Stathmin mediates TNF-α-induced skin fibroblast migration by promoting formation of filopodia
Basic Medicine|更新时间:2026-01-09
|
Stathmin mediates TNF-α-induced skin fibroblast migration by promoting formation of filopodia
Journal of Army Medical UniversityVol. 44, Issue 7, Pages: 630-638(2022)
作者机构:
400042 重庆, 陆军特色医学中心皮肤科
作者简介:
基金信息:
the General Program of National Natural Science Foundation of China(81773348);the National Natural Science Foundation for Young Scholars of China(82003323);the Project of Military Medical Frontier Innovation Program of Daping Hospital(2019CXJSC014)
Ruiyan CEN, Lingfei LI, Yumeng DENG, et al. Stathmin mediates TNF-α-induced skin fibroblast migration by promoting formation of filopodia[J]. Journal of Army Medical University, 2022, 44(7): 630-638.
DOI:
Ruiyan CEN, Lingfei LI, Yumeng DENG, et al. Stathmin mediates TNF-α-induced skin fibroblast migration by promoting formation of filopodia[J]. Journal of Army Medical University, 2022, 44(7): 630-638. DOI: 10.16016/j.2097-0927.202112129.
Stathmin mediates TNF-α-induced skin fibroblast migration by promoting formation of filopodia
To explore the effect and preliminary mechanism of stathmin on skin fibroblast migration in the early inflammatory reaction of wound healing mimicked by TNF-α stimulation.
Methods
2
Human dermal fibroblast was stimulated by TNF-α to establish a cell model of inflammation at the early stage of wound healing. The effect of TNF-α on filopodium formation was observed by immunofluorescence assay
cell migration was detected by scratch wound healing
and stathmin expression level under TNF-α stimulation was measured by immunofluorescence assay and Western blotting. After cytochalasin B stimulation and small interfering RNA were used to interfere stathmin expression
respectively
immunofluorescence assay and scratch wound healing were performed again to observe the changes of filopodia and cell migration.
Results
2
TNF-α treatment promoted the formation of filopodia in human dermal fibroblasts
enhanced cell migration (
P
<
0.05) and increased stathmin expression (
P
<
0.05). Cytochalasin B treatment reduced the formation of filopodia and cell migration (
P
<
0.05); and interference of stathmin expression suppressed the formation of filopodia and reduced cell migration (
P
<
0.05).
Conclusion
2
In early inflammation
stathmin mediates skin fibroblast migration by promoting the formation of filopodia.
关键词
Keywords
references
RODRIGUES M, KOSARIC N, BONHAM C A, et al . Wound healing: a cellular perspective[J ] . Physiol Rev, 2019, 99(1): 665-706. DOI: 10.1152/physrev.00067.2017.
WANG K, CHAO S W. Research progress on related mechanisms of wound healing[J]. Chin J Inj Repair Wound Heal Electron Ed, 2021, 16(1): 81-84. DOI: 10.3877/cma.j.issn.1673-9450.2021.01.017.
HE X J, LIN Y, LIU Q W, et al . Research progress of skin fibroblasts in wound healing[J ] . Chin J Inj Repair Wound Heal Electron Ed, 2021, 16(1): 74-77. DOI: 10.3877/cma.j.issn.1673-9450.2021.01.015.
MAHMOUDI S, MANCINI E, XU L, et al . Heterogeneity in old fibroblasts is linked to variability in reprogramming and wound healing[J ] . Nature, 2019, 574(7779): 553-558. DOI: 10.1038/s41586-019-1658-5.
LI Q Z, YANG Y Q, XIA S, et al . Exploration of comprehensive experiment for labelling and observation of actin cytoskeleton in animal cells[J ] . Bull Biol, 2021, 56(2): 53-57.
TAKAISHI K, KINOSHITA H, FENG G G, et al . Cytoskeleton-disrupting agent cytochalasin B reduces oxidative stress caused by high glucose in the human arterial smooth muscle[J ] . J Pharmacol Sci, 2020, 144(4): 197-203. DOI: 10.1016/j.jphs.2020.08.004.
XING Y L, LI J, GENG M Y. Changes of microtubules and actin filaments in cell migration and the signal transduction in this process[J]. Prog Mod Biomed, 2007, 7(6): 919-922. DOI: 10.13241/j.cnki.pmb.2007.06.042.
YU D, GERNAPUDI R, DRUCKER C, et al . The myristoylated alanine-rich C kinase substrate differentially regulates kinase interacting with stathmin in vascular smooth muscle and endothelial cells and potentiates intimal hyperplasia formation[J ] . J Vasc Surg, 2019, 70(6): 2021-2031. e1. DOI: 10.1016/j.jvs.2018.12.022.
BICHSEL K J, HAMMILLER B, TREMPUS C S, et al . The epidermal growth factor receptor decreases Stathmin 1 and triggers catagen entry in the mouse[J ] . Exp Dermatol, 2016, 25(4): 275-281. DOI: 10.1111/exd.12921.
