Fibroblast Growth Factor 9 Inhibited Apoptosis in Random Flap via the ERK1/2-Nrf2 Pathway to Improve Tissue Survival

doi:10.3390/jcm12030809

科研成果详情

题名	Fibroblast Growth Factor 9 Inhibited Apoptosis in Random Flap via the ERK1/2-Nrf2 Pathway to Improve Tissue Survival
作者	Zhang, Dupiao 1,2,3; Raza, Mazhar Ali 1,2,3; Chen, Jianpeng1,2,3; Li, Baolong 1,2,3; Liu, Wenbin1,2,3; Han, Tao1,2,3; Yan, Hede1,2; Jiang, Liangfu1,2
发表日期	2023-02
发表期刊	JOURNAL OF CLINICAL MEDICINE 影响因子和分区
语种	英语
原始文献类型	Article
关键词	random flap fibroblast growth factor 9 oxidative stress apoptosis angiogenesis
其他关键词	RECONSTRUCTION
摘要	Background: The application of random pattern skin flaps is limited in plastic surgery reconstruction due to necrosis. Fibroblast growth factor 9 (FGF9) was reported to exert a protective effect against myocardial damage and cerebral ischemia injury, but the impact of FGF9 in random flap survival is still unclear. In this study, we used a mouse model of random flaps to verify that FGF9 can directly increase flap survival area and blood flow intensity by promoting angiogenesis. Materials and Methods: In total, 84 male C57BL/6 mice weighing between 22 and 25 g were randomly divided into three groups (n = 28 each group). After skin flap operation, one group served as a control, a treatment group received FGF9, and a treatment group received FGF9+U0126. All flap samples were incised on postoperative day 7. Results: Our results showed that flap survival was significantly increased in the FGF9 group compared with that in the control group. This protective function was restrained by U0126. The results of histopathology, laser Doppler, and fluorescent staining all showed significant increases in capillary count, collagen deposition, and angiogenesis. FGF9 also significantly increased the expression of antioxidant stress proteins SOD1, eNOS, HO-1, vascular marker proteins CD31, VE cadherin, and pericyte marker protein PDGFR beta. Western blot showed that the phosphorylation degree of ERK1/2 increased after FGF9 treatment, and the expression of Nrf2, a downstream factor, was u-regulated. Western blot and immunofluorescence results of apoptosis-related proteins cleaved caspase-3, BAX, and Bcl2 showed that FGF9 inhibited apoptosis. ERK inhibitor U01926 reduced the beneficial effects of FGF9 on skin flap survival, including promoting angiogenesis, and showing antiapoptosis and antioxidative stress activities. Conclusions: Exogenous FGF9 stimulates angiogenesis of random flap and survival of tissue. the impact of FGF9 is closely linked to the prevention of oxidative stress mediated by ERK1/2-Nrf2. In the function of FGF9 in promoting effective angiogenesis, there may be a close interaction in the FGF9-FGFR-PDGFR-ERK-VE cadherin pathway. In particular, PDGFR and VE cadherin may interact.
资助项目	Zhejiang Provincial Natural Science Foundation of China [LY20H060005]
出版者	MDPI
ISSN	2077-0383
EISSN	2077-0383
卷号	12 期号:3
DOI	10.3390/jcm12030809
页数	13
WOS类目	Medicine, General & Internal
WOS研究方向	General & Internal Medicine
WOS记录号	WOS:000930282400001
收录类别	SCIE ; SCOPUS ; PUBMED
URL	查看原文
PubMed ID	36769456
SCOPUSEID	2-s2.0-85147859582
通讯作者地址	[Yan, Hede]Department of Orthopaedics,The Second Affiliated Hospital and Yuying Children’s Hospital,Wenzhou Medical University,Wenzhou,325015,China ; [Jiang, Liangfu]Department of Orthopaedics,The Second Affiliated Hospital and Yuying Children’s Hospital,Wenzhou Medical University,Wenzhou,325015,China
Scopus学科分类	Medicine (all)
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/173065
专题	第二临床医学院、附属第二医院、育英儿童医院附属第二医院_骨科重点学科实验室
通讯作者	Yan, Hede; Jiang, Liangfu
作者单位	1.Department of Orthopaedics,The Second Affiliated Hospital and Yuying Children’s Hospital,Wenzhou Medical University,Wenzhou,325015,China; 2.Key Laboratory of Orthopaedics of Zhejiang Province,Wenzhou Medical University,Wenzhou,325088,China; 3.The Second School of Medicine,Wenzhou Medical University,Wenzhou,325015,China
第一作者单位	附属第二医院; 温州医科大学
通讯作者单位	附属第二医院
第一作者的第一单位	附属第二医院
推荐引用方式 GB/T 7714	Zhang, Dupiao,Raza, Mazhar Ali,Chen, Jianpeng,et al. Fibroblast Growth Factor 9 Inhibited Apoptosis in Random Flap via the ERK1/2-Nrf2 Pathway to Improve Tissue Survival[J]. JOURNAL OF CLINICAL MEDICINE,2023,12(3).
APA	Zhang, Dupiao., Raza, Mazhar Ali., Chen, Jianpeng., Li, Baolong., Liu, Wenbin., ... & Jiang, Liangfu. (2023). Fibroblast Growth Factor 9 Inhibited Apoptosis in Random Flap via the ERK1/2-Nrf2 Pathway to Improve Tissue Survival. JOURNAL OF CLINICAL MEDICINE, 12(3).
MLA	Zhang, Dupiao,et al."Fibroblast Growth Factor 9 Inhibited Apoptosis in Random Flap via the ERK1/2-Nrf2 Pathway to Improve Tissue Survival".JOURNAL OF CLINICAL MEDICINE 12.3(2023).