Journal
MARROW
Volume 1335, Issue -, Pages 100-109Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.12502
Keywords
FSH; hCG; Erk1/2; osteoporosis; osteoblast
Categories
Funding
- NIAMS NIH HHS [AR065407, AR0535, R01 AR055208, R01 AR065407, AR055208] Funding Source: Medline
- NIGMS NIH HHS [U54 GM104942] Funding Source: Medline
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Previously we reported that follicle stimulating hormone (FSH) affects bone degradation in human cells and in follicle stimulating hormone receptor (FSH-R) null mice. Here we describe a FSH-R knockout bone-formation phenotype. We used mesenchymal stem cells (MSCs), osteoblast precursors that express FSH-R, to determine whether FSH regulates bone formation. FSH stimulates MSC cell adhesion 1-3 h and proliferation at 24 h after addition. On the basis of phylogenetic and clinical precedents, we also examined effects of pregnant levels of human chorionic gonadotropin (hCG) on MSCs. We found effects similar to those of FSH, and RNAi knockdown of FSH-R abrogated both FSH and hCG effects on MSCs. In contrast to effects on MSCs, neither FSH nor hCG had significant effects on osteoblast maturation. Also in MSCs, short-term treatment by FSH and hCG altered signaling pathways for proliferation, including Erk1/2 phosphorylation. Our results show augmentation of MSC proliferation by either FSH at menopausal levels or hCG at normal pregnant levels. We conclude that FSH-R participates in regulation of MSC precursor pools in response to either FSH or hCG, integrating the effects of these two glycoprotein hormones.
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