Interleukin-2 Suppresses Endothelin-1 Secretion of Cultured Endothelial Cells

Kazuhisa Taniguchi, Shigeto Morimoto, Keisuke Fukuo, Toshio Ogihara, Masashi Yanagisawa, Tomoh Masaki, Nobuhiro Suzuki

Research output: Contribution to journalArticle

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Abstract

The effect of recombinant interleukin-2 (IL-2) on endothelin-1 (ET-1) secretion was studied in bovine pulmonary arterial endothelial (BPAE) cells. IL-2 at concentrations of 1 to 10 U/ml significantly suppressed the basal secretion of ET-1 from BPAE cells. The maximal suppression, which was obtained with 1 U/ml of IL-2, was 74% of the control value during 24 h incubation. Moreover, incubation for 1 h with IL-2 at a concentration of 1 U/ml significantly lowered the prepro ET-1 mRNA level, measured by Northern blot analysis. Additions of 10‒5 M of NG-nitro-L-arginine, an inhibitor of nitric oxide (NO) synthesis, and of 10‒5 M of methylene blue, an inhibitor of soluble guanylate cyclase, abolished the IL-2-induced suppression of ET-1 secretion. On the other hand, while addition of 10 U/ml of thrombin (TB) for 24 h significantly enhanced the secretion of ET-1 to about 128% of the control value, this enhancement was also inhibited by 100 U/ml of IL-2. IL-2 at more than 1 U/ml significantly increased the concentration of 6-keto-prostaglandin F in the medium. However, addition of indomethacin (10‒5 M) did not affect the IL-2-induced suppression of the basal ET-1 secretion, suggesting that prostaglandin I2 does not participate in the IL-2-induced suppression. These findings indicate that IL-2 suppressed the synthesis of ET-1 at the mRNA transcription level, and that NO/cyclic GMP system enhanced by IL-2 in the endothelial cells may be responsible for IL-2-induced suppression of ET-1 synthesis. (Hypertens Res 1992; 15: 171-175).

Original languageEnglish (US)
Pages (from-to)171-175
Number of pages5
JournalHypertension Research
Volume15
DOIs
StatePublished - 1992

Fingerprint

Endothelin-1
Interleukin-2
Cultured Cells
Endothelial Cells
Nitric Oxide
Lung
Messenger RNA
Nitroarginine
Methylene Blue
Cyclic GMP
Epoprostenol
Thrombin
Indomethacin
Northern Blotting

Keywords

  • endothelial cells
  • endothelin-1
  • Interleukin-2
  • nitric oxide
  • prepro endothelin-1 mRNA
  • prostaglandin I

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Taniguchi, K., Morimoto, S., Fukuo, K., Ogihara, T., Yanagisawa, M., Masaki, T., & Suzuki, N. (1992). Interleukin-2 Suppresses Endothelin-1 Secretion of Cultured Endothelial Cells. Hypertension Research, 15, 171-175. https://doi.org/10.1291/hypres.15.171

Interleukin-2 Suppresses Endothelin-1 Secretion of Cultured Endothelial Cells. / Taniguchi, Kazuhisa; Morimoto, Shigeto; Fukuo, Keisuke; Ogihara, Toshio; Yanagisawa, Masashi; Masaki, Tomoh; Suzuki, Nobuhiro.

In: Hypertension Research, Vol. 15, 1992, p. 171-175.

Research output: Contribution to journalArticle

Taniguchi, K, Morimoto, S, Fukuo, K, Ogihara, T, Yanagisawa, M, Masaki, T & Suzuki, N 1992, 'Interleukin-2 Suppresses Endothelin-1 Secretion of Cultured Endothelial Cells', Hypertension Research, vol. 15, pp. 171-175. https://doi.org/10.1291/hypres.15.171
Taniguchi, Kazuhisa ; Morimoto, Shigeto ; Fukuo, Keisuke ; Ogihara, Toshio ; Yanagisawa, Masashi ; Masaki, Tomoh ; Suzuki, Nobuhiro. / Interleukin-2 Suppresses Endothelin-1 Secretion of Cultured Endothelial Cells. In: Hypertension Research. 1992 ; Vol. 15. pp. 171-175.
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abstract = "The effect of recombinant interleukin-2 (IL-2) on endothelin-1 (ET-1) secretion was studied in bovine pulmonary arterial endothelial (BPAE) cells. IL-2 at concentrations of 1 to 10 U/ml significantly suppressed the basal secretion of ET-1 from BPAE cells. The maximal suppression, which was obtained with 1 U/ml of IL-2, was 74{\%} of the control value during 24 h incubation. Moreover, incubation for 1 h with IL-2 at a concentration of 1 U/ml significantly lowered the prepro ET-1 mRNA level, measured by Northern blot analysis. Additions of 10‒5 M of NG-nitro-L-arginine, an inhibitor of nitric oxide (NO) synthesis, and of 10‒5 M of methylene blue, an inhibitor of soluble guanylate cyclase, abolished the IL-2-induced suppression of ET-1 secretion. On the other hand, while addition of 10 U/ml of thrombin (TB) for 24 h significantly enhanced the secretion of ET-1 to about 128{\%} of the control value, this enhancement was also inhibited by 100 U/ml of IL-2. IL-2 at more than 1 U/ml significantly increased the concentration of 6-keto-prostaglandin F1α in the medium. However, addition of indomethacin (10‒5 M) did not affect the IL-2-induced suppression of the basal ET-1 secretion, suggesting that prostaglandin I2 does not participate in the IL-2-induced suppression. These findings indicate that IL-2 suppressed the synthesis of ET-1 at the mRNA transcription level, and that NO/cyclic GMP system enhanced by IL-2 in the endothelial cells may be responsible for IL-2-induced suppression of ET-1 synthesis. (Hypertens Res 1992; 15: 171-175).",
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AU - Masaki, Tomoh

AU - Suzuki, Nobuhiro

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AB - The effect of recombinant interleukin-2 (IL-2) on endothelin-1 (ET-1) secretion was studied in bovine pulmonary arterial endothelial (BPAE) cells. IL-2 at concentrations of 1 to 10 U/ml significantly suppressed the basal secretion of ET-1 from BPAE cells. The maximal suppression, which was obtained with 1 U/ml of IL-2, was 74% of the control value during 24 h incubation. Moreover, incubation for 1 h with IL-2 at a concentration of 1 U/ml significantly lowered the prepro ET-1 mRNA level, measured by Northern blot analysis. Additions of 10‒5 M of NG-nitro-L-arginine, an inhibitor of nitric oxide (NO) synthesis, and of 10‒5 M of methylene blue, an inhibitor of soluble guanylate cyclase, abolished the IL-2-induced suppression of ET-1 secretion. On the other hand, while addition of 10 U/ml of thrombin (TB) for 24 h significantly enhanced the secretion of ET-1 to about 128% of the control value, this enhancement was also inhibited by 100 U/ml of IL-2. IL-2 at more than 1 U/ml significantly increased the concentration of 6-keto-prostaglandin F1α in the medium. However, addition of indomethacin (10‒5 M) did not affect the IL-2-induced suppression of the basal ET-1 secretion, suggesting that prostaglandin I2 does not participate in the IL-2-induced suppression. These findings indicate that IL-2 suppressed the synthesis of ET-1 at the mRNA transcription level, and that NO/cyclic GMP system enhanced by IL-2 in the endothelial cells may be responsible for IL-2-induced suppression of ET-1 synthesis. (Hypertens Res 1992; 15: 171-175).

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