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Biomedical subjects

L L Lin

Publications and source records attributed to L L Lin.

8 recordsLinked to original sources
PubMed1992

Interleukin-1 alpha induces the accumulation of cytosolic phospholipase A2 and the release of prostaglandin E2 in human fibroblasts.

Treatment of the human lung fibroblast cell line, WI-38, with interleukin-1 alpha (IL-1 alpha) results in a large increase in the production of cytosolic phospholipase A2 (cPLA2) and prostaglandin E2 (PGE2). The IL-1-induced accumulation of cPLA2 is closely correlated with increased PGE2 release. In contrast to cPLA2, the level of cyclooxygenase remains unchanged following IL-1 alpha treatment. The glucocorticoid, dexamethasone, blocks the IL-1 alpha-mediated increases in both cPLA2 and PGE2 without affecting the cyclooxygenase level. Taken together, these data suggest that in these cells, the regulation of prostaglandin production by IL-1 and glucocorticoid can be attributed to the level of cPLA2. These results provide a new mechanism for the effect of IL-1 and glucocorticoids on eicosanoid synthesis and provide additional support for an important role of cPLA2 in the inflammatory response.

Blotting, Western↗
PubMed1992

Cytosolic phospholipase A2 is coupled to hormonally regulated release of arachidonic acid.

Cytosolic phospholipase A2 (cPLA2) binds to natural membrane vesicles in a Ca(2+)-dependent fashion, resulting in the selective release of arachidonic acid, thus implicating cPLA2 in the hormonally regulated production of eicosanoids. Here we report that the treatment of Chinese hamster ovary (CHO) cells overexpressing cPLA2 with ATP or thrombin resulted in an increased release of arachidonic acid as compared with parental CHO cells, demonstrating the hormonal coupling of cPLA2. In contrast, CHO cells overexpressing a secreted form of mammalian PLA2 (sPLA2-II) failed to show any increased hormonal responsiveness. Interestingly, we have noted that the activation of cPLA2 with a wide variety of agents stimulates the phosphorylation of cPLA2 on serine residues. Pretreatment of cells with staurosporin blocked the ATP-mediated phosphorylation of cPLA2 and strongly inhibited the activation of the enzyme. Increased cPLA2 activity was also observed in lysates prepared from ATP-treated cells and was sensitive to phosphatase treatment. These results suggest that in addition to Ca2+, the phosphorylation of cPLA2 plays an important role in the agonist-induced activation of cPLA2.

Adenosine Triphosphate↗
PubMed1992

Phospholipase C-gamma 1 association with CD3 structure in T cells.

Recently, we and others have reported tyrosine phosphorylation of phospholipase C-gamma 1 (PLC gamma 1) enzyme after CD3 activation of T cells, and have proposed that PLC gamma 1 mediates signal transduction through the T cell receptor (TCR/CD3). Here, using immunoblotting and immune complex PLC assays, we show that CD3 stimulation of Jurkat cells induces the association of PLC gamma 1 enzyme with CD3 complex. PLC activity is also found to co-precipitate with the CD3 zeta chain from activated cells. In addition, in vitro PLC assays show that CD3 activation leads to about 10-fold stimulation of PLC gamma 1 activity. These results, along with the observation that Jurkat cells preferentially express PLC gamma 1, indicate that PLC gamma 1 participates in CD3 signaling.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1992

Macrophage colony stimulating factor activates phosphatidylcholine hydrolysis by cytoplasmic phospholipase A2.

The macrophage colony stimulating factor (M-CSF) is required for the proliferation and differentiation of monocytes. Previous studies have demonstrated that M-CSF stimulation is associated with phosphatidylcholine (PC) hydrolysis and increased formation of both diacylglycerol (DAG) and phosphorylcholine. The present work extends those results by demonstrating that treatment of human monocytes with M-CSF is associated with increases in a cytoplasmic Ca(2+)-dependent activity which hydrolyzes 1-palmitoyl,2-arachidonoyl PC to arachidonic acid. The finding that this hydrolysis of PC is associated with increases in production of lysophosphatidylcholine indicates that M-CSF stimulates a cytoplasmic phospholipase A2 (cPLA2) activity. These results are supported by the demonstration that M-CSF induces cPLA2 gene expression. M-CSF-induced increases in cPLA2 mRNA levels were biphasic and corresponded with rapid (30-60 min) and delayed (24-72 h) increases in cPLA2 activity. The results demonstrate that this effect of M-CSF on cPLA2 expression is controlled at least in part by post-transcriptional stabilization of cPLA2 transcripts. The finding that M-CSF treatment is also associated with phosphorylation of the cPLA2 protein further suggests that expression of this enzyme is regulated at multiple levels. Finally, the stimulation of cPLA2 activity and arachidonate release is supported by increases in prostaglandin (PG) synthesis. In this regard, levels of both PGE2 and PGF2 alpha were increased in response to M-CSF. Taken together, these results indicate that M-CSF stimulates PC hydrolysis in human monocytes by inducing cPLA2 activity and thereby formation of eicosanoids.

Arachidonic Acid↗
PubMed1979

Time analysis of corneal endothelial cell density after cataract extraction.

Serial endothelial photographs were taken preoperatively and postoperatively in 200 eyes; 111 eyes contained a Rayner iris clip lens, 54 eyes contained a Fyodorov Sputnik lens, and 35 eyes had no lens. Central endothelial cell density was changed in all instances, with counts in implanted eyes declining 25 to 30%, and in nonimplanted eyes 10 to 15%. In both instances, the decline essentially ceased at about three months. The cause of the greater decline in implanted eyes appeared to be mechanical and subsequent cell loss after the 90-day period was virtually equal for the two groups. Methods that may be used to alter the difference in cell density occurring with implantation are best analyzed by using the 90-day period data for comparison.

Animals↗
PubMedDate not supplied

Longterm timolol therapy.

Of 145 patients registered for an investigation of timolol, 27 patients were dropped for unrelated reasons. Among the remaining 118 patients (212 eyes), a significant reduction in intraocular pressure resulted from twice-a-day topical instillation of 0.25 or 0.5% timolol to ocular hypertensives, primary open-angle glaucoma or aphakic glaucoma patients. Outflow facility improved only slightly, but remained improved throughout the course of this study. A significant reduction in aqueous secretion, however, was the predominant cause of intraocular pressure reduction. Timolol alone controlled intraocular pressure in 87% of ocular hypertensives, in 68% of patients with chronic open-angle glaucoma and in 68% of patients with angle-unobstructed aphakic glaucomas. The addition of epinephrine brought the intraocular pressure to less than 22 mm Hg in 85% of the total group of patients.

Adolescent↗