Literature DB >> 22491873

Thirteen Chinese patients with sporadic Paget's disease of bone: clinical features, SQSTM1 mutation identification, and functional analysis.

Jie-Mei Gu1, Zhen-Lin Zhang, Hao Zhang, Wei-Wei Hu, Chun Wang, Hua Yue, Yao-Hua Ke, Jin-Wei He, Yun-Qiu Hu, Miao Li, Yu-Juan Liu, Wen-Zhen Fu.   

Abstract

To increase awareness of the rarity of Paget's disease of bone (PDB) in the Chinese population, we characterized the clinical manifestations and features of 13 Chinese sporadic PDB patients. The clinical features of our Chinese PDB patients show similarities with cases reported in Western countries. The most common lesion sites were the pelvis, femur, and tibia; the next most common lesion sites were the spine and skull. Most patients had a higher serum alkaline phosphatase (ALP) level. Treatment with bisphosphonates was effective. In addition, we screened for PDB-causing mutations and performed a functional analysis in an attempt to elucidate the molecular pathogenesis of PDB. A total of 216 persons, including 13 sporadic PDB patients, three unaffected relatives of 1 patient, and 200 healthy donors, were recruited. All eight exons and exon-intron boundaries of the SQSTM1 gene were amplified by polymerase chain reaction (PCR) and directly sequenced. We identified a 53-year-old man who harbored a heterozygous T-to-C transversion at position 1250 in exon 8 (1250T > C), which resulted in a methionine-to-threonine (ATG > ACG) substitution at codon 404 (M404T). The M404T mutant SQSTM1 protein exhibited increased NF-κB activation and drove a significantly increased number of osteoclast-like cells (OLCs) that formed in response to RANKL and an increased number of OLC nuclei. This is the first report of an SQSTM1 genetic mutation that contributes to the pathogenesis of PDB in Chinese patients. These results may partially explain the mechanism by which this SQSTM1 mutation contributes to the pathogenesis of sporadic PDB in Chinese patients.

Entities:  

Mesh:

Substances:

Year:  2012        PMID: 22491873     DOI: 10.1007/s00774-012-0352-6

Source DB:  PubMed          Journal:  J Bone Miner Metab        ISSN: 0914-8779            Impact factor:   2.626


  37 in total

1.  A point mutation in the ubiquitin-associated domain of SQSMT1 is sufficient to cause a Paget's disease-like disorder in mice.

Authors:  Anna Daroszewska; Robert J van 't Hof; Javier A Rojas; Robert Layfield; Euphemie Landao-Basonga; Lorraine Rose; Ken Rose; Stuart H Ralston
Journal:  Hum Mol Genet       Date:  2011-04-21       Impact factor: 6.150

Review 2.  Paget's disease of bone.

Authors:  Mickaël Rousière; Laëtitia Michou; François Cornélis; Philippe Orcel
Journal:  Best Pract Res Clin Rheumatol       Date:  2003-12       Impact factor: 4.098

3.  Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice.

Authors:  Masaaki Komatsu; Satoshi Waguri; Masato Koike; Yu-Shin Sou; Takashi Ueno; Taichi Hara; Noboru Mizushima; Jun-Ichi Iwata; Junji Ezaki; Shigeo Murata; Jun Hamazaki; Yasumasa Nishito; Shun-Ichiro Iemura; Tohru Natsume; Toru Yanagawa; Junya Uwayama; Eiji Warabi; Hiroshi Yoshida; Tetsuro Ishii; Akira Kobayashi; Masayuki Yamamoto; Zhenyu Yue; Yasuo Uchiyama; Eiki Kominami; Keiji Tanaka
Journal:  Cell       Date:  2007-12-14       Impact factor: 41.582

4.  On a Form of Chronic Inflammation of Bones (Osteitis Deformans).

Authors:  J Paget
Journal:  Med Chir Trans       Date:  1877

5.  Recurrent mutation of the gene encoding sequestosome 1 (SQSTM1/p62) in Paget disease of bone.

Authors:  Nancy Laurin; Jacques P Brown; Jean Morissette; Vincent Raymond
Journal:  Am J Hum Genet       Date:  2002-04-30       Impact factor: 11.025

6.  p62, a phosphotyrosine-independent ligand of the SH2 domain of p56lck, belongs to a new class of ubiquitin-binding proteins.

Authors:  R K Vadlamudi; I Joung; J L Strominger; J Shin
Journal:  J Biol Chem       Date:  1996-08-23       Impact factor: 5.157

7.  Incidence and natural history of Paget's disease of bone in England and Wales.

Authors:  T P van Staa; P Selby; H G M Leufkens; K Lyles; J M Sprafka; C Cooper
Journal:  J Bone Miner Res       Date:  2002-03       Impact factor: 6.741

Review 8.  Genetics of Paget's disease of bone.

Authors:  Anna Daroszewska; Stuart H Ralston
Journal:  Clin Sci (Lond)       Date:  2005-09       Impact factor: 6.124

9.  Treatment of Paget's disease of bone: a survey of clinical practice in Australia.

Authors:  J P Walsh; R Attewell; B G A Stuckey; M J Hooper; J D Wark; S Fletcher; V Ferrari; J A Eisman
Journal:  Bone       Date:  2008-02-16       Impact factor: 4.398

10.  p62/SQSTM1 binds directly to Atg8/LC3 to facilitate degradation of ubiquitinated protein aggregates by autophagy.

Authors:  Serhiy Pankiv; Terje Høyvarde Clausen; Trond Lamark; Andreas Brech; Jack-Ansgar Bruun; Heidi Outzen; Aud Øvervatn; Geir Bjørkøy; Terje Johansen
Journal:  J Biol Chem       Date:  2007-06-19       Impact factor: 5.157

View more
  3 in total

1.  A FKBP5 mutation is associated with Paget's disease of bone and enhances osteoclastogenesis.

Authors:  Bingru Lu; Yulian Jiao; Yinchang Wang; Jing Dong; Muyun Wei; Bin Cui; Yafang Sun; Laicheng Wang; Bingchang Zhang; Zijiang Chen; Yueran Zhao
Journal:  Exp Mol Med       Date:  2017-05-19       Impact factor: 8.718

Review 2.  Clinical and Genetic Advances in Paget's Disease of Bone: a Review.

Authors:  N Alonso; I Calero-Paniagua; J Del Pino-Montes
Journal:  Clin Rev Bone Miner Metab       Date:  2016-12-19

3.  Clinical Characteristics and Pathogenic Gene Identification in Chinese Patients With Paget's Disease of Bone.

Authors:  Xiaohui Tao; Li Liu; Xingguang Yang; Zhe Wei; Zhongzhong Chen; Ge Zhang; Zhenlin Zhang; Hua Yue
Journal:  Front Endocrinol (Lausanne)       Date:  2022-03-09       Impact factor: 5.555

  3 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.