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Remote Neuronal Activation Coupled with Automated Blood Sampling to Induce and Measure Circulating Luteinizing Hormone in Mice
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Could bone tissue be a target for luteinizing hormone/chorionic gonadotropin?

Jason P Mansell1, Allen J Bailey, Sarah J Yarram

  • 1Department of Oral & Dental Sciences, Division of Child Dental Health, University of Bristol Dental School, Lower Maudlin Street, Bristol BS1 2LY, UK. j.p.mansell@bris.ac.uk

Molecular and Cellular Endocrinology
|March 21, 2007
PubMed
Summary

Ovariectomy and Zoladex had different effects on bone collagen breakdown. Researchers found luteinizing hormone (LH)/human chorionic gonadotropin (hCG) may indirectly influence bone metabolism, with epidermal growth factor (EGF) potentially explaining previous findings.

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Published on: January 22, 2020

Area of Science:

  • Endocrinology
  • Bone Metabolism
  • Cell Biology

Background:

  • Ovariectomy (OVX) and Zoladex administration in rats yielded conflicting results regarding urinary hydroxyproline (OH-Pro) excretion, a marker for bone collagen breakdown.
  • Both procedures induce estrogen deficiency, suggesting luteinizing hormone (LH) status influences bone metabolism.
  • While estrogen's role in bone is known, the direct impact of LH/human chorionic gonadotropin (hCG) on bone metabolism remains under-investigated.

Purpose of the Study:

  • To investigate the differential effects of OVX and Zoladex on bone collagen catabolism.
  • To explore the potential role of LH/hCG in bone metabolism.
  • To identify factors in urinary-derived hCG that influence osteoblast activity.

Main Methods:

  • Administration of OVX and Zoladex to adult rats to assess urinary OH-Pro levels.
  • In vitro culture of osteoblasts treated with urinary-derived and recombinant hCG.
  • Analysis of alkaline phosphatase (ALP) activity, matrix metalloproteinase-2 (MMP-2) levels, and type I collagen expression.
  • Murine calvaria studies to evaluate hCG's bone-resorbing effects.
  • Identification of epidermal growth factor (EGF) as a potential confounding factor.

Main Results:

  • OVX increased OH-Pro early, while Zoladex decreased it over two months.
  • Urinary-derived hCG increased osteoblast alkaline phosphatase, MMP-2, and collagen type I.
  • Recombinant hCG did not affect osteoblast activity, indicating contaminants in the urinary preparation.
  • EGF was identified as a factor in urinary-derived hCG responsible for observed osteoblast changes.

Conclusions:

  • LH/hCG's direct effect on bone tissue appears minimal or indirect.
  • Epidermal growth factor (EGF) in urinary preparations mimics hCG effects on osteoblasts.
  • Bone metabolism changes previously attributed to hCG may be mediated by contaminants like EGF.
  • Further research is needed to clarify the indirect mechanisms of LH/hCG action on bone.