Decreased angiogenic and increased apoptotic activities of bone microvascular endothelial cells in patients with glucocorticoid-induced osteonecrosis of the femoral head

Huachen Yu,Qidong Zhang,Wanshou Guo,Pei Liu,Hongzhi Liu,Wei Zuo,Xiaowei Sun,Feifan Lu

doi:10.1186/s12891-020-03225-1

Abstract

BackgroundGlucocorticoid-induced osteonecrosis of the femoral head (ONFH) is closely associated with the dysfunction of the bone microvascular endothelial cells (BMECs). The present study investigated the angiogenic and apoptotic activity of the BMECs in glucocorticoid-induced ONFH.MethodsThis study enrolled a total of 12 patients, six of whom were assigned to the ONFH group whereas the other six served as the control group. The ONFH group was composed of patients with glucocorticoid-induced ONFH while the control group had femoral neck fractures. BMECs were isolated from the subchondral region of the femoral head. Cell proliferation, cell viability, tube formation assay, Transwell assay, TUNEL assay, and Western blot analysis were performed.ResultsBMECs of the two groups were successfully isolated and identified. No significant differences were noticed in BMECs proliferation between the two groups. However, compared to the control, cell viability, tube formation, and migration of BMECs were significantly decreased and the number of TUNEL positive cells was markedly increased in the ONFH group. In the ONFH group, it was also noted that the amount of Bax and cleaved-caspase3 was elevated while that of Bcl-2 was reduced.ConclusionThe findings of our study revealed that BMECs obtained from the glucocorticoid-induced ONFH patients had decreased angiogenic and increased apoptotic activities, which could explain the pathogenesis and progression of glucocorticoid-induced ONFH.

Highlights

Glucocorticoid-induced osteonecrosis of the femoral head (ONFH) is closely associated with the dysfunction of the bone microvascular endothelial cells (BMECs)
These results indicated that these cells in the two groups were BMECs and were used in the following experiments
This study reveals for the first time that BMECs obtained from patients with glucocorticoidinduced Osteonecrosis of the femoral head (ONFH) have decreased angiogenic and increased apoptotic activities compared with BMECs from patients with femoral neck fractures

Summary

Introduction

Glucocorticoid-induced osteonecrosis of the femoral head (ONFH) is closely associated with the dysfunction of the bone microvascular endothelial cells (BMECs). The present study investigated the angiogenic and apoptotic activity of the BMECs in glucocorticoid-induced ONFH. Recent reports have indicated that the femoral head microcirculation obstacle caused by a dysfunction of the bone microvascular endothelial cells (BMECs) could be significant in the development of glucocorticoid-induced ONFH [10, 11].BMECs line the sinusoids and inner layer of blood vessels and play a crucial role in vascular homeostasis and angiogenesis [12]. Several studies have reported that the dysfunction of regional endothelial cells due to continuous exposure to glucocorticoids can induce cell apoptosis and inhibit angiogenesis [15]. There are currently no reports on whether the angiogenic and apoptotic activity of BMECs is affected in glucocorticoid-induced ONFH patients

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Discussion

Conclusion