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guixing qiu
Peking Union Medical College Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0001-7557-1252
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Background: Scoliosis is a common manifestation of neurofibromatosis type 1, causing significant morbidity. The etiology of dystrophic scoliosis in neurofibromatosis type 1(NF1) is not fully understood and its therapies are lacking. This article focused on how GPR56 affected the development of NF1 cells and the related factors of osteoblast and osteoclast.
Methods: Through RNA-sequencing, G-protein-coupled receptor (GPR56) was found highly differential expressed in the NF1 with scoliosis samples. We measured the GPR56 how affected the NF1 cells in vitro. Then we tested the influence of GPR56 in osteoclasts and osteoblasts.
Results: We reported that knockdown GPR56 promoted the proliferation and cell cycle progression of NF1 cell. Furthermore, knockdown GPR56 can inhibited the osteoblastic differentiation and osteoclast formation, but had greater influence on osteoblastic differentiation, which indicated that knockdown GPR56 can promote the deterioration of NF1 tumors, meanwhile break the dynamic balance of bone formation and bone absorption, leading to increased bone resorption and eventually scoliosis.
Conclusions: In conclusion, we found that GPR56 may inhibit the proliferation and cell cycle progression of NF1. Furthermore, GPR56 can promote osteoblastic differentiation and osteoclast formation, but had greater influence on osteoblastic differentiation, which indicated that knockdown GPR56 can promote the deterioration of NF1 tumors, meanwhile break the dynamic balance of bone formation and bone absorption, leading to increased bone resorption.
Keywords
Neurofibromatosis type 1 with scoliosis, ADGRG1/GPR56, proliferation, cell cycle, osteoblastic differentiation and osteoclast formation
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A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
guixing qiu
Peking Union Medical College Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0001-7557-1252
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 14 Sep, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Scoliosis is a common manifestation of neurofibromatosis type 1, causing significant morbidity. The etiology of dystrophic scoliosis in neurofibromatosis type 1(NF1) is not fully understood and its therapies are lacking. This article focused on how GPR56 affected the development of NF1 cells and the related factors of osteoblast and osteoclast.
Methods: Through RNA-sequencing, G-protein-coupled receptor (GPR56) was found highly differential expressed in the NF1 with scoliosis samples. We measured the GPR56 how affected the NF1 cells in vitro. Then we tested the influence of GPR56 in osteoclasts and osteoblasts.
Results: We reported that knockdown GPR56 promoted the proliferation and cell cycle progression of NF1 cell. Furthermore, knockdown GPR56 can inhibited the osteoblastic differentiation and osteoclast formation, but had greater influence on osteoblastic differentiation, which indicated that knockdown GPR56 can promote the deterioration of NF1 tumors, meanwhile break the dynamic balance of bone formation and bone absorption, leading to increased bone resorption and eventually scoliosis.
Conclusions: In conclusion, we found that GPR56 may inhibit the proliferation and cell cycle progression of NF1. Furthermore, GPR56 can promote osteoblastic differentiation and osteoclast formation, but had greater influence on osteoblastic differentiation, which indicated that knockdown GPR56 can promote the deterioration of NF1 tumors, meanwhile break the dynamic balance of bone formation and bone absorption, leading to increased bone resorption.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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