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TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone

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TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone. / Saito, Hiroaki; Gasser, Andreas; Bolamperti, Simona; Maeda, Miki; Matthies, Levi; Jähn, Katharina; Long, Courtney L; Schlüter, Hartmut; Kwiatkowski, Marcel; Saini, Vaibhav; Pajevic, Paola Divieti; Bellido, Teresita; van Wijnen, Andre J; Mohammad, Khalid S; Guise, Theresa A; Taipaleenmäki, Hanna; Hesse, Eric.

In: NAT COMMUN, Vol. 10, No. 1, 22.03.2019, p. 1354.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Saito, H, Gasser, A, Bolamperti, S, Maeda, M, Matthies, L, Jähn, K, Long, CL, Schlüter, H, Kwiatkowski, M, Saini, V, Pajevic, PD, Bellido, T, van Wijnen, AJ, Mohammad, KS, Guise, TA, Taipaleenmäki, H & Hesse, E 2019, 'TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone', NAT COMMUN, vol. 10, no. 1, pp. 1354. https://doi.org/10.1038/s41467-019-08778-x

APA

Saito, H., Gasser, A., Bolamperti, S., Maeda, M., Matthies, L., Jähn, K., Long, C. L., Schlüter, H., Kwiatkowski, M., Saini, V., Pajevic, P. D., Bellido, T., van Wijnen, A. J., Mohammad, K. S., Guise, T. A., Taipaleenmäki, H., & Hesse, E. (2019). TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone. NAT COMMUN, 10(1), 1354. https://doi.org/10.1038/s41467-019-08778-x

Vancouver

Saito H, Gasser A, Bolamperti S, Maeda M, Matthies L, Jähn K et al. TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone. NAT COMMUN. 2019 Mar 22;10(1):1354. https://doi.org/10.1038/s41467-019-08778-x

Bibtex

@article{12a58400c1f741d0b80f3c733b64b43c,
title = "TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone",
abstract = "Osteoporosis is caused by increased bone resorption and decreased bone formation. Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteoporosis. However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated. Here we show that the absence of the homeodomain protein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a reduced bone formation. Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3E (Sema3E), an osteoclast-inhibiting factor. Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice. Thus, our study identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH anabolic action. These insights contribute to a better understanding of bone metabolism and the anabolic function of PTH.",
keywords = "Journal Article",
author = "Hiroaki Saito and Andreas Gasser and Simona Bolamperti and Miki Maeda and Levi Matthies and Katharina J{\"a}hn and Long, {Courtney L} and Hartmut Schl{\"u}ter and Marcel Kwiatkowski and Vaibhav Saini and Pajevic, {Paola Divieti} and Teresita Bellido and {van Wijnen}, {Andre J} and Mohammad, {Khalid S} and Guise, {Theresa A} and Hanna Taipaleenm{\"a}ki and Eric Hesse",
year = "2019",
month = mar,
day = "22",
doi = "10.1038/s41467-019-08778-x",
language = "English",
volume = "10",
pages = "1354",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone

AU - Saito, Hiroaki

AU - Gasser, Andreas

AU - Bolamperti, Simona

AU - Maeda, Miki

AU - Matthies, Levi

AU - Jähn, Katharina

AU - Long, Courtney L

AU - Schlüter, Hartmut

AU - Kwiatkowski, Marcel

AU - Saini, Vaibhav

AU - Pajevic, Paola Divieti

AU - Bellido, Teresita

AU - van Wijnen, Andre J

AU - Mohammad, Khalid S

AU - Guise, Theresa A

AU - Taipaleenmäki, Hanna

AU - Hesse, Eric

PY - 2019/3/22

Y1 - 2019/3/22

N2 - Osteoporosis is caused by increased bone resorption and decreased bone formation. Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteoporosis. However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated. Here we show that the absence of the homeodomain protein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a reduced bone formation. Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3E (Sema3E), an osteoclast-inhibiting factor. Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice. Thus, our study identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH anabolic action. These insights contribute to a better understanding of bone metabolism and the anabolic function of PTH.

AB - Osteoporosis is caused by increased bone resorption and decreased bone formation. Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteoporosis. However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated. Here we show that the absence of the homeodomain protein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a reduced bone formation. Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3E (Sema3E), an osteoclast-inhibiting factor. Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice. Thus, our study identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH anabolic action. These insights contribute to a better understanding of bone metabolism and the anabolic function of PTH.

KW - Journal Article

U2 - 10.1038/s41467-019-08778-x

DO - 10.1038/s41467-019-08778-x

M3 - SCORING: Journal article

C2 - 30902975

VL - 10

SP - 1354

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

ER -