Human Keratinocytes Adhere to and Spread on Synthetic Peptide FN-C/H-V Derived from Fibronectin

• Published in: Journal of investigative dermatology Vol. 101; no. 1; pp. 43 - 48
• Main Authors: Wilke, Mark S., Vespa, Jeff, Skubitz, Amy P.N., Furcht, Leo T., McCarthy, James B.
• Format: Journal Article
• Language: English
• Published: Danvers, MA Elsevier Inc 01.07.1993; Nature Publishing
• Subjects: Amino Acid Sequence; Biological and medical sciences; Cell Adhesion - drug effects; Cell Division - drug effects; Cell interactions, adhesion; Collagen; Fibronectins - chemistry; Fibronectins - pharmacology; Fundamental and applied biological sciences. Psychology; Humans; Keratinocytes - drug effects; Laminin; Molecular and cellular biology; Molecular Sequence Data; Peptide Fragments - genetics; Peptide Fragments - pharmacology; Human; Cell culture; Immunocytochemistry; Cell adhesion molecule; Exploration; Cell surface; In vitro; Fibronectin; Pathology; Keratinocyte; Skin; Physiology; Biological receptor
• ISSN: 0022-202X; 1523-1747
• DOI: 10.1111/1523-1747.ep12358823

In a previous study, we reported that two synthetic peptides derived from the 33-kD carboxyl terminal cell/heparin- binding fragment of fibronectin A chain promoted keratinocyte adhesion but not spreading. Because keratinocytes are capable of spreading on the 33/66-kD fragments, we focused on identifying additional chemically synthesized peptides from the cell/heparin-binding fragments of fibronectin that might promote cell spreading. When plastic substrata were coated with peptide FN-C/H-V (WQPPRARI), which is derived from the carboxyl-terminal heparin-binding domain of all plasma fibronectin isoforms, keratinocytes adhered and displayed a spread morphology. In solution, soluble peptide FN-C/H-V inhibited cell spreading on intact fibronectin and on the 33/66-kD fragments. Furthermore, polyclonal antibodies raised against peptide FN-C/H-V also inhibited keratinocyte spreading on fibronectin and the 33/66-kD fragments. These data support the hypothesis that keratinocyte cell adhesion and cell spreading on fibronectin are mediated by multiple distinct domains and different regulatory processes.