lncRNA ANRIL accelerates wound healing in diabetic foot ulcers via modulating HIF1A/VEGFA signaling through interacting with FUS

Wan, Jia; Bao, Yan; Hou, Li-Juan; Li, Guojian; Du, Lingjuan; Ma, Zhenzhen; Yang, Guo-Kai; Hou, Yi; Li, Zhaoxiang; Yang, Yilin

doi:10.1002/jgm.3462

Cited by 8 publications

(3 citation statements)

References 45 publications

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“…LncRNA GAS6-AS1 regulated colorectal cancer (CRC) proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) via recruiting FUS to stable TRIM14 mRNA stability [41]. Recent study has shown that ANRIL recruited and interacted with FUS to stable HIFA to mediate transcription of VEGFA and ANRIL, which accelerated wound healing in diabetic foot ulcers [42]. In the present study, the interaction between LINC00323 and FUS was con rmed by veri ed by RNA pull-down and RIP assays.…”

Section: Discussionmentioning

confidence: 99%

LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

黄,

Wang,

Sun

et al. 2024

Preprint

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Intermittent hypoxia has been reported to contribute beneficial effects on fracture healing depending on various factors like duration, frequency, and severity. Yet, little is known about the underlying molecular mechanism. Our previous study found that LINC00323 was up-regulated under hypoxic conditions, suggesting that it might play a final role in hypoxia-induced fracture repair. The present study is to investigate the osteogenic effect of LINC00323 in vitro and in vivo. Upregulation of LINC00323 enhanced the mineralization and activity ALP and increased the expression of osteogenic markers. Further analysis revealed that LINC00323 promoted PDGFB expression by binding FUS to regulate the growth and osteogenic differentiation of MC3T3-E1. Lentivirus mediated LINC00323 particles were injected into the fracture site of the tibia of mice, and fracture healing was evaluated by X-rays, micro-CT examination, biomechanical test and histological staining. Local injection of Lentivirus-LINC00323 increased bone mass, biomechanical strength and cartilage callus formation. These findings indicated that LINC00323 induced the differentiation of osteoblast-like cells via regulation of the expression of PDGFB, represents a theoretical basis to accelerate fracture healing.

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Section: Discussionmentioning

confidence: 99%

LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

黄,

Wang,

Sun

et al. 2024

Preprint

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“…ANRIL regulates the HIF1A/VEGFA signalling in an FUS (fused in sarcoma)-dependent manner, accelerating DFU wound healing. 45 The apoptotic effects of lncRNAs in DFUs are listed in Table 3 These findings provide new information for the clinical treatment of diabetic chronic non-healing wounds.…”

Section: Lncrnamentioning

confidence: 98%

The role of programmed cell death in diabetic foot ulcers

Li,

Jiang,

Xia

2023

International Wound Journal

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Diabetic foot ulcer, is a chronic complication afflicting individuals with diabetes, continue to increase worldwide, immensely burdening society. Programmed cell death, which includes apoptosis, autophagy, ferroptosis, necroptosis and pyroptosis, has been increasingly implicated in the pathogenesis of diabetic foot ulcer. This review is based on an exhaustive examination of the literature on ‘programmed cell death’ and ‘diabetic foot ulcers’ via PubMed. The findings revealed that natural bioactive compounds, noncoding RNAs and certain proteins play crucial roles in the healing of diabetic foot ulcers through various forms of programmed cell death, including apoptosis, autophagy, ferroptosis and pyroptosis.

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“…As a transcription factor, HIF1A is implicated in various biological activities, such as angiogenesis, glucose metabolism, cell proliferation, survival, and apoptosis; HIF1A can also promote tumor cell migration in different tumors [ 12 ]. Vascular endothelial growth factor (VEGF), accepted as the target gene of HIF1A, is one of the most potent angiogenic factors [ 13 ]. The HIF1A/VEGFA axis has been found to play a crucial role in angiogenesis [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

The HIFIA/LINC02913/IGF1R axis promotes the cell function of adipose-derived mesenchymal stem cells under hypoxia via activating the PI3K/AKT pathway

Xiong,

Yuan,

Yang

et al. 2023

J Transl Med

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Objective Promoting angiogenesis is crucial for tissue repair. Adipose-derived mesenchymal stem cells (ADSCs) are endowed with the ability of paracrine secretion of various angiogenic cytokines and the differentiation potential into endothelium-like cells to directly participate in angiogenesis. ADSCs are key seed cells for promoting angiogenesis in regenerative medicine and tissue engineering. This study aimed to explore the role and mechanism of C9orf106 (LINC02913) in the angiogenesis of ADSCs. Methods The microarray dataset GSE12884 was analyzed to identify the differentially expressed lncRNAs in ADSCs under normoxia and hypoxia. The expression of the key genes was detected using qRT-PCR, western blot assay (western blot), and immunofluorescence (IF) staining. The adipogenic ability and tube formation ability of ADSCs was detected using oil red O staining and tube formation assay, respectively. The regulatory relationship between hypoxia-inducible factor-1alpha (HIF1A) and LINC02913 was verified using chromatin immunoprecipitation (ChIP) assay and dual-luciferase reporter gene assay. A skin wound healing nude mice model was established. Hematoxylin and eosin (H&E) staining was applied to detect pathological skin damage. Immunohistochemistry (IHC) staining was used to determine the level of CD31 in skin tissues. Results LINC02913 expression was decreased in ADSCs under hypoxia; LINC02913 overexpression inhibited the proliferation, adipogenic ability, endothelial differentiation ability, and tube formation ability of ADSCs. ChIP assay and dual-luciferase reporter gene assay results showed that HIF1A could directly bind to the LINC02913 promoter region to inhibit its transcription. Through RNAact prediction and analysis of the correlation with LINC02913 expression, it was found that IGF1R may directly interact with LINCO02913. The HIF1A/LINC02913/IGF1R axis could activate the PI3K/AKT pathway to promote the biological function of ADSCs. Hypoxia-ADSCs significantly promoted vascularization in the wounded skin. The regulatory effect of LINC02913/IGF1R axis on hypoxia-ADSCs treated skin wound healing were verified. Conclusion The HIF1A/LINC02913/IGF1R axis promoted the proliferation, adipogenic ability, and tube formation ability of ADSCs under hypoxia via activating the PI3K/AKT pathway.

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lncRNA ANRIL accelerates wound healing in diabetic foot ulcers via modulating HIF1A/VEGFA signaling through interacting with FUS

Cited by 8 publications

References 45 publications

LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

The role of programmed cell death in diabetic foot ulcers

The HIFIA/LINC02913/IGF1R axis promotes the cell function of adipose-derived mesenchymal stem cells under hypoxia via activating the PI3K/AKT pathway

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