The effects of hypoxia-inducible factor (HIF)-1α protein on bone regeneration during distraction osteogenesis: an animal study

Jiang, Xiaowen; Zhang, Y.; Fan, Xiaodong; Deng, Xiao-Dong; Zhu, Yunqing; Li, F.

doi:10.1016/j.ijom.2015.09.021

Cited by 16 publications

(16 citation statements)

References 25 publications

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“…Similar findings were registered by Jiang et al, 23 who observed that the administration of hypoxia-inducible factor (HIF) -1α accelerated osteogenesis in a mandibular distraction model in rabbits, which was dose-dependent; p<0.001. Also, Oishi et al, 24 found an increase in the expression of HIF-1α, VEGF, alkaline phosphatase and bone morphogenetic protein-2 (BMP-2) after intermittent exposure to hypoxia.…”

Section: [ E P U B a H E A D O F P R I N T ]supporting

confidence: 86%

Effects of NSAIDs and environmental oxygen pressure on bone regeneration.

et al. 2019

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Métodos: Participaron 36 cobayos distribuidos en dos grupos iguales. A ambos grupos se les realizaron defectos óseos mandibulares. El Grupo A fue controlado bajo presión de oxígeno en altura (3320msnm, 107mm Hg). El Grupo B fue controlado bajo presión de oxígeno a nivel del mar (150msnm, 157mm Hg). Cada grupo fue dividido en 3 subgrupos iguales (A1, A2, A3 y B1, B2, B3). Los subgrupos A1 y B1 recibieron diclofenaco; A2 y B2, ketoprofeno; A3 y B3, NaCl. La regeneración ósea fue evaluada histológicamente a los 15 y 30 días. Resultados: A nivel del mar, a los 15 días, hubo una significativa mayor cantidad de osteoblastos en el subgrupo control (28,00±2,65) comparado con el subgrupo diclofenaco (16,00±6.25) y ketoprofeno (18,00±4.36); (p=0,041). En altura, a los 15 días, hubo una significativa mayor cantidad de osteblastos en el subgrupo control (38,00±5,29) comparado con el subgrupo diclofenaco (21,67±6,35) y ketoprofeno (19,33±2,52); p=0,007. A nivel del mar, a los 30 días, no se encontró diferencia en el conteo celular; p>0,05. En altura, a los 30 días, se encontró una significativa mayor cantidad de osteoblastos en el subgrupo control (58,00±4,58) comparado con el subgrupo diclofenaco (34,33±4,73) y ketoprofeno (34,00±11,14); (p=0,003). Conclusión: La administración de diclofenaco y ketoprofeno produjeron una menor regeneración ósea mandibular, siendo este efecto significativamente más negativo a nivel del mar. Palabras Clave: Regeneración ósea; presión atmosférica; antiinflamatorios no esteroideos; hipoxia; factor 1 inducible por la hipoxia.

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Section: [ E P U B a H E A D O F P R I N T ]supporting

confidence: 86%

Effects of NSAIDs and environmental oxygen pressure on bone regeneration.

et al. 2019

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“…The rats were divided into four groups: the sham group, sham + HIF‐1α group, acute kidney injury group (AKI), AKI + HIF‐1α group. In a previous study, Jiang et al studied the effects of HIF‐1α on bone regeneration, and each rabbit received 10 μg or 20 μg recombinant HIF‐1α protein. In our study, we tested 50 mg/kg, 100 mg/kg, and 200 mg/kg, among which the dose at 200 mg/kg produced best protective effect.…”

Section: Methodsmentioning

confidence: 99%

Nephropreventing effect of hypoxia‐inducible factor 1α in a rat model of ischaemic/reperfusion acute kidney injury

Wang

Liu

et al. 2018

Clin Exp Pharma Physio

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Acute kidney injury (AKI) occurs in 5% of hospitalized patients and in 50% of sepsis patients with acute renal dysfunction. However, there have been no safe and effective therapeutic strategies. The hypoxia condition is closely related to renal injury and function under AKI. As hypoxia-inducible factor 1α (HIF-1α) is critical for the cellular response to hypoxia, we investigated the protective effect of HIF-1α in a rat AKI model. We found that HIF-1α injection improved the survival of rat with AKI, and the level of creatinine and blood urea nitrogen (BUN) was also increased. Our data showed that HIF-1α treatment significantly alleviated ischaemic/reperfusion injury to kidney tubules and nephrocytes. We also found the downstream factors, such as EPOR, VEGF, and PHD3, were also upregulated by HIF-1α. Finally, it was observed that HIF-1α treatment also increased the percentage of adult resident progenitor cells (ARPC) in vitro and in vivo. In conclusion, HIF-1α plays a protective role in the ischaemic AKI model through stimulating the proliferation of ARPC, and our study provided a potential therapeutic strategy for AKI.

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“…Previous studies have confirmed that HIF-1α can markedly enhance both vessel number and the bone regeneration area in ischemic tissue after a local injection of HIF-1α vectors [18][19][20]. Although HIF-1α have not been used in angiogenesis and osteogenesis in tissue-engineered bone using adenoviruses and a gelatin scaffold, Jiang et al [21] recently investigated the effects of hypoxiainducible factor-1α protein on bone regeneration during distraction osteogenesis using a rabbit model. The results obtained revealed that HIF-1α may represent a new agent for promoteingdistraction osteogenesis by accelerating osteogenesis and mineralization [21].…”

Section: Discussionmentioning

confidence: 99%

“…Although HIF-1α have not been used in angiogenesis and osteogenesis in tissue-engineered bone using adenoviruses and a gelatin scaffold, Jiang et al [21] recently investigated the effects of hypoxiainducible factor-1α protein on bone regeneration during distraction osteogenesis using a rabbit model. The results obtained revealed that HIF-1α may represent a new agent for promoteingdistraction osteogenesis by accelerating osteogenesis and mineralization [21]. These associations were consistent with the interpretation that HIF-1α had a crucial role in mediating the effects of angiogenesis and osteogenesis on bone.…”

Section: Discussionmentioning

confidence: 99%