Department of Orthopaedics, Affiliated Hospital of North Sichuan Medical College, Nanchong, P.R. China.
Key Laboratory of Emergency and Trauma, Ministry of Education, College of Emergency and Trauma, Hainan Medical University, Haikou, P.R. China.
J Microbiol Biotechnol. 2023 Mar 28;33(3):339-347. doi: 10.4014/jmb.2209.09033. Epub 2023 Feb 15.
Transforming growth factor-β is a key factor in regulating adhesion formation during tendon healing. We investigated the effectiveness of SMAD family members, SMAD7 and SMAD3, in the TGF-β/Smad signaling during flexor tendon repair. Mouse flexor toe deep tendon rupture anastomosis models were made. On days 3, 7, 14, 21, and 28, the expressions of smad7 and smad3 in flexor tendon tissues were detected by RT-qPCR and western blot. Furthermore, postoperative intraperitoneal injections of SMAD7 agonists or SMAD3 antagonists were given. The degree of tendon healing was evaluated by adhesion testing and biomechanical experiments. Hematoxylin and eosin (HE) staining was used to observe the pathological changes. Immunohistochemistry was used to evaluate the expressions of collagen III, SMAD3, and SMAD7. The mRNA levels of matrix metalloproteinases, and , and scleraxis (SCX) in flexor tendon tissue were detected by RT-qPCR. expression increased and expression decreased in flexor tendon tissue after injury. In addition, the SMAD7 agonist blocked SMAD3 phosphorylation. SMAD7 agonist and SMAD3 antagonist both improved adhesion formation during flexor tendon healing, and decreased the expressions of collagen III, , and SCX, while increasing expression. This study provides a possible theoretical basis for the SMAD7-SMAD3 signal cascade during flexor tendon adhesion healing.
转化生长因子-β是调节肌腱愈合过程中粘连形成的关键因素。我们研究了 SMAD 家族成员 SMAD7 和 SMAD3 在 TGF-β/Smad 信号通路中的作用在屈肌腱修复中的作用。建立了小鼠屈趾深肌腱断裂吻合模型。在第 3、7、14、21 和 28 天，通过 RT-qPCR 和 Western blot 检测屈肌腱组织中 smad7 和 smad3 的表达。此外，还进行了术后腹腔内注射 SMAD7 激动剂或 SMAD3 拮抗剂。通过粘连试验和生物力学实验评估肌腱愈合程度。苏木精和伊红（HE）染色观察病理变化。免疫组织化学检测胶原 III、SMAD3 和 SMAD7 的表达。通过 RT-qPCR 检测屈肌腱组织中基质金属蛋白酶和 Scleraxis (SCX)的表达。受伤后，屈肌腱组织中 表达增加， 表达减少。此外，SMAD7 激动剂阻断了 SMAD3 的磷酸化。SMAD7 激动剂和 SMAD3 拮抗剂均改善了屈肌腱愈合过程中的粘连形成，降低了胶原 III、和 SCX 的表达，同时增加了 表达。这项研究为屈肌腱粘连愈合过程中的 SMAD7-SMAD3 信号级联提供了可能的理论基础。
