VEGF and FGF-2: Promising targets for the treatment of respiratory disorders

Laddha, Ankit P.; Kulkarni, Yogesh A.

doi:10.1016/j.rmed.2019.08.003

Cited by 129 publications

(98 citation statements)

References 123 publications

(97 reference statements)

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“…Previous studies indicated that hypoxia could upregulate the HIF pathway and might subsequently initiate a pathological process or protective biofunction in cartilage (Bouaziz et al, 2016a;Laddha and Kulkarni, 2019). Indeed, the HIF-1 pathway was previously shown to play a vital role in the maintenance of chondrocyte homeostasis and chondrogenic capacity (Dunwoodie, 2009).…”

Section: Discussionmentioning

confidence: 99%

Low-Intensity Pulsed Ultrasound Alleviates Hypoxia-Induced Chondrocyte Damage in Temporomandibular Disorders by Modulating the Hypoxia-Inducible Factor Pathway

et al. 2020

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Temporomandibular disorders are a common cause of chronic pain in the orofacial region and have a complex and multi-factorial pathophysiology. Mechanical loading or inflammatory conditions have been shown to decrease oxygen tension within the joint cartilage and activate the hypoxia-inducible factor (HIF) pathway, which in turn aggravates the pathological processes underlying temporomandibular joint (TMJ) disorders. We previously showed that low-intensity pulsed ultrasound (LIPUS) treatment effectively repairs TMJ injury induced by chronic sleep deprivation (CSD). Here, we explored the effects of LIPUS treatment on hypoxia-induced chondrocyte injury. We found that it effectively restored the proliferation capacity of mandibular chondrocytes under hypoxic conditions and lowered their rate of apoptosis. Chondrogenic capacity, as assessed by type II collagen levels, and mucin-positive areas were also significantly increased after LIPUS treatment. Levels of matrix metalloprotein-3 and interleukin-6 decreased in mandibular chondrocytes following this treatment, whereas the expression of tissue inhibitor of metalloproteinase-1 increased. We also found that HIF-1a expression was upregulated in mandibular chondrocytes under hypoxic conditions and was further enhanced by LIPUS treatment. Similarly, HIF-2a levels increased in mandibular chondrocytes under hypoxic conditions but decreased following LIPUS treatment. Subsequently, we established a CSD-induced TMJ injury model and found that LIPUS increased mucin-positive areas as well as HIF-1a expression and decreased HIF-2 level in the chondrocyte layer. Together, our results indicate that the protective effect of LIPUS on chondrocyte is partly associated with the HIF pathway.

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Section: Discussionmentioning

confidence: 99%

Low-Intensity Pulsed Ultrasound Alleviates Hypoxia-Induced Chondrocyte Damage in Temporomandibular Disorders by Modulating the Hypoxia-Inducible Factor Pathway

et al. 2020

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“…330 Considering that FGF2 acts as an angiogenic mediator involved in various lung disorders such as COPD, pulmonary fibrosis, pulmonary hypertension, asthma, and lung cancer, FGF2 could also be an crucial target for the treatment of these lung disorders. 331 FGF7 stimulates proliferation of lung epithelial cells and has been considered as a potential therapy for lung injury. 332 FGF9 is a strong candidate contributing to the progression of IPF, which makes it a potential target for the therapies of IPF.…”

Section: Expressions Of Fgf Ligands and Receptors In The Lungmentioning

confidence: 99%

FGF/FGFR signaling in health and disease

Xie

Yang

et al. 2020

Sig Transduct Target Ther

514

391

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Growing evidences suggest that the fibroblast growth factor/FGF receptor (FGF/FGFR) signaling has crucial roles in a multitude of processes during embryonic development and adult homeostasis by regulating cellular lineage commitment, differentiation, proliferation, and apoptosis of various types of cells. In this review, we provide a comprehensive overview of the current understanding of FGF signaling and its roles in organ development, injury repair, and the pathophysiology of spectrum of diseases, which is a consequence of FGF signaling dysregulation, including cancers and chronic kidney disease (CKD). In this context, the agonists and antagonists for FGF-FGFRs might have therapeutic benefits in multiple systems.

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“…This study also verified the angiogenic role of exosomesdelivered miR-23a in molecular levels, as our data shown that VEGF expression was markedly increased, while TSP-1 expression was reduced by GC cell-derived exosomal miR-23a. VEGF, one of the powerful activators of angiogenesis, stimulates endothelial cell migration and proliferation abilities in existing vessels, thereby enhancing the generation and stabilization of new blood vessels (41,42). TSP-1 is a multidomain glycoprotein participated in intercellular and cell to matrix interactions, and particularly related to angiogenesis and tumorigenesis (43).…”

Section: Discussionmentioning

confidence: 99%

Gastric Cancer Cell-Derived Exosomal microRNA-23a Promotes Angiogenesis by Targeting PTEN

Liu

et al. 2020

Front. Oncol.

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Hypoxia-exposed lung cancer-released exosomal microRNA-23a (miR-23a) has been shown to enhance angiogenesis as well as vascular permeability, contributing to the close correlation between exosomal miR-23a and tumorigenesis. The current study aimed to investigate whether gastric cancer (GC) cell-derived exosomal miR-23a could induce angiogenesis and to elucidate the potential mechanisms associated with the process. Differentially expressed miRNAs in GC were initially screened from the Gene Expression Omnibus database. Target genes were selected following miRNA-mRNA prediction and subsequently verified by dual luciferase reporter assay. RT-qPCR was conducted to detect miR-23a and PTEN expression in GC tissues, cells and exosomes. Human umbilical venous endothelial cells (HUVECs) were co-cultured with GC cell-derived exosomes to assess the angiogenesis mediated by exosomes in vitro. Additionally, PTEN was overexpressed in HUVECs to analyze the mechanism by which miR-23a regulates angiogenesis. miR-23a was highly expressed in GC tissues and cells and GC cell-derived exosomes. Angiogenesis was promoted by the co-culture of HUVECs and GC cells-derived exosomes, as evidenced by the increased expression of VEGF but decreased expression of TSP-1. PTEN was targeted by miR-23a and was lowly expressed in GC tissues. In a co-culture system, miR-23a carried by GC cells-derived exosomes promoted angiogenesis via the repression of PTEN. Collectively, GC cell-derived exosomal miR-23a could promote angiogenesis and provide blood supply for growth of GC cells. This study contributes to advancement of miRNA-targeted therapeutics.

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VEGF and FGF-2: Promising targets for the treatment of respiratory disorders

Cited by 129 publications

References 123 publications

Low-Intensity Pulsed Ultrasound Alleviates Hypoxia-Induced Chondrocyte Damage in Temporomandibular Disorders by Modulating the Hypoxia-Inducible Factor Pathway

Low-Intensity Pulsed Ultrasound Alleviates Hypoxia-Induced Chondrocyte Damage in Temporomandibular Disorders by Modulating the Hypoxia-Inducible Factor Pathway

FGF/FGFR signaling in health and disease

Gastric Cancer Cell-Derived Exosomal microRNA-23a Promotes Angiogenesis by Targeting PTEN

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