Forkhead box A1 induces angiogenesis through activation of the S100A8/p38 MAPK axis in cutaneous wound healing

Zhou, Zhong-Zhi; Zou, Meilin; Chen, Zhidong; Zhu, Furong; Wang, Tingting; Huang, Xinling

doi:10.1080/08923973.2023.2233693

Cited by 2 publications

(1 citation statement)

References 40 publications

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“…Inflammation is also connected with angiogenesis ( Jeong, Ojha & Lee, 2021 ). p38, same as VEGFA, is also key in regulating angiogenesis ( Zhou et al, 2023 ). Research also showed that VEGFA can activate the p38 pathway and induce the phosphorylation of p38 to regulate cell angiogenesis ( Cheng et al, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

Sun,

Wu,

Lan

et al. 2024

PeerJ

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Ischemic stroke (IS) is a disease with a high mortality and disability rate worldwide, and its incidence is increasing per year. Angiogenesis after IS improves blood supply to ischemic areas, accelerating neurological recovery. β-asarone has been reported to exhibit a significant protective effect against hypoxia injury. The ability of β-asarone to improve IS injury by inducing angiogenesis has not been distinctly clarified. The experimental rats were induced with middle cerebral artery occlusion (MCAO), and oxygen-glucose deprivation (OGD) model cells were constructed using human microvascular endothelial cell line (HMEC-1) cells. Cerebral infarction and pathological damage were first determined via triphenyl tetrazolium chloride (TTC) and hematoxylin and eosin (H&E) staining. Then, cell viability, apoptosis, and angiogenesis were assessed by utilizing cell counting kit-8 (CCK-8), flow cytometry, spheroid-based angiogenesis, and tube formation assays in OGD HMEC-1 cells. Besides, angiogenesis and other related proteins were identified with western blot. The study confirms that β-asarone, like nimodipine, can ameliorate cerebral infarction and pathological damage. β-asarone can also upregulate vascular endothelial growth factor A (VEGFA) and endothelial nitric oxide synthase (eNOS) and induce phosphorylation of p38. Besides, the study proves that β-asarone can protect against IS injury by increasing the expression of VEGFA. In vitro experiments affirmed that β-asarone can induce viability and suppress apoptosis in OGD-mediated HMEC-1 cells and promote angiogenesis of OGD HMEC-1 cells by upregulating VEGFA. This establishes the potential for β-asarone to be a latent drug for IS therapy.

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Section: Discussionmentioning

confidence: 99%

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

Sun,

Wu,

Lan

et al. 2024

PeerJ

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Niobium Nanoparticles Activates Endothelial Tip Cells and Promotes Angiogenesis by FOXA1-PAK4-YAP Signaling Pathway

Mo,

Xie,

Chen

et al. 2024

ACS Appl. Nano Mater.

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Inadequate vascularization is a major challenge in tissue engineering and can lead to the failure of tissue defect repair. Currently, the use of nanomaterials has emerged as a critical strategy for tissue engineering. Nanoparticles can be utilized as additives in composite materials to enhance the development of bone tissue engineering. Niobium (Nb), a transition metal element with notable biocompatibility, has potential in angiogenesis. However, the effect of Nb nanoparticles (a form of niobium in the nanoparticle state) on endothelial cell behavior remains unclear. This study focused on the effect of Nb nanoparticles on the differentiation of tip cells and its in-depth regulatory mechanism. Our results revealed that Nb nanoparticles promoted angiogenesis at an early stage and increased bone regeneration in calvarial bone defects. In addition, Nb nanoparticles activated tip cell differentiation and thereby promoted cell migration and tube formation. Furthermore, we verified that Nb nanoparticles promoted endothelial tip cell formation by activating YAP. Nb nanoparticles regulates YAP through the newly identified upstream regulatory molecules FOXA1 and PAK4. When FOXA1 or PAK4 was inhibited, YAP expression and tip cell activation were inhibited. Thus, Nb nanoparticles promoted angiogenesis by activating endothelial tip cells, and the FOXA1-PAK4-YAP signaling cascade regulated this process. The insights garnered from this study suggest a strategy for tissue engineering and lay a theoretical foundation for the expanded application of Nb nanoparticles in this field.

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Forkhead box A1 induces angiogenesis through activation of the S100A8/p38 MAPK axis in cutaneous wound healing

Cited by 2 publications

References 40 publications

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A

Niobium Nanoparticles Activates Endothelial Tip Cells and Promotes Angiogenesis by FOXA1-PAK4-YAP Signaling Pathway

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