responsabili del normale invecchiamento", ha affermato l'autore principale Robert D. Goldman, Ph.D., Stephen Walter Ranson Professor e Chair, Cell and Molecular Biology, Northwestern University, Feinberg School of Medicine. "Questo studio evidenzia l'importanza del gene Lamin A nel mantenimento della struttura e della funzione cellulare".<\/p>\n

Nell'aprile 2003, un team di ricercatori riunito dalla Progeria Research Foundation (PRF), e comprendente il National Human Genome Research Institute (NHGRI), uno dei 27 istituti e centri che compongono i National Institutes of Health (NIH), ha annunciato la scoperta del gene che causa la Progeria. Quello studio, pubblicato nel numero del 16 aprile 2003 di Nature, ha scoperto che la malattia non \u00e8 ereditaria, ma \u00e8 causata da mutazioni casuali del gene LMNA (Lamin A). La proteina Lamin A \u00e8 l'impalcatura strutturale che tiene insieme il nucleo ed \u00e8 coinvolta nell'espressione genica e nella replicazione del DNA.<\/p>\n

Nel PNAS<\/em> studio, il risultato di uno sforzo collaborativo avviato da ricercatori della Northwestern, della Progeria Research Foundation e del NIH, sono state utilizzate tecniche microscopiche e molecolari per esaminare la struttura nucleare delle cellule di bambini con Progeria. Con l'invecchiamento delle cellule di Progeria, si \u00e8 verificato un graduale aumento dei difetti nella loro struttura e funzione nucleare, che riflette un accumulo anomalo della proteina difettosa Lamin A. Cambiamenti molto simili sono stati osservati nelle normali cellule umane di bambini e anziani trattati con la proteina difettosa Lamin A. Questi ricercatori ora credono che con l'invecchiamento delle cellule di Progeria, si verifichino cambiamenti significativi nella funzione cellulare che sono direttamente attribuibili alla quantit\u00e0 di proteina mutante Lamin A.<\/p>\n

\"Progeria<\/p>\n


Fotografie dei nuclei delle cellule di Progeria mentre invecchiano in una capsula di coltura, che mostrano i cambiamenti dalle cellule pi\u00f9 giovani (a) a quelle pi\u00f9 vecchie (c).<\/em><\/p>\n

\"Dr.\u00a0Dott.ssa Frances Collins, Direttrice del National Human Genome Research Institute<\/em><\/p>\n

"Queste scoperte rafforzano i nostri sospetti che l'instabilit\u00e0 della membrana nucleare della cellula svolga un ruolo chiave nella sindrome di Hutchinson-Gilford Progeria. Ora sappiamo molto di pi\u00f9 su come una minuscola cellula genetica Dott. <\/em>"La mutazione pu\u00f2 portare a una situazione in cui l'architettura della cellula \u00e8 gravemente e progressivamente danneggiata", ha affermato il dott. Francis Collins, direttore dell'NHGRI e autore principale dello studio.<\/p>\n

\"Leslie\u00a0Dott.ssa Leslie Gordon, Direttore medico della Progeria Research Foundation<\/em><\/p>\n

"I risultati di questo studio sono fondamentali per comprendere meglio la causa delle malattie cardiache e dell'invecchiamento cellulare nella Progeria", ha affermato Leslie Gordon, MD, Ph.D., autore dello studio e direttore medico della Progeria Research Foundation. "Siamo ottimisti sul fatto che con ogni nuovo studio e scoperta nel campo della Progeria, siamo un passo pi\u00f9 vicini a trovare una cura".<\/p>\n

[\/et_pb_text][\/et_pb_column][\/et_pb_row][\/et_pb_section]<\/p>","protected":false},"excerpt":{"rendered":"

[et_pb_section fb_built=”1″ _builder_version=”3.22″][et_pb_row _builder_version=”3.25″ background_size=”initial” background_position=”top_left” background_repeat=”repeat”][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”4.6.5″ background_size=”initial” background_position=”top_left” background_repeat=”repeat”] New Study Advances Drive for Treatment and Cure for Fatal Rapid-Aging Disease [Boston, MA – June 8, 2004] – Researchers today announced that a mutation of the Lamin A gene gradually causes devastating effects on cellular structure and function in […]<\/p>","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":"

