Abstract
Mitochondrial function following rotator cuff tendon injury (RCI) influences the tendon healing. We examined the mitochondrial morphology and function under hypoxia in the shoulder tendon tissue from surgically-induced tenotomy-RCI rat model and cultured swine tenocytes. The tendon tissue was collected post-injury on 3–5 (Group-A), 10–12 (Group-B), and 22–24 (Group-C), days and the corresponding contralateral tendons were used as control for each group. There was higher protein expression of citrate synthase (P < 0.0001) [10.22 MFI (mean fluorescent intensity)] and complex-1 (P = 0.0008) (7.86 MFI) in Group-A and Group-B that decreased in Group-C [(P = 0.0201) (5.78 MFI and (P = 0.7915) (2.32 MFI), respectively] compared to control tendons. The ratio of BAX:Bcl2 (Bcl2 associated x protein:B cell lymphoma 2) in RCI tendons increased by 50.5% (Group-A) and 68.4% (Group-B) and decreased by 25.8% (Group-C) compared to normoxic controls. Hypoxia increased β-tubulin expression (P = 0067) and reduced PGC1-α (P = 0412) expression in the isolated swine tenocytes with no effect on the protein expression of Complex-1 (P = 7409) and citrate synthase (P = 0.3290). Also, the hypoxic tenocytes exhibited about 4-fold increase in mitochondrial superoxide (P < 0.0001), altered morphology and mitochondrial pore integrity, and increase in mitochondrial density compared to normoxic controls. These findings suggest the critical role of mitochondria in the RCI healing response.
Highlights
Departments of Clinical & Translational Science and Orthopedic Surgery, Creighton University School of Medicine, Omaha, NE, 68178, USA
The present study aims at the investigation of mitochondrial health status in the tendon tissue of tenotomy-RCI-rat model and cultured swine tenocytes under hypoxic conditions
Tenotomy was surgically induced in rat shoulder tendon to develop the RCI model and the injured tendon showed a visible difference in appearance when compared with the contralateral shoulder tendon as the control[19]
Summary
Departments of Clinical & Translational Science and Orthopedic Surgery, Creighton University School of Medicine, Omaha, NE, 68178, USA. The increasing demand for cellular energy in tenocytes during RCI is believed to trigger mitochondrial biogenesis[12]. The association of mitochondrial function and activity and the effect of hypoxia in the shoulder tendon tissues following RCI have not yet been studied. We hypothesize that the health status of mitochondria under the hypoxic environment following acute RCI is strongly associated with the severity and delayed healing responses. The tenocyte in culture responds to hypoxic conditions by increasing the mitochondrial activity. The present study aims at the investigation of mitochondrial health status in the tendon tissue of tenotomy-RCI-rat model and cultured swine tenocytes under hypoxic conditions
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