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Periostin splice variants affect craniofacial growth by influencing chondrocyte hypertrophy. | LitMetric

AI Article Synopsis

  • - Periostin is a key protein involved in bone and cartilage development, with different variants playing distinct roles, particularly in chondrogenesis and craniofacial bone formation.
  • - In a study using mice with different periostin variants, researchers found that variants lacking specific exons resulted in smaller craniofacial skeletons, especially in the mandibular bone, and increased numbers of hypertrophic chondrocytes.
  • - The findings suggest that the absence of certain periostin variants may impair chondrocyte differentiation, ultimately hindering proper bone formation in the craniofacial region.

Article Abstract

Introduction: Periostin, an extracellular matrix protein, plays an important role in osteogenesis and is also known to activate several signals that contribute to chondrogenesis. The absence of periostin in periostin knockout mice leads to several disorders such as craniosynostosis and periostitis. There are several splice variants with different roles in heart disease and myocardial infarction. However, little is known about each variant's role in chondrogenesis, followed by bone formation. Therefore, the aim of this study is to investigate the role of several variants in chondrogenesis differentiation and bone formation in the craniofacial region. Periostin splice variants included a full-length variant (Control), a variant lacking exon 17 (ΔEx17), a variant lacking exon 21 (ΔEx21), and another variant lacking both exon 17 and 21 ***(ΔEx17&21).

Materials And Methods: We used C56BL6/N mice (n = 6) for the wild type (Control)*** and the three variant type mice (n = 6 each) to identify the effect of each variant morphologically and histologically. Micro-computed tomography demonstrated a smaller craniofacial skeleton in ΔEx17s, ΔEx21s, and ΔEx17&21s compared to Controls, especially the mandibular bone. We, thus, focused on the mandibular condyle.

Results: The most distinctive histological observation was that each defected mouse appeared to have more hypertrophic chondrocytes than Controls. Real-time PCR demonstrated the differences among the group. Moreover, the lack of exon 17 or exon 21 in periostin leads to inadequate chondrocyte differentiation and presents in a diminutive craniofacial skeleton.

Discussion: Therefore, these findings suggested that each variant has a significant role in chondrocyte hypertrophy, leading to suppression of bone formation.

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Source
http://dx.doi.org/10.1007/s00774-023-01409-yDOI Listing

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