ArticleAmerican journal of physiology. Cell physiology2014
Delayed skin wound repair in proline-rich protein tyrosine kinase 2 knockout mice.
Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 22 citations in OpenAlex.
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- Abnormally Elevated PKCδ Delays Diabetic Wound Healing by Inhibiting the GAD1-GABA Pathway.Diabetes & metabolism journal · 2026Article
- Genome-wide detection of RNA editing events during the hair follicles cycle of Tianzhu white yak.BMC genomics · 2022Article
- Pyk2 regulates cell-edge protrusion dynamics by interacting with Crk.Molecular biology of the cell · 2021Article
- Sperm-oocyte signaling: the role of IZUMO1R and CD9 in PTK2B activation and actin remodeling at the sperm binding site†.Biology of reproduction · 2021Article
- PYK2 Is Involved in Premalignant Acinar Cell Reprogramming and Pancreatic Ductal Adenocarcinoma Maintenance by Phosphorylating β-CateninCellular and molecular gastroenterology and hepatology · 2019Article
- Sperm-oocyte contact induces outside-in signaling via PYK2 activation.Developmental biology · 2017Article
- An in silico high-throughput screen identifies potential selective inhibitors for the non-receptor tyrosine kinase Pyk2.Drug design, development and therapy · 2017Article
- Targeting focal adhesion kinase renders pancreatic cancers responsive to checkpoint immunotherapy.Nature medicine · 2016Article
- Proline-rich tyrosine kinase 2 via enhancing signal transducer and activator of transcription 3-dependent cJun expression mediates retinal neovascularization.Scientific reports · 2016Article
- Metalloproteinases and Wound Healing.Advances in wound care · 2015Article
- FOXO1, TGF-β regulation and wound healing.International journal of molecular sciences · 2014Review
- Pyk2 contributes to reepithelialization by promoting MMP expression. Focus on "Delayed skin wound repair in proline-rich protein tyrosine kinase 2 knockout mice".American journal of physiology. Cell physiology · 2014Article
- Transcriptional-secretory uncoupling in RDEB skin creates a non-permissive microenvironment for sensory nerve regeneration.Neurobiology of pain (Cambridge, Mass.)Article
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8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Proline-rich protein tyrosine kinase 2 (Pyk2) is a member of the focal adhesion kinase family. We used Pyk2 knockout (Pyk2-KO) mice to study the role of Pyk2 in cutaneous wound repair. We report that the rate of wound closure was delayed in Pyk2-KO compared with control mice. To examine whether impaired wound healing of Pyk2-KO mice was caused by a keratinocyte cell-autonomous defect, the capacities of primary keratinocytes from Pyk2-KO and wild-type (WT) littermates to heal scratch wounds in vitro were compared. The rate of scratch wound repair was decreased in Pyk2-KO keratinocytes compared with WT cells. Moreover, cultured human epidermal keratinocytes overexpressing the dominant-negative mutant of Pyk2 failed to heal scratch wounds. Conversely, stimulation of Pyk2-dependent signaling via WT Pyk2 overexpression induced accelerated scratch wound closure and was associated with increased expression of matrix metalloproteinase (MMP)-1, MMP-9, and MMP-10. The Pyk2-stimulated increase in the rate of scratch wound repair was abolished by coexpression of the dominant-negative mutant of PKCδ and by GM-6001, a broad-spectrum inhibitor of MMP activity. These results suggest that Pyk2 is essential for skin wound reepithelialization in vivo and in vitro and that it regulates epidermal keratinocyte migration via a pathway that requires PKCδ and MMP functions.
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