Display options
Share it on

Life (Basel). 2021 Sep 29;11(10). doi: 10.3390/life11101028.

NMUR1 in the NMU-Mediated Regulation of Bone Remodeling.

Life (Basel, Switzerland)

Yu-Tin Hsiao, Kelli J Manikowski, Samantha Snyder, Nicole Griffin, Ashley L Orr, Elizabeth Q Hulsey, Gabriella Born-Evers, Tara Zukosky, Maria E Squire, Julia M Hum, Corinne E Metzger, Matthew R Allen, Jonathan W Lowery

Affiliations

  1. Division of Biomedical Science, Marian University College of Osteopathic Medicine, Indianapolis, IN 46022, USA.
  2. Bone and Muscle Research Group, Marian University, Indianapolis, IN 46022, USA.
  3. Department of Biology, The University of Scranton, Scranton, PA 18503, USA.
  4. Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
  5. Indiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

PMID: 34685399 PMCID: PMC8538501 DOI: 10.3390/life11101028

Abstract

Neuromedin-U (NMU) is an evolutionarily conserved peptide that regulates varying physiologic effects including blood pressure, stress and allergic responses, metabolic and feeding behavior, pain perception, and neuroendocrine functions. Recently, several lines of investigation implicate NMU in regulating bone remodeling. For instance, global loss of NMU expression in male and female mice leads to high bone mass due to elevated bone formation rate with no alteration in bone resorption rate or observable defect in skeletal patterning. Additionally, NMU treatment regulates the activity of osteoblasts in vitro. The downstream pathway utilized by NMU to carry out these effects is unknown as NMU signals via two G-protein-coupled receptors (GPCRs), NMU receptor 1 (NMUR1), and NMU receptor 2 (NMUR2), and both are expressed in the postnatal skeleton. Here, we sought to address this open question and build a better understanding of the downstream pathway utilized by NMU. Our approach involved the knockdown of

Keywords: NMU; NMUR1; NMUR2; Neuromedin-U; bone; osteoblast; osteoporosis

References

  1. Biochem Biophys Res Commun. 2020 Apr 16;524(4):890-894 - PubMed
  2. Endocr Pract. 2016 Sep 2;22(Suppl 4):1-42 - PubMed
  3. J Physiol Biochem. 2018 Feb;74(1):3-8 - PubMed
  4. Pharmacol Rev. 2004 Jun;56(2):231-48 - PubMed
  5. Mol Cell Biol. 2006 Dec;26(24):9352-63 - PubMed
  6. J Clin Invest. 2005 Dec;115(12):3318-25 - PubMed
  7. Nature. 2017 Sep 14;549(7671):282-286 - PubMed
  8. Mayo Clin Proc. 2015 Jan;90(1):53-62 - PubMed
  9. Joint Bone Spine. 2010 Dec;77 Suppl 2:S107-12 - PubMed
  10. Nat Med. 2007 Oct;13(10):1234-40 - PubMed
  11. Osteoporos Int. 1997;7(5):407-13 - PubMed
  12. Front Endocrinol (Lausanne). 2012 Dec 05;3:156 - PubMed
  13. J Bone Miner Res. 2013 Jan;28(1):2-17 - PubMed
  14. Arthritis Res Ther. 2012 Feb 07;14(1):R29 - PubMed
  15. Nature. 2017 Sep 21;549(7672):351-356 - PubMed
  16. J Bone Miner Res. 2010 Jul;25(7):1468-86 - PubMed
  17. Int J Mol Med. 2008 Sep;22(3):363-8 - PubMed

Publication Types

Grant support