Alterations in cellular adhesion and apoptosis in epithelial cells overexpressing prostaglandin endoperoxide synthase 2

Article Abstract:

The overexpression of cyclooxegenase (COX) 2 leads to alterations in cell adhesion and prevention of apoptosis. Rat intestinal epithelial cells exhibit resistance to apoptosis induced by butyrate. Sulindac sulfide, a suppressor of COX 2, reverses the effect indicating that COX 2 stimulates tumorigenesis. The expression of COX 2 is elevated in colorectal carcinoma in humans which is reducible by nonsteroidal anti-inflammatory drugs such as aspirin. A better understanding of the molecular mechanisms of COX 2 action will help in the development of drugs to prevent cancers.

Physiological aspects, Nonsteroidal anti-inflammatory drugs, Nonsteroidal anti-inflammatory agents

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Prostaglandin synthase 1 gene disruption in mice reduces arachidonic acid-induced inflammation and indomethacin-induced gastric ulceration

Article Abstract:

Mice lacking cyclooxegenase (COX) 1 are more healthy and less prone to indomethacin-induced stomach ulcers than the wild-type mice. The homozygous mutant mice exhibit a decrease in platelet aggregation and a reduction in inflammatory responses to archadionic acid. COX 1 and 2 are essential enzymes in prostaglandin synthesis. Female mice with mutations in the gene encoding COX 1 produce few live young ones when mated with homozygous mutant males.

Prostaglandins, Prostaglandin synthesis

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Prostaglandin synthase 2 gene disruption causes severe renal pathology in the mouse

Article Abstract:

The absence of the prostaglandin endoperoxide H synthase isoform 2, cyclooxegenase 2 (COX-2), causes abnormalities in the kidney that increase with age. A study conducted on mice with mutations in COX-2 indicates no difference from the wild-type animals in the gastrointestinal pathology. Mutations in the COX-1 gene fail to show any abnormality but the female homozygotes give birth to few live young ones when mated with the males.

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