Impaired bone formation in Pdia3 deficient mice.

1α,25-Dihydroxyvitamin D3 [1α,25(OH)2D3] is crucial for normal skeletal development and bone homeostasis. Protein disulfide isomerase family A, member 3 (PDIA3) mediates 1α,25(OH)2D3 initiated-rapid membrane signaling in several cell types. To understand its role in regulating skeletal development, we generated Pdia3-deficient mice and examined the physiologic consequence of Pdia3-disruption in embryos and Pdia3+/- heterozygotes at different ages.

Endogenous regeneration of critical-size chondral defects in immunocompromised rat xiphoid cartilage using decellularized human bone matrix scaffolds.

Clinical efforts to repair cartilage defects delivering cells or engineered cartilage implants into the lesions have met with limited success. This study used a critical-size chondral defect model in immunocompromised rat xiphoid cartilage to test whether endogenous chondrogenesis could be achieved using human bone matrix scaffolds to deliver human cartilage particles and/or a variant isoform of fibroblast growth factor-2 (FGF2-variant). Seventy-two male athymic RNU rats were enrolled in this study with eight rats per experimental group.

Disruption of Pdia3 gene results in bone abnormality and affects 1alpha,25-dihydroxy-vitamin D3-induced rapid activation of PKC.

1,25-dihydroxy-vitamin D3 [1alpha,25(OH)2D3] is a critical regulator of bone development. Protein disulfide isomerase A3 (Pdia3) is a multifunctional protein that has been associated with rapid membrane-initiated signalling by 1alpha,25(OH)2D3 in several cell types. To identify the physiological roles of Pdia3 in skeletal development, we generated Pdia3-deficient mice.