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Platelet interaction with vascular smooth muscle in synthesis of prostacyclin.
Am J Physiol. 1991 May; 260(5 Pt 2):H1544-51.AJ

Abstract

Because vascular smooth muscle cells (SMC) can be exposed to platelets at sites of significant arterial injury, we studied whether cultured rat aorta SMC can utilize platelet-derived arachidonate and prostaglandin (PG) endoperoxides (PGG2/PGH2) in the synthesis of prostacyclin (PGI2). SMC converted exogenous PGH2 to PGI2, measured by radioimmunoassay (RIA) of 6-keto-PGF1 alpha, despite cyclooxygenase inhibition or PGH2-receptor blockade. SMC produced increasing amounts of PGI2 in the presence of an increasing number of platelets when the two cell types were coincubated with arachidonate. Furthermore, aspirin-pretreated SMC produced PGI2 in response to arachidonate, ionophore A23187, or thrombin in the presence of platelets but not in their absence. SMC, by themselves unresponsive to thrombin, produced PGI2 during coincubation with thrombin-stimulated aspirin-pretreated platelets. Separation of the SMC monolayer and platelets with a filter did not prevent platelet-dependent PGI2 formation by the SMC. Finally, aspirin-pretreated SMC, in cosuspension with platelets, inhibited platelet aggregation in association with PGI2 production. These data indicate that 1) SMC can synthesize PGI2 from exogenously added PGH2 and from platelet-derived arachidonate or endoperoxides, 2) direct cell-cell contact is not required for intercellular endoperoxide transfer, and 3) SMC can inhibit platelet aggregation possibly through PGI2 production from platelet-derived endoperoxides.

Authors+Show Affiliations

Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

1903602

Citation

Hechtman, D H., et al. "Platelet Interaction With Vascular Smooth Muscle in Synthesis of Prostacyclin." The American Journal of Physiology, vol. 260, no. 5 Pt 2, 1991, pp. H1544-51.
Hechtman DH, Kroll MH, Gimbrone MA, et al. Platelet interaction with vascular smooth muscle in synthesis of prostacyclin. Am J Physiol. 1991;260(5 Pt 2):H1544-51.
Hechtman, D. H., Kroll, M. H., Gimbrone, M. A., & Schafer, A. I. (1991). Platelet interaction with vascular smooth muscle in synthesis of prostacyclin. The American Journal of Physiology, 260(5 Pt 2), H1544-51.
Hechtman DH, et al. Platelet Interaction With Vascular Smooth Muscle in Synthesis of Prostacyclin. Am J Physiol. 1991;260(5 Pt 2):H1544-51. PubMed PMID: 1903602.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Platelet interaction with vascular smooth muscle in synthesis of prostacyclin. AU - Hechtman,D H, AU - Kroll,M H, AU - Gimbrone,M A,Jr AU - Schafer,A I, PY - 1991/5/11/pubmed PY - 1991/5/11/medline PY - 1991/5/11/entrez SP - H1544 EP - 51 JF - The American journal of physiology JO - Am J Physiol VL - 260 IS - 5 Pt 2 N2 - Because vascular smooth muscle cells (SMC) can be exposed to platelets at sites of significant arterial injury, we studied whether cultured rat aorta SMC can utilize platelet-derived arachidonate and prostaglandin (PG) endoperoxides (PGG2/PGH2) in the synthesis of prostacyclin (PGI2). SMC converted exogenous PGH2 to PGI2, measured by radioimmunoassay (RIA) of 6-keto-PGF1 alpha, despite cyclooxygenase inhibition or PGH2-receptor blockade. SMC produced increasing amounts of PGI2 in the presence of an increasing number of platelets when the two cell types were coincubated with arachidonate. Furthermore, aspirin-pretreated SMC produced PGI2 in response to arachidonate, ionophore A23187, or thrombin in the presence of platelets but not in their absence. SMC, by themselves unresponsive to thrombin, produced PGI2 during coincubation with thrombin-stimulated aspirin-pretreated platelets. Separation of the SMC monolayer and platelets with a filter did not prevent platelet-dependent PGI2 formation by the SMC. Finally, aspirin-pretreated SMC, in cosuspension with platelets, inhibited platelet aggregation in association with PGI2 production. These data indicate that 1) SMC can synthesize PGI2 from exogenously added PGH2 and from platelet-derived arachidonate or endoperoxides, 2) direct cell-cell contact is not required for intercellular endoperoxide transfer, and 3) SMC can inhibit platelet aggregation possibly through PGI2 production from platelet-derived endoperoxides. SN - 0002-9513 UR - https://www.unboundmedicine.com/medline/citation/1903602/Platelet_interaction_with_vascular_smooth_muscle_in_synthesis_of_prostacyclin_ L2 - https://journals.physiology.org/doi/10.1152/ajpheart.1991.260.5.H1544?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -