Literature DB >> 15694405

Regulation of apoptosis in osteoclasts and osteoblastic cells.

Lianping Xing1, Brendan F Boyce.   

Abstract

In postnatal life, the skeleton undergoes continuous remodeling in which osteoclasts resorb aged or damaged bone, leaving space for osteoblasts to make new bone. The balance of proliferation, differentiation, and apoptosis of bone cells determines the size of osteoclast or osteoblast populations at any given time. Bone cells constantly receive signals from adjacent cells, hormones, and bone matrix that regulate their proliferation, activity, and survival. Thus, the amount of bone and its microarchitecture before and after the menopause or following therapeutic intervention with drugs, such as sex hormones, glucocorticoids, parathyroid hormone, and bisphosphonates, is determined in part by effects of these on survival of osteoclasts, osteoblasts, and osteocytes. Understanding the mechanisms and regulation of bone cell apoptosis will enhance our knowledge of bone cell function and help us to develop better therapeutics for the management of osteoporosis and other bone diseases.

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Year:  2005        PMID: 15694405     DOI: 10.1016/j.bbrc.2004.11.072

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  46 in total

1.  Selective regulation of bone cell apoptosis by translational isoforms of the glucocorticoid receptor.

Authors:  Nick Z Lu; Jennifer B Collins; Sherry F Grissom; John A Cidlowski
Journal:  Mol Cell Biol       Date:  2007-08-06       Impact factor: 4.272

Review 2.  Normal bone anatomy and physiology.

Authors:  Bart Clarke
Journal:  Clin J Am Soc Nephrol       Date:  2008-11       Impact factor: 8.237

3.  Cadmium exposure activates the ERK signaling pathway leading to altered osteoblast gene expression and apoptotic death in Saos-2 cells.

Authors:  Kate S Arbon; Cody M Christensen; Wendy A Harvey; Sara J Heggland
Journal:  Food Chem Toxicol       Date:  2011-10-13       Impact factor: 6.023

Review 4.  Functional impairment of bone formation in the pathogenesis of osteoporosis: the bone marrow regenerative competence.

Authors:  Joseph P Bidwell; Marta B Alvarez; Mark Hood; Paul Childress
Journal:  Curr Osteoporos Rep       Date:  2013-06       Impact factor: 5.096

5.  Activation of the acquired immune response reduces coupled bone formation in response to a periodontal pathogen.

Authors:  Yugal Behl; Michelle Siqueira; Javier Ortiz; Jingchao Li; Tesfahun Desta; Dan Faibish; Dana T Graves
Journal:  J Immunol       Date:  2008-12-15       Impact factor: 5.422

6.  Long-term safety and efficacy of raloxifene in the prevention and treatment of postmenopausal osteoporosis: an update.

Authors:  Enrico M Messalli; Cono Scaffa
Journal:  Int J Womens Health       Date:  2010-08-09

7.  Ferulic acid impairs osteoclast fusion and exacerbates survival of mature osteoclasts.

Authors:  Travers Sagar; Mpho Rantlha; Marlena C Kruger; Magdalena Coetzee; Vishwa Deepak
Journal:  Cytotechnology       Date:  2016-07-23       Impact factor: 2.058

8.  Immunohistochemical detection of estrogen receptor beta in alveolar bone cells of estradiol-treated female rats: possible direct action of estrogen on osteoclast life span.

Authors:  Mady Crusodé de Souza; Mady Cruzoé-Souza; Estela Sasso-Cerri; Paulo S Cerri
Journal:  J Anat       Date:  2009-12       Impact factor: 2.610

9.  RANKL increases the level of Mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitro.

Authors:  Karen A Sutherland; Helena L Rogers; Denise Tosh; Michael J Rogers
Journal:  Arthritis Res Ther       Date:  2009-04-30       Impact factor: 5.156

10.  Differentiation dependent expression of urocortin's mRNA and peptide in human osteoprogenitor cells: influence of BMP-2, TGF-beta-1 and dexamethasone.

Authors:  Mohammad Tezval; Hossein Tezval; Klaus Dresing; Ewa Klara Stuermer; Martina Blaschke; Klaus Michael Stuermer; Heide Siggelkow
Journal:  J Mol Histol       Date:  2009-12-01       Impact factor: 2.611

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