Hypoxia-induced HIF-1 α accumulation is augmented in a co-culture of keloid fibroblasts and human mast cells: Involvement of ERK1/2 and PI-3K/Akt

Zhang, Qunzhou; Oh, Chad K.; Messadi, Diana V.; Duong, Hai S.; Kelly, A. Paul; Soo, Chia; Wang, Lina; Le, Anh D.

doi:10.1016/j.yexcr.2005.10.006

Cited by 66 publications

(68 citation statements)

References 62 publications

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“…20 VEGF production stimulated by hypoxia in this model is anticipated to be defective in Akt1 -/-mice, since Akt is directly involved in the regulation of VEGF expression. 52 This particular feature is distinct from other in vivo models of pathological angiogenesis, where VEGF is constantly supplied by implanted tumors, matrigel or delivered by VEGF-encoding adenovirus. 5 Thus, while comparing results of different studies on angiogenesis one should take into consideration the differences between experimental models as well as endpoints of the studies.…”

Section: Akt Signaling In Endothelial Cellsmentioning

confidence: 95%

“…19 Second, Akt is Akt1 in Endothelial Cell and Angiogenesis activated in ECs in response to exogenous VEGF. 9 Finally, in addition to VEGF, 52 Akt might affect the protein levels and activities of several key regulators of angiogenesis, including Angiopoetin 2. 3 Recent studies clearly demonstrate that, due to the diversity of Akt downstream targets (Fig.…”

Section: Akt Signaling In Endothelial Cellsmentioning

confidence: 99%

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Akt1 in Endothelial Cell and Angiogenesis

et al. 2006

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Section: Akt Signaling In Endothelial Cellsmentioning

confidence: 95%

Section: Akt Signaling In Endothelial Cellsmentioning

confidence: 99%

Akt1 in Endothelial Cell and Angiogenesis

et al. 2006

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“…It was proposed that keloid formation may be caused by inflammation arising from the abnormal secretion of proinflammatory mediators and irregular response to other inflammatory signals mediated by keloid fibroblasts (12). It was also proven that, as a special form of wound healing, keloids exhibit characteristics similar to the long-lasting inflammatory responses, immune abnormalities and invasive growth characteristics of tumors (31,32).…”

Section: Chronic Inflammation In Keloidsmentioning

confidence: 99%

Upregulation of proinflammatory genes in skin lesions may be the cause of keloid formation (Review)

2013

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Abstract. It was previously demonstrated that the main cause behind keloid formation may be keloid fibroblast abnormalities, which are closely associated with the microenvironment of the keloid lesion. The post-traumatic and chronic inflammation of the keloid lesion area suggest that inflammatory mediators play an important role in the keloid microenvironment and are crucial for keloid fibroblast abnormalities. In this study, we hypothesized that the mechanism underlying keloid formation may involve the continuous upregulation of proinflammatory gene expression in keloid lesions. This hypothesis may explain the inflammatory response, invasive growth and recurrence following resection of keloids, as well as the selective localization of keloids in specific parts of a patient's body and the differences in localization among different patients.

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“…Studies suggest that the level of active AKT, as well as its short-term and long-term activation states, in vascular cells can regulate various signaling pathways to affect the balance of pro-and anti-angiogenic factors (19)(20)(21). In addition to VEGF, AKT might affect the protein levels and activities of several key regulators of angiogenesis, including Anhiopoetin (15,22). Thus, AKT/VEGF pathway may constitute a therapeutic target for angiogenesis anomaly in HCC.…”

Section: Introductionmentioning

confidence: 99%

Bufalin enhances anti-angiogenic effect of sorafenib via AKT/VEGF signaling

Wang

Zhang

Ning

et al. 2016

International Journal of Oncology

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Abstract. Sorafenib mainly exerts its anti-hepatoma effect by inhibiting tumor angiogenesis. However, its curative effect is limited. Thus, application of drugs which could augment its anti-angiogenic effect is necessary. Bufalin has been reported to possess anticancer properties. In the present study, we investigated the synergistic anti-angiogenic effect of sorafenib combined with bufalin. The enhanced anti-angiogenic effect of the combination treatment was firstly assessed in nude mice bearing human HCC intradermal tumors. In addition, we found that proliferation was significantly inhibited and the morphology was obviously changed in the combinationtreated human umbilical vein endothelial cells (HUVEC) at 48 h of treatment. In addition, the combination treatment was found to suppress vessel formation potently as proved in the tube formation, chick chorioallantoic membrane and rat aortic rings. Mechanistically, HUVEC incubated with the combination treatment showed increased apoptosis, decreased migration, which might account for its capacity against angiogenesis. Vascular endothelial cells have been reported to secrete cytokines to affect angiogenesis. Therefore, suspensions from HUVECs with different treatments were collected as conditioned medium (CM). The combinationtreated CM significantly inhibited the migration of HUVEC and blood vessel formation in vitro. Importantly, multiple cytokines associated with angiogenesis were downregulated in the combination-treated CM. Furthermore, we verified that the secretion of VEGF was downregulated and revealed that the reduction might be regulated through the inhibition of the PI3K/AKT pathway. Taken together, our findings demonstrated for the first time that bufalin can enhance anti-angiogenic effect of sorafenib via modulating the AKT/ VEGF signaling pathway.

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Hypoxia-induced HIF-1 α accumulation is augmented in a co-culture of keloid fibroblasts and human mast cells: Involvement of ERK1/2 and PI-3K/Akt

Cited by 66 publications

References 62 publications

Akt1 in Endothelial Cell and Angiogenesis

Akt1 in Endothelial Cell and Angiogenesis

Upregulation of proinflammatory genes in skin lesions may be the cause of keloid formation (Review)

Bufalin enhances anti-angiogenic effect of sorafenib via AKT/VEGF signaling

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