Reticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation

Abstract Tendon plays a critical role in the joint movement by transmitting force from muscle to bone. This transmission of force is facilitated by its specialized structure, which consists of highly aligned extracellular matrix consisting predominantly of type I collagen. Tenocytes, fibroblast-like...

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Autores principales: Na Rae Park, Snehal S. Shetye, Igor Bogush, Douglas R. Keene, Sara Tufa, David M. Hudson, Marilyn Archer, Ling Qin, Louis J. Soslowsky, Nathaniel A. Dyment, Kyu Sang Joeng
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/45c74eb3cdcf4f63868318236fda9957
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spelling oai:doaj.org-article:45c74eb3cdcf4f63868318236fda99572021-12-02T15:00:19ZReticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation10.1038/s41598-021-90258-82045-2322https://doaj.org/article/45c74eb3cdcf4f63868318236fda99572021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-90258-8https://doaj.org/toc/2045-2322Abstract Tendon plays a critical role in the joint movement by transmitting force from muscle to bone. This transmission of force is facilitated by its specialized structure, which consists of highly aligned extracellular matrix consisting predominantly of type I collagen. Tenocytes, fibroblast-like tendon cells residing between the parallel collagen fibers, regulate this specialized tendon matrix. Despite the importance of collagen structure and tenocyte function, the biological mechanisms regulating fibrillogenesis and tenocyte maturation are not well understood. Here we examine the function of Reticulocalbin 3 (Rcn3) in collagen fibrillogenesis and tenocyte maturation during postnatal tendon development using a genetic mouse model. Loss of Rcn3 in tendon caused decreased tendon thickness, abnormal tendon cell maturation, and decreased mechanical properties. Interestingly, Rcn3 deficient mice exhibited a smaller collagen fibril distribution and over-hydroxylation in C-telopeptide cross-linking lysine from α1(1) chain. Additionally, the proline 3-hydroxylation sites in type I collagen were also over-hydroxylated in Rcn3 deficient mice. Our data collectively suggest that Rcn3 is a pivotal regulator of collagen fibrillogenesis and tenocyte maturation during postnatal tendon development.Na Rae ParkSnehal S. ShetyeIgor BogushDouglas R. KeeneSara TufaDavid M. HudsonMarilyn ArcherLing QinLouis J. SoslowskyNathaniel A. DymentKyu Sang JoengNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Na Rae Park
Snehal S. Shetye
Igor Bogush
Douglas R. Keene
Sara Tufa
David M. Hudson
Marilyn Archer
Ling Qin
Louis J. Soslowsky
Nathaniel A. Dyment
Kyu Sang Joeng
Reticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation
description Abstract Tendon plays a critical role in the joint movement by transmitting force from muscle to bone. This transmission of force is facilitated by its specialized structure, which consists of highly aligned extracellular matrix consisting predominantly of type I collagen. Tenocytes, fibroblast-like tendon cells residing between the parallel collagen fibers, regulate this specialized tendon matrix. Despite the importance of collagen structure and tenocyte function, the biological mechanisms regulating fibrillogenesis and tenocyte maturation are not well understood. Here we examine the function of Reticulocalbin 3 (Rcn3) in collagen fibrillogenesis and tenocyte maturation during postnatal tendon development using a genetic mouse model. Loss of Rcn3 in tendon caused decreased tendon thickness, abnormal tendon cell maturation, and decreased mechanical properties. Interestingly, Rcn3 deficient mice exhibited a smaller collagen fibril distribution and over-hydroxylation in C-telopeptide cross-linking lysine from α1(1) chain. Additionally, the proline 3-hydroxylation sites in type I collagen were also over-hydroxylated in Rcn3 deficient mice. Our data collectively suggest that Rcn3 is a pivotal regulator of collagen fibrillogenesis and tenocyte maturation during postnatal tendon development.
format article
author Na Rae Park
Snehal S. Shetye
Igor Bogush
Douglas R. Keene
Sara Tufa
David M. Hudson
Marilyn Archer
Ling Qin
Louis J. Soslowsky
Nathaniel A. Dyment
Kyu Sang Joeng
author_facet Na Rae Park
Snehal S. Shetye
Igor Bogush
Douglas R. Keene
Sara Tufa
David M. Hudson
Marilyn Archer
Ling Qin
Louis J. Soslowsky
Nathaniel A. Dyment
Kyu Sang Joeng
author_sort Na Rae Park
title Reticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation
title_short Reticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation
title_full Reticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation
title_fullStr Reticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation
title_full_unstemmed Reticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation
title_sort reticulocalbin 3 is involved in postnatal tendon development by regulating collagen fibrillogenesis and cellular maturation
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/45c74eb3cdcf4f63868318236fda9957
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