Genome scans provide evidence for keloid susceptibility loci on chromosomes 2q23 and 7p11

被引:134
作者
Marneros, AG
Norris, JEC
Watanabe, S
Reichenberger, E
Olsen, BR
机构
[1] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA
[2] Univ Cologne, Dept Dermatol, D-5000 Cologne, Germany
[3] St Lukes Roosevelt Hosp, Dept Plast Surg, New York, NY USA
[4] Saitama Childrens Med Ctr, Div Plast Surg, Saitama, Japan
[5] Harvard Univ, Sch Dent, Dept Oral Biol, Boston, MA 02115 USA
关键词
autosomal dominant inheritance; keloid; linkage analysis; wound healing;
D O I
10.1111/j.0022-202X.2004.22327.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Keloids are proliferative fibrous growths that result from an excessive tissue response to skin trauma. They often occur sporadically, but in some families a genetic predisposition to keloids has been observed. Here we studied two families with an autosomal dominant inheritance pattern of keloids. One African-American family showed a high degree of variability in the extent of keloid formation between family members, whereas the second family from Japan showed a pattern of full penetrance and the formation of only small keloids. We performed a genome-wide linkage search for genes predisposing to keloid formation in these two families. We identified linkage to chromosome 2q23 (maximal two-point LOD score of 3.01) for the Japanese family. The African-American family showed evidence for a keloid susceptibility locus on chromosome 7p11 (maximal two-point LOD score of 3.16). The observed locus heterogeneity in autosomal dominant keloid disease is consistent with the clinical heterogeneity of this scarring disorder. Dense microsatellite analysis in these two loci was performed and candidate genes were identified. This study provides the first genetic evidence for keloid susceptibility loci and serves as a basis for the identification of responsible genes.
引用
收藏
页码:1126 / 1132
页数:7
相关论文
共 24 条
[1]   KELOID FIBROBLASTS EXHIBIT AN ALTERED RESPONSE TO TGF-BETA [J].
BABU, M ;
DIEGELMANN, R ;
OLIVER, N .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1992, 99 (05) :650-655
[2]   FIBRONECTIN IS OVERPRODUCED BY KELOID FIBROBLASTS DURING ABNORMAL WOUND-HEALING [J].
BABU, M ;
DIEGELMANN, R ;
OLIVER, N .
MOLECULAR AND CELLULAR BIOLOGY, 1989, 9 (04) :1642-1650
[3]   The effect of TGF-beta on keloid fibroblast proliferation and collagen synthesis [J].
Bettinger, DA ;
Yager, DR ;
Diegelmann, RF ;
Cohen, IK .
PLASTIC AND RECONSTRUCTIVE SURGERY, 1996, 98 (05) :827-833
[4]   Cellular signaling by tyrosine phosphorylation in keloid and normal human dermal fibroblasts [J].
Chin, GS ;
Liu, W ;
Steinbrech, D ;
Hsu, M ;
Levinson, H ;
Longaker, MT .
PLASTIC AND RECONSTRUCTIVE SURGERY, 2000, 106 (07) :1532-1540
[5]   Keloid-derived fibroblasts are refractory to Fas-mediated apoptosis and neutralization of autocrine transforming growth factor-β1 can abrogate this resistance [J].
Chodon, T ;
Sugihara, T ;
Igawa, HH ;
Funayama, E ;
Furukawa, H .
AMERICAN JOURNAL OF PATHOLOGY, 2000, 157 (05) :1661-1669
[6]   SURGICAL TREATMENT OF KELOIDS [J].
COSMAN, B ;
CRIKELAIR, GF ;
GAULIN, C ;
JU, DMC ;
LATTES, R .
PLASTIC AND RECONSTRUCTIVE SURGERY, 1961, 27 (04) :335-+
[7]   Keloids and hypertrophic scars [J].
English, RS ;
Shenefelt, PD .
DERMATOLOGIC SURGERY, 1999, 25 (08) :631-638
[8]   ELEVATED LEVELS OF PDGF-ALPHA RECEPTORS IN KELOID FIBROBLASTS CONTRIBUTE TO AN ENHANCED RESPONSE TO PDGF [J].
HAISA, M ;
OKOCHI, H ;
GROTENDORST, GR .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1994, 103 (04) :560-563
[9]   Keloid fibroblasts resist ceramide-induced apoptosis by overexpression of insulin-like growth factor I receptor [J].
Ishihara, H ;
Yoshimoto, H ;
Fujioka, M ;
Murakami, R ;
Hirano, A ;
Fujii, T ;
Ohtsuru, A ;
Namba, H ;
Yamashita, S .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2000, 115 (06) :1065-1071
[10]  
KELLY AP, 1988, DERMATOL CLIN, V6, P407