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The influence of fibrillin-1 and physical activity upon tendon tissue morphology and mechanical properties in mice

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@article{6fba64d73a834b0589cb6f567b54f0e0,
title = "The influence of fibrillin-1 and physical activity upon tendon tissue morphology and mechanical properties in mice",
abstract = "Fibrillin-1 mutations cause pathological changes in connective tissue that constitute the complex phenotype of Marfan syndrome. In this study, we used fibrillin-1 hypomorphic and haploinsufficient mice (Fbn1mgr/mgR and Fbn1+/- mice, respectively) to investigate the impact of fibrillin-1 deficiency alone or in combination with regular physical activity on tendon tissue morphology and mechanical properties. Morphological and biomechanical analyses revealed that Fbn1mgr/mgR but not Fbn1+/- mice displayed smaller tendons with physical properties that were unremarkable when normalized to tendon size. Fbn1mgR/mgR mice (n = 43) Fbn1+/- mice (n = 27) and wild-type mice (WT, n = 25) were randomly assigned to either control cage conditions (n = 54) or to a running on a running wheel for 4 weeks (n = 41). Both fibrillin-1-deficient mice ran voluntarily on the running wheel in a manner similar to WT mice (3-4 km/24 h). Regular exercise did not mitigate aneurysm progression in Fbn1mgR/mgR mice (P < 0.05) as evidenced by unmodified median survival. In spite of the smaller size, tendons of fibrillin-1-deficient mice subjected to regular exercise showed no evidence of overt histopathological changes or tissue overload. We therefore concluded that lack of optimal fibrillin-1 synthesis leads to a down regulation of integrated tendon formation, rather than to a loss of tendon quality, which also implies that fibrillin-1 deficiency in combination with exercise is not a suitable animal model for studying the development of tendon overuse (tendinopathy).",
author = "Tran, {Peter H T} and Tanja Skrba and Elisabeth Wondimu and Giuseppina Galatioto and Svensson, {Ren{\'e} Br{\"u}ggebusch} and Olesen, {Annesofie T} and Mackey, {Abigail L} and Magnusson, {S Peter} and Francesco Ramirez and Michael Kjaer",
note = "{\textcopyright} 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.",
year = "2019",
month = nov,
doi = "10.14814/phy2.14267",
language = "English",
volume = "7",
pages = "e14267",
journal = "Physiological Reports",
issn = "2051-817X",
publisher = "Wiley Periodicals, Inc.",
number = "21",

}

RIS

TY - JOUR

T1 - The influence of fibrillin-1 and physical activity upon tendon tissue morphology and mechanical properties in mice

AU - Tran, Peter H T

AU - Skrba, Tanja

AU - Wondimu, Elisabeth

AU - Galatioto, Giuseppina

AU - Svensson, René Brüggebusch

AU - Olesen, Annesofie T

AU - Mackey, Abigail L

AU - Magnusson, S Peter

AU - Ramirez, Francesco

AU - Kjaer, Michael

N1 - © 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

PY - 2019/11

Y1 - 2019/11

N2 - Fibrillin-1 mutations cause pathological changes in connective tissue that constitute the complex phenotype of Marfan syndrome. In this study, we used fibrillin-1 hypomorphic and haploinsufficient mice (Fbn1mgr/mgR and Fbn1+/- mice, respectively) to investigate the impact of fibrillin-1 deficiency alone or in combination with regular physical activity on tendon tissue morphology and mechanical properties. Morphological and biomechanical analyses revealed that Fbn1mgr/mgR but not Fbn1+/- mice displayed smaller tendons with physical properties that were unremarkable when normalized to tendon size. Fbn1mgR/mgR mice (n = 43) Fbn1+/- mice (n = 27) and wild-type mice (WT, n = 25) were randomly assigned to either control cage conditions (n = 54) or to a running on a running wheel for 4 weeks (n = 41). Both fibrillin-1-deficient mice ran voluntarily on the running wheel in a manner similar to WT mice (3-4 km/24 h). Regular exercise did not mitigate aneurysm progression in Fbn1mgR/mgR mice (P < 0.05) as evidenced by unmodified median survival. In spite of the smaller size, tendons of fibrillin-1-deficient mice subjected to regular exercise showed no evidence of overt histopathological changes or tissue overload. We therefore concluded that lack of optimal fibrillin-1 synthesis leads to a down regulation of integrated tendon formation, rather than to a loss of tendon quality, which also implies that fibrillin-1 deficiency in combination with exercise is not a suitable animal model for studying the development of tendon overuse (tendinopathy).

AB - Fibrillin-1 mutations cause pathological changes in connective tissue that constitute the complex phenotype of Marfan syndrome. In this study, we used fibrillin-1 hypomorphic and haploinsufficient mice (Fbn1mgr/mgR and Fbn1+/- mice, respectively) to investigate the impact of fibrillin-1 deficiency alone or in combination with regular physical activity on tendon tissue morphology and mechanical properties. Morphological and biomechanical analyses revealed that Fbn1mgr/mgR but not Fbn1+/- mice displayed smaller tendons with physical properties that were unremarkable when normalized to tendon size. Fbn1mgR/mgR mice (n = 43) Fbn1+/- mice (n = 27) and wild-type mice (WT, n = 25) were randomly assigned to either control cage conditions (n = 54) or to a running on a running wheel for 4 weeks (n = 41). Both fibrillin-1-deficient mice ran voluntarily on the running wheel in a manner similar to WT mice (3-4 km/24 h). Regular exercise did not mitigate aneurysm progression in Fbn1mgR/mgR mice (P < 0.05) as evidenced by unmodified median survival. In spite of the smaller size, tendons of fibrillin-1-deficient mice subjected to regular exercise showed no evidence of overt histopathological changes or tissue overload. We therefore concluded that lack of optimal fibrillin-1 synthesis leads to a down regulation of integrated tendon formation, rather than to a loss of tendon quality, which also implies that fibrillin-1 deficiency in combination with exercise is not a suitable animal model for studying the development of tendon overuse (tendinopathy).

U2 - 10.14814/phy2.14267

DO - 10.14814/phy2.14267

M3 - Journal article

C2 - 31724332

VL - 7

SP - e14267

JO - Physiological Reports

JF - Physiological Reports

SN - 2051-817X

IS - 21

ER -

ID: 58971715