Vertaisarvioitu alkuperäisartikkeli tai data-artikkeli tieteellisessä aikakauslehdessä (A1)

Collagen XIII-derived ectodomain regulates bone angiogenesis and intracortical remodeling




Julkaisun tekijät: Koivunen J, Kemppainen AV, Finnila MA, Keski-Filppula R, Haronen H, Tu HM, Pellikka H, Heikkinen A, Kylmaoja E, Sormunen R, Miinalainen I, Saarakkala S, Izzi V, Pihlajaniemi T

Kustantaja: ELSEVIER

Julkaisuvuosi: 2019

Journal: Matrix Biology

Tietokannassa oleva lehden nimi: MATRIX BIOLOGY

Lehden akronyymi: MATRIX BIOL

Volyymi: 83

Aloitussivu: 6

Lopetussivun numero: 25

Sivujen määrä: 20

ISSN: 0945-053X

DOI: http://dx.doi.org/10.1016/j.matbio.2019.06.005


Tiivistelmä
Osteoporosis is the most common degenerative bone disease that occurs when the balance of bone production and resorption is perturbed. Loss of bone mass or alteration in its quality leads to significant weakening of the bones and subsequently to higher fracture risk. Collagen XIII (ColXIII) is a conserved transmembrane protein expressed in many mesenchymal tissues. Here we show that CoIXIII is a regulator of bone remodeling niche. In this study, we found that CoIXIII expression is significantly upregulated in osteoporotic patients. In view of that, we studied bone homeostasis in CoIXIII-overexpressing mice (Col13a1(oe)) up to 72 weeks of age and observed a cortical bone overgrowth followed by a drastic bone loss, together with increased bone vascularization. Moreover, our results demonstrate that the CoIXIII-derived ectodomain enhances angiogenesis through beta 1-integrins and the JNK pathway. Consequently, these data suggest that CoIXIII has a role in age-dependent cortical bone deterioration with possible implications for osteoporosis and fracture risk. (C) 2019 Elsevier B.V. All rights reserved.


Last updated on 2022-01-12 at 11:12