Collagen type I degradation fragments act through the collagen receptor LAIR-1 to provide a negative feedback for osteoclast formation

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Collagen type I degradation fragments act through the collagen receptor LAIR-1 to provide a negative feedback for osteoclast formation. / Boraschi-Diaz, Iris; Mort, John S.; Brömme, Dieter; Senis, Yotis A.; Mazharian, Alexandra; Komarova, Svetlana V.

In: Bone, Vol. 117, 01.12.2018, p. 23-30.

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@article{da486ff3d23540a2b7ab913a29d6e918,
title = "Collagen type I degradation fragments act through the collagen receptor LAIR-1 to provide a negative feedback for osteoclast formation",
abstract = "The major organic component of bone is collagen type I. Osteoclasts are terminally differentiated multinucleated cells of hematopoietic origin that are essential for physiological development of bone and teeth. We examined if osteoclast differentiation from murine bone marrow precursors is affected by collagen type I, or by its degradation products produced by human recombinant cathepsin K. Osteoclasts formation was dose-dependently inhibited in the presence of full length collagen type I or its 30–75 kDa degradation products added to the osteoclast differentiation media for the duration of an experiment. Collagen degradation fragments signaled through SH-2 phosphatases, inhibiting calcium signaling and NFATc1 translocation in osteoclast precursors. Osteoclasts and their precursors expressed a collagen receptor of leukocyte receptor complex family, LAIR-1. Importantly, collagen fragments failed to inhibit osteoclast formation from LAIR-1 deficient murine osteoclast precursors. This study demonstrates that collagen degradation fragments inhibit osteoclast formation acting through LAIR-1, providing a novel mechanism for the physiologically-relevant negative control of osteoclastogenesis.",
keywords = "Cathepsin K, Collagen type I, LAIR-1, Leukocyte receptor complex, NFATc1, Osteoclast",
author = "Iris Boraschi-Diaz and Mort, {John S.} and Dieter Br{\"o}mme and Senis, {Yotis A.} and Alexandra Mazharian and Komarova, {Svetlana V.}",
year = "2018",
month = dec,
day = "1",
doi = "10.1016/j.bone.2018.09.006",
language = "English",
volume = "117",
pages = "23--30",
journal = "Bone",
issn = "8756-3282",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Collagen type I degradation fragments act through the collagen receptor LAIR-1 to provide a negative feedback for osteoclast formation

AU - Boraschi-Diaz, Iris

AU - Mort, John S.

AU - Brömme, Dieter

AU - Senis, Yotis A.

AU - Mazharian, Alexandra

AU - Komarova, Svetlana V.

PY - 2018/12/1

Y1 - 2018/12/1

N2 - The major organic component of bone is collagen type I. Osteoclasts are terminally differentiated multinucleated cells of hematopoietic origin that are essential for physiological development of bone and teeth. We examined if osteoclast differentiation from murine bone marrow precursors is affected by collagen type I, or by its degradation products produced by human recombinant cathepsin K. Osteoclasts formation was dose-dependently inhibited in the presence of full length collagen type I or its 30–75 kDa degradation products added to the osteoclast differentiation media for the duration of an experiment. Collagen degradation fragments signaled through SH-2 phosphatases, inhibiting calcium signaling and NFATc1 translocation in osteoclast precursors. Osteoclasts and their precursors expressed a collagen receptor of leukocyte receptor complex family, LAIR-1. Importantly, collagen fragments failed to inhibit osteoclast formation from LAIR-1 deficient murine osteoclast precursors. This study demonstrates that collagen degradation fragments inhibit osteoclast formation acting through LAIR-1, providing a novel mechanism for the physiologically-relevant negative control of osteoclastogenesis.

AB - The major organic component of bone is collagen type I. Osteoclasts are terminally differentiated multinucleated cells of hematopoietic origin that are essential for physiological development of bone and teeth. We examined if osteoclast differentiation from murine bone marrow precursors is affected by collagen type I, or by its degradation products produced by human recombinant cathepsin K. Osteoclasts formation was dose-dependently inhibited in the presence of full length collagen type I or its 30–75 kDa degradation products added to the osteoclast differentiation media for the duration of an experiment. Collagen degradation fragments signaled through SH-2 phosphatases, inhibiting calcium signaling and NFATc1 translocation in osteoclast precursors. Osteoclasts and their precursors expressed a collagen receptor of leukocyte receptor complex family, LAIR-1. Importantly, collagen fragments failed to inhibit osteoclast formation from LAIR-1 deficient murine osteoclast precursors. This study demonstrates that collagen degradation fragments inhibit osteoclast formation acting through LAIR-1, providing a novel mechanism for the physiologically-relevant negative control of osteoclastogenesis.

KW - Cathepsin K

KW - Collagen type I

KW - LAIR-1

KW - Leukocyte receptor complex

KW - NFATc1

KW - Osteoclast

UR - http://www.scopus.com/inward/record.url?scp=85053204712&partnerID=8YFLogxK

U2 - 10.1016/j.bone.2018.09.006

DO - 10.1016/j.bone.2018.09.006

M3 - Article

AN - SCOPUS:85053204712

VL - 117

SP - 23

EP - 30

JO - Bone

JF - Bone

SN - 8756-3282

ER -