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iTRAQ-Based Proteomic Analysis of Spontaneous Achilles Tendon Rupture
Bayixiati Qianman1, Tuomilisi Jiasharete2, Ayinazi Badalihan3
1Department of Osteopathy and Orthopedics (Ankle) Surgery, The Sixth Teaching Hospital of Xinjiang Medical University, No. 39 Wuxing South Road, Urumqi 830001, Xinjiang Uygur Autonomous Region, China.
Journal of Proteome Research
|November 27, 2024
Summary
Spontaneous Achilles tendon rupture (SATR) involves complex molecular changes. This study identified key proteins and pathways, revealing potential targets for diagnosing and treating this condition.
Area of Science:
- Biochemistry
- Molecular Biology
- Orthopedics
Background:
- Spontaneous Achilles tendon rupture (SATR) primarily affects middle-aged and elderly individuals, often linked to chronic injury.
- The precise mechanisms and molecular underpinnings of SATR remain poorly understood, limiting effective therapeutic and preventive strategies.
Purpose of the Study:
- To identify critical pathological molecules and signaling pathways involved in the etiology of SATR using advanced proteomic techniques.
- To provide novel insights into the diagnosis, treatment, and prognosis of spontaneous Achilles tendon rupture.
Main Methods:
- iTRAQ proteomics was employed to analyze protein expression profiles in SATR patients.
- Bioinformatic analyses including KEGG pathway, Gene Ontology (GO) enrichment, and protein-protein interaction (PPI) network analysis were performed.
- Western blot (WB) and immunohistochemical staining were used to validate key protein and collagen expression levels.
Main Results:
- iTRAQ analysis identified 2432 candidate proteins, with 307 differentially expressed proteins (DEPs) linked to pathways like focal adhesion and ECM organization.
- Hub genes such as fibronectin (FN1) and serum albumin (ALB) were identified. FN1 and RACK1 were found to be downregulated in SATR tendons.
- Collagen I and III expression were suppressed, while collagen II and APOA4 expression were elevated in SATR tissues. SATR tenocytes exhibited increased proliferation with altered collagen profiles.
Conclusions:
- The study elucidates key molecular targets and pathways implicated in the progression of spontaneous Achilles tendon rupture.
- Findings offer a new perspective for developing diagnostic markers and therapeutic interventions for SATR.
