Regulation function of MMP-1 downregulated by siRNA on migration of heat-denatured dermal fibroblasts

ABSTRACT Cutaneous wound healing is a complex physiological process that requires the efforts of various cell types and signaling pathways and often results in thickened collagen-enriched healed tissue called a scar. Therefore, the identification of the mechanism of cutaneous wound healing is necessary and has great value in providing better treatment. Here, we demonstrated that MMP-1 inhibition could promote cell proliferation in dermal fibroblasts via the MTT assay. Meanwhile, we investigated cell migration by flow cytometry and tested type I collagenase activity. We found that MMP-1 inhibition promoted cell proliferation and inhibited cell migration and type I collagenase activity. In conclusion, our study demonstrated that MMP-1 might be a potential therapeutic target in cutaneous wound healing.

[1]  Youliang Wang,et al.  MicroRNA Let‐7b inhibits keratinocyte migration in cutaneous wound healing by targeting IGF2BP2 , 2017, Experimental dermatology.

[2]  Jakub Toczek,et al.  Matrix Metalloproteinase–Targeted Imaging of Lung Inflammation and Remodeling , 2017, The Journal of Nuclear Medicine.

[3]  Jie Cheng,et al.  Overexpression of miR-29b reduces collagen biosynthesis by inhibiting heat shock protein 47 during skin wound healing. , 2016, Translational research : the journal of laboratory and clinical medicine.

[4]  S. Akita,et al.  Effectiveness of basic fibroblast growth factor for pediatric hand burns. , 2016, Journal of tissue viability.

[5]  Chao Zhang,et al.  Tiron Inhibits UVB-Induced AP-1 Binding Sites Transcriptional Activation on MMP-1 and MMP-3 Promoters by MAPK Signaling Pathway in Human Dermal Fibroblasts , 2016, PloS one.

[6]  Takashi Sato,et al.  Novel Antitumor Invasive Actions of p-Cymene by Decreasing MMP-9/TIMP-1 Expression Ratio in Human Fibrosarcoma HT-1080 Cells. , 2016, Biological & pharmaceutical bulletin.

[7]  P. Muangman,et al.  Clinical Efficacy Test of Polyester Containing Herbal Extract Dressings in Burn Wound Healing , 2016, The international journal of lower extremity wounds.

[8]  Xiaofei Lu,et al.  Evaluation of MMP-9 and MMP-2 and their suppressor TIMP-1 and TIMP-2 in adenocarcinoma of esophagogastric junction , 2016, OncoTargets and therapy.

[9]  Y. Koh,et al.  Matrix metalloproteinases in exercise and obesity , 2016, Vascular health and risk management.

[10]  Y. Miao,et al.  Expression of matrix metalloproteinases and tissue inhibitor of matrix metalloproteinases in the hair cycle , 2016, Experimental and therapeutic medicine.

[11]  Bingchang Zhang,et al.  Visfatin Triggers the Cell Motility of Non‐Small Cell Lung Cancer via Up‐Regulation of Matrix Metalloproteinases , 2016, Basic & clinical pharmacology & toxicology.

[12]  J. Ulrichová,et al.  Effects of Silver Nanoparticles on Primary Cell Cultures of Fibroblasts and Keratinocytes in a Wound-Healing Model , 2016, Journal of applied biomaterials & functional materials.

[13]  F. Sharp,et al.  Implications of MMP9 for Blood Brain Barrier Disruption and Hemorrhagic Transformation Following Ischemic Stroke , 2016, Front. Cell. Neurosci..

[14]  Fan Zhang,et al.  Let-7c miRNA Inhibits the Proliferation and Migration of Heat-Denatured Dermal Fibroblasts Through Down-Regulating HSP70 , 2016, Molecules and cells.

[15]  N. Lee,et al.  Diphlorethohydroxycarmalol Suppresses Ultraviolet B-Induced Matrix Metalloproteinases via Inhibition of JNK and ERK Signaling in Human Keratinocytes , 2015, Biomolecules & therapeutics.

[16]  B. Marelli,et al.  Newly identified interfibrillar collagen crosslinking suppresses cell proliferation and remodelling. , 2015, Biomaterials.

[17]  A. Doğan,et al.  Boron and Poloxamer (F68 and F127) Containing Hydrogel Formulation for Burn Wound Healing , 2015, Biological Trace Element Research.

[18]  X. Yang,et al.  Serum Levels of Copper and Zinc in Patients with Rheumatoid Arthritis: a Meta-analysis , 2015, Biological Trace Element Research.

[19]  Bin Zhao,et al.  MiR‐10a and miR‐181c regulate collagen type I generation in hypertrophic scars by targeting PAI‐1 and uPA , 2015, FEBS letters.

[20]  M. Slimane,et al.  Matrix metalloproteinase-1 and matrix metalloproteinase-12 gene polymorphisms and the risk of ischemic stroke in a Tunisian population , 2014, Journal of the Neurological Sciences.

[21]  A. Pant,et al.  Activation of the δ-opioid receptor promotes cutaneous wound healing by affecting keratinocyte intercellular adhesion and migration , 2014, British journal of pharmacology.

[22]  D. Chung,et al.  The stimulatory effects of Stewartia koreana extract on the proliferation and migration of fibroblasts and the wound healing activity of the extract in mice. , 2014, International journal of molecular medicine.

[23]  Hyung-Seok Kim,et al.  Melatonin improves functional outcome via inhibition of matrix metalloproteinases-9 after photothrombotic spinal cord injury in rats , 2014, Acta Neurochirurgica.

[24]  B. Lin,et al.  NGF Accelerates Cutaneous Wound Healing by Promoting the Migration of Dermal Fibroblasts via the PI3K/Akt-Rac1-JNK and ERK Pathways , 2014, BioMed research international.

[25]  Jie Cheng,et al.  Identification of Collagen 1 as a Post-transcriptional Target of miR-29b in Skin Fibroblasts: Therapeutic Implication for Scar Reduction , 2013, The American journal of the medical sciences.

[26]  Jong-Suk Kim,et al.  Curcumin inhibits UVB‐induced matrix metalloproteinase‐1/3 expression by suppressing the MAPK‐p38/JNK pathways in human dermal fibroblasts , 2013, Experimental dermatology.

[27]  L. Qiao,et al.  [Treatment strategies of sequelae following burn wound]. , 2016, Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns.

[28]  J. Trojanek.  [Role of matrix metalloproteinases and tissue inhibitors of metalloproteinases in hypertension. Pathogenesis of hypertension and obesity]. , 2015, Postepy biochemii.

[29]  Li Yan,et al.  Changes in biological behaviors of rat dermal fibroblasts induced by high expression of MMP9. , 2014, World Journal of Emergency Medicine.