1. Volume 9, Issue 2, Pages 63-74 (January 2003)
Endothelial cell activation in inflammation: lessons from mutant mouse models 
Christopher G Kevil 
Pathophysiology 
Volume 9, Issue 2, Pages (January 2003)
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2. Fig. 1
Generation of a gene-targeted mutation. This figure summarizes the major steps involved in generating gene targeted mutant mice. The first step is to electroporate and select (G418 antibiotic) murine embryonic stem cells containing the targeting vector (1). PCR or southern blotting techniques are then used to identify clones that have been correctly targeted through homologous recombination (2). These clones are injected into blastocytes (3), which are then implanted into pseudopregnant females (4). Chimeric progeny are identified and bred with wild type mice to determine germline transmission (5). Lastly, heterozygous mutant mice are intercrossed to generate homozygous mutant mice (6).
Pathophysiology 2003 9, 63-74DOI: ( /S )

3. Fig. 2
Mechanisms of leukocyte recruitment. Leukocyte extravasation is accomplished through successive interactions including leukocyte rolling on, firm adhesion to, and emigration across endothelial cells. This inflammation response can be stimulated from extravascular sources, as well as within the lumen. Depending upon where the stimulus is initiated, the endothelium, the leukocyte, or both cell types can be activated. Leukocyte rolling is predominately mediated by the selectin family of molecules (e.g. P- and E-selectin). Whereas, leukocyte firm adhesion and emigration primarily involves members of the immunoglobulin superfamily (e.g. ICAM-1, VCAM-1, and PECAM-1).
Pathophysiology 2003 9, 63-74DOI: ( /S )

4. Fig. 3
Structural features of endothelial cell adhesion molecules. Members of the selectin family contain variable numbers of SCR domains, one EGF like domain, and a Ca++ dependent lectin binding domain. The extracellular domain of immunoglobulin superfamily proteins contains variable numbers of Ig like domains.
Pathophysiology 2003 9, 63-74DOI: ( /S )

5. Fig. 4
Conditional genome mutagenesis using Cre-recombinase. Conditional genome mutagenesis can be accomplished by breeding transgenic mice containing the bacterial Cre DNA recombinase with loxP flanked gene targeted mice. The resulting progeny will contain both the Cre-recombinase transgene and the loxP targeted sites that enable the recombinase to specifically remove genomic material contained within these two sites.
Pathophysiology 2003 9, 63-74DOI: ( /S )

6. Fig. 5
Tissue specific mutagenesis using Cre-recombinase. Tissue specific genome mutations are performed by using a TSP to drive Cre-recombinase gene expression. Cell type A illustrates how tissue specific induction of Cre-recombinase expression facilitates removal of genomic material flanked by loxP motifs. However, lack of promoter utilization by cell type B fails to induce Cre-recombinase expression leaving the genome unaltered.
Pathophysiology 2003 9, 63-74DOI: ( /S )