ArticleExperimental cell research2010
A novel signaling pathway of tissue kallikrein in promoting keratinocyte migration: activation of proteinase-activated receptor 1 and epidermal growth factor receptor.
Article in Experimental cell research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 56 citations in OpenAlex.
- mTORC1 signaling pathway integrates estrogen and growth factor to coordinate vaginal epithelial cells proliferation and differentiation.Cell death & disease · 2022Article
- Therapeutic values of chick early amniotic fluid (ceAF) that facilitates wound healing via potentiating a SASP-mediated transient senescence.Genes & diseases · 2022Article
- Role of Serine Proteases at the Tumor-Stroma Interface.Frontiers in immunology · 2022Review
- Effectivity of zinc oxide-turmeric extract dressing in stimulating the reepithelization phase of wound healing.Veterinary world · 2020Article
- Kallikreins: Essential epidermal messengers for regulation of the skin microenvironment during homeostasis, repair and disease.Matrix biology plus · 2020Article
- Kinin B1 Receptor Signaling in Skin Homeostasis and Wound Healing.The Yale journal of biology and medicine · 2020Review
- Protease-Activated Receptors in the Intestine: Focus on Inflammation and Cancer.Frontiers in endocrinology · 2019Review
- Human tissue kallikrein in the treatment of acute ischemic stroke.Therapeutic advances in neurological disorders · 2019Review
- Matrix metalloproteinase-1 facilitates MSC migration via cleavage of IGF-2/IGFBP2 complex.FEBS open bio · 2018Article
- Plasmin reduces fibronectin deposition by mesangial cells in a protease-activated receptor-1 independent manner.Biochemistry and biophysics reports · 2017Article
- Protease-activated receptor-1 deficiency protects against streptozotocin-induced diabetic nephropathy in mice.Scientific reports · 2016Article
- Gingipains of Porphyromonas gingivalis Affect the Stability and Function of Serine Protease Inhibitor of Kazal-type 6 (SPINK6), a Tissue Inhibitor of Human Kallikreins.The Journal of biological chemistry · 2016Article
- Kallikreins - The melting pot of activity and function.Biochimie · 2016Review
- Role of Sirtuins in Linking Metabolic Syndrome with Depression.Frontiers in cellular neuroscience · 2016Review
- Pharmacological effects of recombinant human tissue kallikrein on bradykinin B2 receptors.Pharmacology research & perspectives · 2015Article
- Protease-activated receptors and itch.Handbook of experimental pharmacology · 2015Review
- Article
- Metastasis of ovarian cancer is mediated by kallikrein related peptidases.Clinical & experimental metastasis · 2014Review
- Proteinase-activated receptors (PARs) - focus on receptor-receptor-interactions and their physiological and pathophysiological impact.Cell communication and signaling : CCS · 2013Review
- Senescent fibroblasts enhance early skin carcinogenic events via a paracrine MMP-PAR-1 axis.PloS one · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Biological functions of tissue kallikrein (TK, KLK1) are mainly mediated by kinin generation and subsequent kinin B2 receptor activation. In this study, we investigated the potential role of TK and its signaling pathways in cultured human keratinocyte migration and in a rat skin wound healing model. Herein, we show that TK promoted cell migration and proliferation in a concentration- and time-dependent manner. Inactive TK or kinin had no significant effect on cell migration. Interestingly, cell migration induced by active TK was not blocked by icatibant or L-NAME, indicating an event independent of kinin B2 receptor and nitric oxide formation. TK's stimulatory effect on cell migration was inhibited by small interfering RNA for proteinase-activated receptor 1 (PAR(1)), and by PAR(1) inhibitor. TK-induced migration was associated with increased phosphorylation of epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinase (ERK), which was blocked by inhibition of protein kinase C (PKC), Src, EGFR and ERK. TK-induced cell migration and EGFR phosphorylation were blocked by metalloproteinase (MMP) inhibitor, heparin, and antibodies against EGFR external domain, heparin-binding EGF-like growth factor (HB-EGF) and amphiregulin (AR). Local application of TK promoted skin wound healing in rats, whereas icatibant and EGFR inhibitor blocked TK's effect. Skin wound healing was further delayed by aprotinin and neutralizing TK antibody. This study demonstrates a novel role of TK in skin wound healing and uncovers new signaling pathways mediated by TK in promoting keratinocyte migration through activation of the PAR(1)-PKC-Src-MMP pathway and HB-EGF/AR shedding-dependent EGFR transactivation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.