LU S L. To master the rules and characteristics of wound repair for wound healing promotion[J]. Chin J Burns, 2021, 37(5): 401-403. DOI: 10.3760/cma.j.cn501120-20210322-00100.
CAÑEDO-DORANTES L, CAÑEDO-AYALA M. Skin acute wound healing: a comprehensive review[J]. Int J Inflam, 2019, 2019: 3706315. DOI: 10.1155/2019/3706315.
SINGAMPALLI K L, BALAJI S, WANG X Y, et al . The role of an IL-10/hyaluronan axis in dermal wound healing[J ] . Front Cell Dev Biol, 2020, 8: 636. DOI: 10.3389/fcell.2020.00636.
LI H L, LIU X T, HUANG S M, et al . Repair function of essential oil from Crocodylus Siamensis(Schneider, 1801) on the burn wound healing via up-regulated growth factor expression and anti-inflammatory effect[J ] . J Ethnopharmacol, 2021, 264: 113286. DOI: 10.1016/j.jep.2020.113286..
SUN H J, DOU L J, GONG Y, et al . Correlation between the prognosis of diabetic foot wounds and inflammation factor[J ] . J Med Res, 2016, 45(11): 162-164. DOI: 10.11969/j.issn.1673-548X.2016.11.041.
LANDÉN N X, LI D Q, STÅHLE M. Transition from inflammation to proliferation: a critical step during wound healing[J]. Cell Mol Life Sci, 2016, 73(20): 3861-3885. DOI: 10.1007/s00018-016-2268-0.
BROUGHTON G 2nd, JANIS J E, ATTINGER C E. Wound healing: an overview[J]. Plast Reconstr Surg, 2006, 117 (7 Suppl): 1e-S-32e-S. DOI: 10.1097/01.prs.0000222562.60260.f9.
DESJARDINS-PARK H E, FOSTER D S, LONGAKER M T. Fibroblasts and wound healing: an update[J]. Regen Med, 2018, 13(5): 491-495. DOI: 10.2217/rme-2018-0073.
SHU F, ZOU X Q, TUO H, et al . Stathmin gene silencing suppresses proliferation, migration and invasion of gastric cancer cells via AKT/sCLU and STAT3 signaling[J ] . Int J Oncol, 2019, 54(3): 1086-1098. DOI: 10.3892/ijo.2019.4674..
QIU H, YU R. The interactions of microtubules and microfilaments[J]. Chin J Cell Biol, 2009, 31(4): 476-480.
MATTILA P K, LAPPALAINEN P. Filopodia: molecular architecture and cellular functions[J]. Nat Rev Mol Cell Biol, 2008, 9(6): 446-454. DOI: 10.1038/nrm2406.
ALESI G N, JIN L, LI D, et al . RSK2 signals through stathmin to promote microtubule dynamics and tumor metastasis[J ] . Oncogene, 2016, 35(41): 5412-5421. DOI: 10.1038/onc.2016.79.
ZHAO L, ZHANG D J, SHEN Q, et al . KIAA1199 promotes metastasis of colorectal cancer cells via microtubule destabilization regulated by a PP2A/stathmin pathway[J ] . Oncogene, 2019, 38(7): 935-949. DOI: 10.1038/s41388-018-0493-8..
SEETHARAMAN S, ETIENNE-MANNEVILLE S. Cytoskeletal crosstalk in cell migration[J]. Trends Cell Biol, 2020, 30(9): 720-735. DOI: 10.1016/j.tcb.2020.06.004.
MARDAKHEH F K, PAUL A, KVMPER S, et al . Global analysis of mRNA, translation, and protein localization: local translation is a key regulator of cell protrusions[J ] . Dev Cell, 2015, 35(3): 344-357. DOI: 10.1016/j.devcel.2015.10.005.
Effect of fibroblast growth factor 21 on migration and invasion of human pancreatic cancer cells in an inflammatory environment
Loss-of-function MAVS mutation causes antiviral immunodeficiency: unveiling a novel mechanism linking viral infection to generalized pustular psoriasis in children
Z-Ligustilide ameliorates retinitis pigmentosa via inhibiting PI3K/AKT-inflammation axis: Validation based on network pharmacology and molecular docking
Promoting effect of ultra-low dose DMSO on fibroblast proliferation and its underlying mechanism
ATF3 regulates macrophage autophagy and inflammatory responses by suppressing ATG5 and ATG16L1 expression
Related Author
Wei XIAO
Shasha ZHU
Panchun ZHENG
Yaying YANG
SUN Yanan
ZHOU Jiahong
LIU Yaqin
YANG Juan
Related Institution
Department of Pathology, Molecular Medicine Diagnostics Center, Chongqing Medical University
Center for Clinical Molecular Medical Detection, the First Affiliated Hospital of Chongqing Medical University
Department of Dermatology, Children’s Hospital of Chongqing Medical University
Department of Pediatric Research Institute,Children’s Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders
Department of Ophthalmology, General Hospital of Southern Theater Command