PT  - JOURNAL ARTICLE
AU  - Na Rae Park
AU  - Snehal Shetye
AU  - Douglas R. Keene
AU  - Sara Tufa
AU  - David M. Hudson
AU  - Marilyn Archer
AU  - Louis J Soslowsky
AU  - Nathaniel A. Dyment
AU  - Kyu Sang Joeng
TI  - Rcn3 is Involved in Postnatal Tendon Development by Regulating Collagen Modification and Fibrillogenesis
AID  - 10.1101/2020.09.25.313098
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.09.25.313098
4099  - http://biorxiv.org/content/early/2020/09/25/2020.09.25.313098.short
4100  - http://biorxiv.org/content/early/2020/09/25/2020.09.25.313098.full
AB  - Tendon plays a critical role in the joint movement by transmitting force from muscle to bone. This transmission of force is facilitated by its structure, which consists of an aligned and organized type I collagen. Despite the importance of collagen structure, the biological mechanisms regulating fibrillogenesis are not well understood. Here we examine the function of Rcn3 in postnatal tendon development and collagen fibrillogenesis using a genetic mouse model. Loss of Rcn3 in tendon caused decreased tendon thickness, abnormal tendon cellular maturation, and decreased mechanical properties. Interestingly, Rcn3 deficient mice exhibited a relatively smaller distribution of collagen fibril and over-hydroxylation in C-telopeptide cross-linking lysine from α1(1) chain. Besides, the proline 3-hydroxylation sites in type I collagen were also over-hydroxylated in Rcn3 deficient mice. Our data collectively suggest that Rcn3 is required for proper postnatal tendon development via regulation of collagen modification and fibrillogenesis.Competing Interest StatementThe authors have declared no competing interest.