New Study Advances Drive for Treatment and Cure <\/em>for Fatal Rapid-Aging Disease<\/em><\/p>

[Boston, MA - June 8, 2004] - Researchers today announced that a mutation of the Lamin A gene gradually causes devastating effects on cellular structure and function in children with Hutchinson-Gilford Progeria Syndrome (HGPS or Progeria). The study was published in this week's Proceedings of the National Academy of Sciences (PNAS).<\/em> Progeria is a rare, fatal genetic condition characterized by an appearance of accelerated aging in children.<\/p>

\"Robert<\/p>

Robert D. Goldman, Ph.D.
Northwestern University, Feinberg School of Medicine<\/em><\/p>

\"Although it is a rare disease, Progeria has long been considered to be a model for studying the mechanisms responsible for normal aging\" said lead author Robert D. Goldman, Ph.D., Stephen Walter Ranson Professor and Chair, Cell and Molecular Biology, Northwestern University, Feinberg School of Medicine. \"This study highlights the importance of the Lamin A gene in the maintenance of cell structure and function.\"<\/p>

In April 2003, a team of researchers assembled by The Progeria Research Foundation (PRF), and including the National Human Genome Research Institute (NHGRI), one of the 27 institutes and centers that make up the National Institutes of Health (NIH), announced the discovery of the gene that causes Progeria. That study, published in the April 16th 2003 issue of Nature, found that the disease is not inherited, but instead is caused by chance mutations to the LMNA gene (Lamin A). The Lamin A protein is the structural scaffolding that holds the nucleus together, and is involved in gene expression and DNA replication.<\/p>

In the PNAS<\/em> study, the result of a collaborative effort launched by researchers from Northwestern, The Progeria Research Foundation and NIH, microscopic and molecular techniques were used to examine the nuclear structure of cells from children with Progeria. As the Progeria cells aged, there was a gradual increase in defects in their nuclear structure and function, reflecting an abnormal accumulation of the defective Lamin A protein. Very similar changes were seen in normal human cells from both children and elderly persons treated with the defective Lamin A. These researchers now believe that as Progeria cells age, there are significant changes in cell function that are directly attributable to the amount of mutant Lamin A protein.<\/p>

\"Progeria<\/p>

Photographs nuclei of Progeria cells as they age in a culture dish showing changes from younger (a) to older (c) cells.<\/em><\/p>

\u00a0<\/p>

\"Dr.\u00a0Dr. Frances Collins, Director National Human Genome Research Institute<\/em><\/p>

\"These findings strengthen our suspicions that instability of the cell's nuclear membrane plays a key role in Hutchinson-Gilford Progeria Syndrome. We now know far more about how one tiny, genetic Dr. <\/em>mutation can lead to a situation in which the cell's architecture is severely and progressively damaged,\" said Dr. Francis Collins, Director of NHGRI and the study's senior author.<\/p>

\u00a0<\/p>

\"Leslie\u00a0Dr. Leslie Gordon, Medical Director The Progeria Research Foundation<\/em><\/p>

\"The findings of this study are critical to further understanding the cause of heart disease and cellular aging in Progeria,\" said Leslie Gordon, M.D., Ph.D., study author and Medical Director of The Progeria Research Foundation. \"We are optimistic that with every new study and discovery in the field of Progeria, we are one step closer to finding a cure.\"<\/p><\/div><\/div><\/div><\/div>","_et_gb_content_width":"","footnotes":"","_links_to":"","_links_to_target":""},"categories":[2],"tags":[],"class_list":["post-2150","post","type-post","status-publish","format-standard","hentry","category-news"],"yoast_head":"\nGene Mutation Causes Progressive Changes to Cell Structure in Children with Progeria - The Progeria Research Foundation<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" 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