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Research Article

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Mol. Cells 2012; 33(4): 401-406

Published online February 28, 2012

https://doi.org/10.1007/s10059-012-0009-2

© The Korean Society for Molecular and Cellular Biology

The Transmembrane Adaptor Protein, Linker for Activation of T cells (LAT), Regulates RANKL-Induced Osteoclast Differentiation

Kabsun Kim*, Jung Ha Kim, Jang Bae Moon, Jongwon Lee, Han bok Kwak, Yong-Wook Park1,and Nacksung Kim*

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National Research Laboratory for Regulation of Bone Metabolism and Disease, Department of Pharmacology, Chonnam National University Medical School, Gwangju 501-746, Korea, 1Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju 501-757, Korea

Correspondence to : *Correspondence: kabsun@hanmail.net (KK); nacksung@chonnam.ac.kr (NK)

Received: January 6, 2012; Revised: January 26, 2012; Accepted: January 27, 2012

Abstract

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RANKL induces the formation of osteoclasts, which are responsible for bone resorption. Herein we investigate the role of the transmembrane adaptor proteins in RANKL-induced osteoclastogenesis. LAT positively regulates osteoclast differentiation and is up-regulated by RANKL via c-Fos and NFATc1, whereas LAB and LIME act as negative modulators of osteoclastogenesis. In addition, silencing of LAT by RNA interference or overexpression of a LAT dominant negative in bone marrow-derived macrophage cells attenuates RANKL-induced osteoclast formation. Furthermore, LAT is in-volved in RANKL-induced PLC? activation and NFATc1 induction. Thus, our data suggest that LAT acts as a positive regulator of RANKL-induced osteoclastogenesis.

Keywords gene expression, LAT, osteoclast, RANKL, transmembrane adaptor

Article

Research Article

Mol. Cells 2012; 33(4): 401-406

Published online April 30, 2012 https://doi.org/10.1007/s10059-012-0009-2

Copyright © The Korean Society for Molecular and Cellular Biology.

The Transmembrane Adaptor Protein, Linker for Activation of T cells (LAT), Regulates RANKL-Induced Osteoclast Differentiation

Kabsun Kim*, Jung Ha Kim, Jang Bae Moon, Jongwon Lee, Han bok Kwak, Yong-Wook Park1,and Nacksung Kim*

National Research Laboratory for Regulation of Bone Metabolism and Disease, Department of Pharmacology, Chonnam National University Medical School, Gwangju 501-746, Korea, 1Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju 501-757, Korea

Correspondence to:*Correspondence: kabsun@hanmail.net (KK); nacksung@chonnam.ac.kr (NK)

Received: January 6, 2012; Revised: January 26, 2012; Accepted: January 27, 2012

Abstract

RANKL induces the formation of osteoclasts, which are responsible for bone resorption. Herein we investigate the role of the transmembrane adaptor proteins in RANKL-induced osteoclastogenesis. LAT positively regulates osteoclast differentiation and is up-regulated by RANKL via c-Fos and NFATc1, whereas LAB and LIME act as negative modulators of osteoclastogenesis. In addition, silencing of LAT by RNA interference or overexpression of a LAT dominant negative in bone marrow-derived macrophage cells attenuates RANKL-induced osteoclast formation. Furthermore, LAT is in-volved in RANKL-induced PLC? activation and NFATc1 induction. Thus, our data suggest that LAT acts as a positive regulator of RANKL-induced osteoclastogenesis.

Keywords: gene expression, LAT, osteoclast, RANKL, transmembrane adaptor

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.
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