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Effets de l'estradiol et du chargement mécanique sur la régulation de la POC5 et du récepteur ADGRG7 dans la scoliose idiopathique
| Content Provider | Semantic Scholar |
|---|---|
| Author | Hassan, Amani |
| Copyright Year | 2019 |
| Abstract | The physiological role and the regulation of ADGRG7 are not yet elucidated. The functional involvement of this receptor was linked with different physiological process such as reduced body weight, gastrointestinal function and recently, a gene variant in ADGRG7 was observed in patients with idiopathic scoliosis. The physiological role and the regulation of Adhesion G protein coupled receptor7 (ADGRG7) are not yet elucidated. The functional involvement of this receptor was linked with different physiological process such as reduced body weight, gastrointestinal function and recently, a gene variant in ADGRG7 was observed in patients with adolescent idiopathic scoliosis (AIS). Here, we identify the ADGRG7 as an estrogenresponsive gene under the regulation of estrogen receptor ER in different cells lines. We found that ADGRG7 expression was upregulated in response to estrogen (E2) in normal osteoblasts (NOB) but not in AIS cells. ADGRG7 promoter studies indicate the presence of an ER response half site in close vicinity of an SP1 binding site. Mutation of the SP1 site completely abrogated the response to E2, indicating its essential requirement. ChIP confirmed the binding of SP1 and ERα to the ADGRG7 promoter. Our results identify the ADGRG7 gene as an estrogen-responsive gene under the control of ER and SP1 tethered actions, suggesting a possible role of estrogens in the regulation of ADGRG7. Introduction: Adolescent idiopathic scoliosis (AIS) is a complex three-dimensional deformity of the spine that mostly occurs during late childhood or puberty (Konieczny, Senyurt et al. 2013). Severe forms of AIS are more common in girls as compared to boys (Cheng, Castelein et al. 2015). The difference between girls and boys, as well as the etiology of AIS are still unclear. Several studies suggest that AIS could be an endocrinal disease and that various hormones, especially |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://papyrus.bib.umontreal.ca/xmlui/bitstream/handle/1866/21839/HASSAN_Amani_2018_these.pdf?isAllowed=y&sequence=2 |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
