Original articles
Differences in cellular properties and responses to growth factors between human ACL and MCL cells

https://doi.org/10.1007/s007760050106Get rights and content

Abstract

The anterior cruciate ligament (ACL) has poor healing responses compared with those of the medial collateral ligament (MCL). It has been implied that this is partially due to the poor reparative capacity of ACL cells for ligament injury. The present study was designed to elucidate the reparative capacities of human ACL and MCL cells by investigating their cellular properties and their responses to growth factors. Human ACL and MCL were obtained from seven fresh human cadavers. The cells were isolated from each tissue, and primary cultures were used for the examination. The growth rates of all the human ACL cells were lower than those of the human MCL cells; consistent with this, the doubling time of the ACL cells was 30 ± 7.4% longer than that of the MCL cells. The chemotactic migration of human ACL cells was 33 ± 8.1% slower and the synthesis of DNA and collagen in human ACL cells was 29 ± 6.3% and 31 ± 9.7% lower, respectively, in comparison with those of MCL cells. Cellular responses, in terms of DNA synthesis, in human ACL cells to either basic-fibroblast growth factor (1.0 and 10.0 ng/ml) or transforming growth factor-β (1.0ng/ml) were lower than those of human MCL cells. However, no differences in the cellular responses in terms of collagen synthesis were found. Composite data show that human ACL cells have poorer cellular properties and lower responses to growth factors compared with those of human MCL cells, which suggests that the reparative capacity of human ACL cells may be poorer than that of human MCL cells.

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Cited by (47)

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    So far, multiple explanations for this phenomenon have been suggested. These include different ultrastructural characteristics of the connective tissue cells in the MCL and ACL (Lyon et al., 1991); variations in the proliferative potential of fibroblasts (Amiel et al., 1995; Yoshida and Fujii, 1999); higher levels of nitric oxide produced by the ACL which inhibit collagen and proteoglycan synthesis (Cao et al., 2000); a superior capacity of the MCL to increase its blood supply after injury through angiogenesis and increased blood flow (Bray et al., 2003); distinctive, ligament-specific properties of stem cells (Furumatsu et al., 2010; Zhang et al., 2011); differential expression of MMP-2, -9 and -13 (Georgiev et al., 2018; Nishikawa et al., 2018). The unsatisfactory healing of the ACL may also be due to the failure of cells and blood vessels to bridge the gap between the ruptured ends of the ACL in an adequate way, as well as the lack of the wound-site to fill within the intra-articular environment (Chen, 2009).

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    One possible explanation is the higher cellular response in hamstring tenocytes to injury-induced growth factors, as compared to that of ACL tenocytes, which have been known to be very poor. Yoshida and Fujii reported that the Deoxyribonucleic Acid (DNA) synthesis of human Medial Collateral Ligament (MCL) cells when exposed to β-fibroblast growth factor (β-FGF) and transforming growth factor-β (TGF-β) was notably higher as compared to human ACL cells [10]. Furthermore, Sanchez et al. noted that the application of a particular platelet-rich plasma preparation rich in growth factors (PRGF) to hamstring autografts during ACL reconstruction resulted in postoperative histological changes [11].

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    Although ACL and MCL injury and repair processes are very complex, the intrinsic differences between ACL and MCL could help to explain their differential healing abilities. Previous reports had shown substantial differences in ACL and MCL, such as tissue structure feature, cell morphology, adhesion forces, expressions of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs).9–14 It is reported that the mRNA expression levels of pro-collagen and collagen are higher in MCL tissues than in ACL tissues for both normal and injury states.15

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