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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2021
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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) |
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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 |
work_keys_str_mv |
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