Hao Yang
Indiana University
5 Papers
49 Citations
Hao Yang is an academic researcher from Indiana University. The author has contributed to research in topics: Osteoclast & Transforming growth factor. The author has an hindex of 4, co-authored 5 publications.
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Papers
Hyperactive transforming growth factor-β1 signaling potentiates skeletal defects in a neurofibromatosis type 1 mouse model.
Steven D. Rhodes,Xiaohua Wu,Yongzheng He,Shi Chen,Hao Yang,Karl 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 +18 more
TL;DR: In this article, the authors provide genetic and pharmacologic evidence that hyperactive TGFβ1 signaling pivotally underpins osseous defects in Nf1(flox/-) ;Col2.3Cre mice, a model which closely recapitulates the skeletal abnormalities found in the human disease.
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Hyperactive transforming growth factor-β1 signaling potentiates skeletal defects in a neurofibromatosis type 1 mouse model
Steven D. Rhodes,Xiaohua Wu,Yongzheng He,Shi Chen,Hao Yang,Karl 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 +18 more
- 01 Dec 2013
TL;DR: It is demonstrated that administration of the TGF‐β receptor 1 (TβRI) kinase inhibitor, SD‐208, can rescue bone mass deficits and prevent tibial fracture nonunion in Nf1flox/−;Col2.3Cre mice, thus implicating the T GF‐β signaling pathway as a potential therapeutic target in the treatment of NF1 osseous defects that are refractory to current therapies.
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Dystrophic spinal deformities in a neurofibromatosis type 1 murine model
Steven D. Rhodes,Wei Zhang,Dalong Yang,Hao Yang,Shi Chen,Xiahoua Wu,Xianlin Yang,Khalid S. Mohammad,Theresa A. Guise,Amanda L. Bergner,David A. Stevenson,Feng Chun Yang +11 more
- 18 Mar 2015
TL;DR: In this paper, two case reports of intervertebral disc (IVD) defects and interarticular vertebral fusion were reported in patients with dystrophic scoliosis.
11
Nf1 haploinsufficiency alters myeloid lineage commitment and function, leading to deranged skeletal homeostasis
Steven D. Rhodes,Hao Yang,Ruizhi Dong,Keshav Menon,Yongzheng He,Zhaomin Li,Shi Chen,Karl Staser,Li Jiang,Xiaohua Wu,Xianlin Yang,Xianghong Peng,Khalid S. Mohammad,Theresa A. Guise,Mingjiang Xu,Feng Chun Yang +15 more
TL;DR: In this article, conditional inactivation of a single Nf1 allele within the myeloid progenitor cell population (Nf1-LysM) is shown to promote multiple osteoclast gains-in-function, resulting in enhanced osteocyteogenesis and accelerated osteoclastic bone lytic activity in response to proresorptive challenge.
Dystrophic spinal deformities in a neurofibromatosis type 1 murine model.
Steven D. Rhodes,Wei Zhang,Dalong Yang,Dalong Yang,Hao Yang,Shi Chen,Xiaohua Wu,Xiaohong Li,Xianlin Yang,Khalid S. Mohammad,Theresa A. Guise,Amanda L. Bergner,David A. Stevenson,Feng Chun Yang +13 more
TL;DR: Collectively, these data provide novel insights regarding the pathophysiology of dystrophic spinal anomalies in NF1, and provide impetus for future radiographic analyses of larger patient cohorts to determine whether IVD and vertebral fusion defects may have been previously overlooked or underreported in the NF1 patient population.