Literature DB >> 17317783

Multiple roles for neurofibromin in skeletal development and growth.

Mateusz Kolanczyk1, Nadine Kossler, Jirko Kühnisch, Liron Lavitas, Sigmar Stricker, Ulrich Wilkening, Inderchand Manjubala, Peter Fratzl, Ralf Spörle, Bernhard G Herrmann, Luis F Parada, Uwe Kornak, Stefan Mundlos.   

Abstract

Neurofibromatosis type 1 (NF1) is a prevalent genetic disorder primarily characterized by the formation of neurofibromas, café-au-lait spots and freckling. Skeletal abnormalities such as short stature or bowing/pseudarthrosis of the tibia are relatively common. To investigate the role of the neurofibromin in skeletal development, we crossed Nf1flox mice with Prx1Cre mice to inactivate Nf1 in undifferentiated mesenchymal cells of the developing limbs. Similar to NF1 affected individuals, Nf1(Prx1) mice show bowing of the tibia and diminished growth. Tibial bowing is caused by decreased stability of the cortical bone due to a high degree of porosity, decreased stiffness and reduction in the mineral content as well as hyperosteoidosis. Accordingly, osteoblasts show an increase in proliferation and a decreased ability to differentiate and mineralize in vitro. The reduction in growth is due to lower proliferation rates and a differentiation defect of chondrocytes. Abnormal vascularization of skeletal tissues is likely to contribute to this pathology as it exerts a negative effect on cortical bone stability. Furthermore, Nf1 has an important role in the development of joints, as shown by fusion of the hip joints and other joint abnormalities, which are not observed in neurofibromatosis type I. Thus, neurofibromin has multiple essential roles in skeletal development and growth.

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Year:  2007        PMID: 17317783     DOI: 10.1093/hmg/ddm032

Source DB:  PubMed          Journal:  Hum Mol Genet        ISSN: 0964-6906            Impact factor:   6.150


  49 in total

1.  Cephalometry in adults and children with neurofibromatosis type 1: Implications for the pathogenesis of sphenoid wing dysplasia and the "NF1 facies".

Authors:  Winnie Cung; Laura A Freedman; Nicholas E Khan; Elaine Romberg; Pamela J Gardner; Carol W Bassim; Andrea M Baldwin; Brigitte C Widemann; Douglas R Stewart
Journal:  Eur J Med Genet       Date:  2015-09-08       Impact factor: 2.708

Review 2.  Regulation of Long Bone Growth in Vertebrates; It Is Time to Catch Up.

Authors:  Alberto Roselló-Díez; Alexandra L Joyner
Journal:  Endocr Rev       Date:  2015-10-20       Impact factor: 19.871

3.  Loss of BMPR2 leads to high bone mass due to increased osteoblast activity.

Authors:  Jonathan W Lowery; Giuseppe Intini; Laura Gamer; Sutada Lotinun; Valerie S Salazar; Satoshi Ote; Karen Cox; Roland Baron; Vicki Rosen
Journal:  J Cell Sci       Date:  2015-02-06       Impact factor: 5.285

4.  Mice lacking Nf1 in osteochondroprogenitor cells display skeletal dysplasia similar to patients with neurofibromatosis type I.

Authors:  Weixi Wang; Jeffry S Nyman; Koichiro Ono; David A Stevenson; Xiangli Yang; Florent Elefteriou
Journal:  Hum Mol Genet       Date:  2011-07-14       Impact factor: 6.150

5.  Combined MEK inhibition and BMP2 treatment promotes osteoblast differentiation and bone healing in Nf1Osx -/- mice.

Authors:  Jean de la Croix Ndong; David M Stevens; Guillaume Vignaux; Sasidhar Uppuganti; Daniel S Perrien; Xiangli Yang; Jeffry S Nyman; Eva Harth; Florent Elefteriou
Journal:  J Bone Miner Res       Date:  2015-01       Impact factor: 6.741

6.  Bone resorption in syndromes of the Ras/MAPK pathway.

Authors:  D A Stevenson; E L Schwarz; J C Carey; D H Viskochil; H Hanson; S Bauer; H-Y Cindy Weng; T Greene; K Reinker; J Swensen; R J Chan; F-C Yang; L Senbanjo; Z Yang; R Mao; M Pasquali
Journal:  Clin Genet       Date:  2011-01-19       Impact factor: 4.438

7.  Decreased bone mineralization in children with Noonan syndrome: another consequence of dysregulated RAS MAPKinase pathway?

Authors:  Kiran S Choudhry; Monica Grover; Alyssa A Tran; E O'Brian Smith; Kenneth J Ellis; Brendan H Lee
Journal:  Mol Genet Metab       Date:  2012-04-11       Impact factor: 4.797

8.  Neurofibromin deficiency-associated transcriptional dysregulation suggests a novel therapy for tibial pseudoarthrosis in NF1.

Authors:  Nandina Paria; Tae-Joon Cho; In Ho Choi; Nobuhiro Kamiya; Kay Kayembe; Rong Mao; Rebecca L Margraf; Gerlinde Obermosser; Ila Oxendine; David W Sant; Mi Hyun Song; David A Stevenson; David H Viskochil; Carol A Wise; Harry K W Kim; Jonathan J Rios
Journal:  J Bone Miner Res       Date:  2014-12       Impact factor: 6.741

9.  Hyperactive transforming growth factor-β1 signaling potentiates skeletal defects in a neurofibromatosis type 1 mouse model.

Authors:  Steven D Rhodes; Xiaohua Wu; Yongzheng He; Shi Chen; Hao Yang; Karl W Staser; Jiapeng Wang; Ping Zhang; Chang Jiang; Hiroki Yokota; Ruizhi Dong; Xianghong Peng; Xianlin Yang; Sreemala Murthy; Mohamad Azhar; Khalid S Mohammad; Mingjiang Xu; Theresa A Guise; Feng-Chun Yang
Journal:  J Bone Miner Res       Date:  2013-12       Impact factor: 6.741

Review 10.  Aberrant Myeloid Differentiation Contributes to the Development of Osteoporosis in Neurofibromatosis Type 1.

Authors:  Steven D Rhodes; Feng-Chun Yang
Journal:  Curr Osteoporos Rep       Date:  2016-02       Impact factor: 5.096

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