TY - JOUR
T1 - High-affinity binding sites for prostaglandin E on human lymphocytes
AU - Goodwin, James S.
AU - Wiik, Alan
AU - Lewis, Mary
AU - Bankhurst, Arthur D.
AU - Williams, Ralph C.
N1 - Funding Information:
1 This work was supported in part by U.S. Public Health Service Grants AM AI 13824-08and AM 13690-07a nd in part by grants from the Arthritis Foundation, the KROC Foundation, and the American Cancer Society. * Present address: Laboratory of Immunology, Belgdamshospitalet, Rigshospitalets Epidemiafdeling M, Blegdamsvej 3, 2200 Kobenhavn N, Denmark.
PY - 1979/3/1
Y1 - 1979/3/1
N2 - Binding sites on human lymphocytes for prostaglandins were examined by incubating cells with [3H]prostaglandin (PG) A1, E1, E2, F1α, and F2α. Specific reversible binding for [3H]PGE1 and E2 was found with a Kd of ~2 × 10-9M and a B max of ~200 binding sites per cell, assuming uniform distribution. We detected no specific binding of [3H]PGA1, F1α, or F2α to lymphocytes. Also, the addition of 10- to 1000-fold greater amounts of unlabeled PGA, F1α, or F2α did not inhibit the binding of [3H]PGE. The time course of [3H]PGE binding appeared to be bimodal with one component complete within 5 min at 37 °C and another component of binding increasing over a 40-min incubation. We feel that the rapid component of binding may represent cell surface receptors for PGE while the slower component may represent a specific uptake mechanism for PGE into the cell. Glass adherent cells had fewer binding sites than nonadherent cells. Preincubation of the cells overnight resulted in a loss of binding sites.
AB - Binding sites on human lymphocytes for prostaglandins were examined by incubating cells with [3H]prostaglandin (PG) A1, E1, E2, F1α, and F2α. Specific reversible binding for [3H]PGE1 and E2 was found with a Kd of ~2 × 10-9M and a B max of ~200 binding sites per cell, assuming uniform distribution. We detected no specific binding of [3H]PGA1, F1α, or F2α to lymphocytes. Also, the addition of 10- to 1000-fold greater amounts of unlabeled PGA, F1α, or F2α did not inhibit the binding of [3H]PGE. The time course of [3H]PGE binding appeared to be bimodal with one component complete within 5 min at 37 °C and another component of binding increasing over a 40-min incubation. We feel that the rapid component of binding may represent cell surface receptors for PGE while the slower component may represent a specific uptake mechanism for PGE into the cell. Glass adherent cells had fewer binding sites than nonadherent cells. Preincubation of the cells overnight resulted in a loss of binding sites.
UR - http://www.scopus.com/inward/record.url?scp=0018777750&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0018777750&partnerID=8YFLogxK
U2 - 10.1016/0008-8749(79)90158-8
DO - 10.1016/0008-8749(79)90158-8
M3 - Article
C2 - 223765
AN - SCOPUS:0018777750
SN - 0008-8749
VL - 43
SP - 150
EP - 159
JO - Cellular Immunology
JF - Cellular Immunology
IS - 1
ER -