Prostacyclin receptor-dependent inhibition of human erythroleukemia cell differentiation is STAT3-dependent

Alaster H.Y. Lau; Henry K.H. Lai; Barry H.S. Yeung; Sze Lee Leung; Suk Ying Tsang; Yung H. Wong; Helen Wise

doi:10.1016/j.plefa.2011.12.002

Prostacyclin receptor-dependent inhibition of human erythroleukemia cell differentiation is STAT3-dependent

Alaster H.Y. Lau, Henry K.H. Lai, Barry H.S. Yeung, Sze Lee Leung, Suk Ying Tsang, Yung H. Wong, Helen Wise^*

^*Corresponding author for this work

Division of Life Science

Research output: Contribution to journal › Journal Article › peer-review

2 Citations (Scopus)

Abstract

We have previously demonstrated that activation of prostacyclin (IP) receptors in human erythroleukemia (HEL) cells phosphorylates the signal transducer and activator of transcription 3 (STAT3) via Gα_s and Gα₁₆ hybrid signalling. This current study was designed to determine if functional responses to cicaprost in HEL cells were dependent on STAT3 phosphorylation. Cicaprost significantly enhanced the rapid change in HEL cell morphology induced by phorbol-12-myristate-13-acetate (PMA), and this effect was inhibited by the IP receptor antagonist RO1138452 and a STAT3 inhibitory peptide. Other indicators of PMA-induced HEL cell differentiation, such as increased expression of CD41/CD61 and an increase in cell complexity/granularity, were inhibited by cicaprost in an IP receptor-dependent and STAT3-dependent manner. Although thrombopoietic cytokines promote megakaryocytic differentiation and platelet production via activation of STAT3, the predominant STAT3-dependent effects of cicaprost in HEL cells were inhibitory towards the process of PMA-induced megakaryocytopoeisis.

Original language	English
Pages (from-to)	119-126
Number of pages	8
Journal	Prostaglandins Leukotrienes and Essential Fatty Acids
Volume	86
Issue number	3
DOIs	https://doi.org/10.1016/j.plefa.2011.12.002
Publication status	Published - Mar 2012

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This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

HEL cells
IP receptors
Megakaryocytopoeisis
STAT3

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10.1016/j.plefa.2011.12.002

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title = "Prostacyclin receptor-dependent inhibition of human erythroleukemia cell differentiation is STAT3-dependent",

abstract = "We have previously demonstrated that activation of prostacyclin (IP) receptors in human erythroleukemia (HEL) cells phosphorylates the signal transducer and activator of transcription 3 (STAT3) via Gαs and Gα16 hybrid signalling. This current study was designed to determine if functional responses to cicaprost in HEL cells were dependent on STAT3 phosphorylation. Cicaprost significantly enhanced the rapid change in HEL cell morphology induced by phorbol-12-myristate-13-acetate (PMA), and this effect was inhibited by the IP receptor antagonist RO1138452 and a STAT3 inhibitory peptide. Other indicators of PMA-induced HEL cell differentiation, such as increased expression of CD41/CD61 and an increase in cell complexity/granularity, were inhibited by cicaprost in an IP receptor-dependent and STAT3-dependent manner. Although thrombopoietic cytokines promote megakaryocytic differentiation and platelet production via activation of STAT3, the predominant STAT3-dependent effects of cicaprost in HEL cells were inhibitory towards the process of PMA-induced megakaryocytopoeisis.",

keywords = "HEL cells, IP receptors, Megakaryocytopoeisis, STAT3",

author = "Lau, \{Alaster H.Y.\} and Lai, \{Henry K.H.\} and Yeung, \{Barry H.S.\} and \{Lee Leung\}, Sze and \{Ying Tsang\}, Suk and Wong, \{Yung H.\} and Helen Wise",

year = "2012",

month = mar,

doi = "10.1016/j.plefa.2011.12.002",

language = "English",

volume = "86",

pages = "119--126",

journal = "Prostaglandins Leukotrienes and Essential Fatty Acids",

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T1 - Prostacyclin receptor-dependent inhibition of human erythroleukemia cell differentiation is STAT3-dependent

AU - Lau, Alaster H.Y.

AU - Lai, Henry K.H.

AU - Yeung, Barry H.S.

AU - Lee Leung, Sze

AU - Ying Tsang, Suk

AU - Wong, Yung H.

AU - Wise, Helen

PY - 2012/3

Y1 - 2012/3

N2 - We have previously demonstrated that activation of prostacyclin (IP) receptors in human erythroleukemia (HEL) cells phosphorylates the signal transducer and activator of transcription 3 (STAT3) via Gαs and Gα16 hybrid signalling. This current study was designed to determine if functional responses to cicaprost in HEL cells were dependent on STAT3 phosphorylation. Cicaprost significantly enhanced the rapid change in HEL cell morphology induced by phorbol-12-myristate-13-acetate (PMA), and this effect was inhibited by the IP receptor antagonist RO1138452 and a STAT3 inhibitory peptide. Other indicators of PMA-induced HEL cell differentiation, such as increased expression of CD41/CD61 and an increase in cell complexity/granularity, were inhibited by cicaprost in an IP receptor-dependent and STAT3-dependent manner. Although thrombopoietic cytokines promote megakaryocytic differentiation and platelet production via activation of STAT3, the predominant STAT3-dependent effects of cicaprost in HEL cells were inhibitory towards the process of PMA-induced megakaryocytopoeisis.

AB - We have previously demonstrated that activation of prostacyclin (IP) receptors in human erythroleukemia (HEL) cells phosphorylates the signal transducer and activator of transcription 3 (STAT3) via Gαs and Gα16 hybrid signalling. This current study was designed to determine if functional responses to cicaprost in HEL cells were dependent on STAT3 phosphorylation. Cicaprost significantly enhanced the rapid change in HEL cell morphology induced by phorbol-12-myristate-13-acetate (PMA), and this effect was inhibited by the IP receptor antagonist RO1138452 and a STAT3 inhibitory peptide. Other indicators of PMA-induced HEL cell differentiation, such as increased expression of CD41/CD61 and an increase in cell complexity/granularity, were inhibited by cicaprost in an IP receptor-dependent and STAT3-dependent manner. Although thrombopoietic cytokines promote megakaryocytic differentiation and platelet production via activation of STAT3, the predominant STAT3-dependent effects of cicaprost in HEL cells were inhibitory towards the process of PMA-induced megakaryocytopoeisis.

KW - HEL cells

KW - IP receptors

KW - Megakaryocytopoeisis

KW - STAT3

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UR - https://openalex.org/W2167276296

UR - https://www.scopus.com/pages/publications/84858447106

U2 - 10.1016/j.plefa.2011.12.002

DO - 10.1016/j.plefa.2011.12.002

M3 - Journal Article

C2 - 22336225

SN - 0952-3278

VL - 86

SP - 119

EP - 126

JO - Prostaglandins Leukotrienes and Essential Fatty Acids

JF - Prostaglandins Leukotrienes and Essential Fatty Acids

IS - 3

ER -

Prostacyclin receptor-dependent inhibition of human erythroleukemia cell differentiation is STAT3-dependent

Abstract

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Keywords

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