Abstract
9-cis Retinoic acid (9-CRA) is a lipophilic molecule that binds to the retinoid X receptor (RXR). Although retinoic acid (RA) has been known to regulate neutrophil differentiation, a specific role for 9-CRA in chemokine-mediated cellular processes remains obscure. We investigated the effects of 9-CRA on expression of CC chemokine receptors (CCRs) in human monocytic THP-1 cells and peripheral blood monocytes. RNase protection assay was performed to examine the mRNA levels of CCRs in 9-CRA-treated THP-1 cells. mRNA expression of CCR1 and CCR2 was induced in both a dose and time dependent manner. CCR1 and CCR2 mRNA expression began to increase from 6 h after a 100 nM 9-CRA treatment and reached a maximal level at 12 h. Surface expression of CCRs was monitored by flow cytometry. CCR1 and CCR2 surface expression increased in 9-CRA-treated THP-1 cells, but not in untreated cells. Calcium mobilization and chemotactic activity were determined to examine the effect of 9-CRA on cell movement. The intracellular Ca2+ concentration and the chemotactic activity increased in 9-CRA-treated cells in response to the CCR1-dependent chemokines Lkn-1, MIP-1α, and RANTES, and the CCR2-specific chemokine MCP-1. Increased surface expression of CCR1 and the Ca2+ influx due to 9-CRA were confirmed in peripheral blood monocytes. Taken together, 9-CRA increases the expression levels of mRNA and protein of both CCR1 and CCR2, and the cell migration ability in THP-1 cells and peripheral blood monocytes, indicating that 9-CRA may regulate inflammatory processes through an increased response to CCR1- and CCR2-dependent chemokines.
| Original language | English |
|---|---|
| Pages (from-to) | 611-620 |
| Number of pages | 10 |
| Journal | Biochemical Pharmacology |
| Volume | 68 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 2004 Aug 15 |
| Externally published | Yes |
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Keywords
- Chemokine
- Chemokine receptor
- Chemotaxis
- Inflammation
- Monocyte
- Retinoic acid
ASJC Scopus subject areas
- Pharmacology
Cite this
Differential effects of 9-cis retinoic acid on expression of CC chemokine receptors in human monocytes. / Kim, In Sik; Kim, Yoon Suk; Jang, Sung Wuk; Sung, Ho Joong; Han, Ki Hoon; Na, Doe Sun; Ko, Je Sang.
In: Biochemical Pharmacology, Vol. 68, No. 4, 15.08.2004, p. 611-620.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Differential effects of 9-cis retinoic acid on expression of CC chemokine receptors in human monocytes
AU - Kim, In Sik
AU - Kim, Yoon Suk
AU - Jang, Sung Wuk
AU - Sung, Ho Joong
AU - Han, Ki Hoon
AU - Na, Doe Sun
AU - Ko, Je Sang
PY - 2004/8/15
Y1 - 2004/8/15
N2 - 9-cis Retinoic acid (9-CRA) is a lipophilic molecule that binds to the retinoid X receptor (RXR). Although retinoic acid (RA) has been known to regulate neutrophil differentiation, a specific role for 9-CRA in chemokine-mediated cellular processes remains obscure. We investigated the effects of 9-CRA on expression of CC chemokine receptors (CCRs) in human monocytic THP-1 cells and peripheral blood monocytes. RNase protection assay was performed to examine the mRNA levels of CCRs in 9-CRA-treated THP-1 cells. mRNA expression of CCR1 and CCR2 was induced in both a dose and time dependent manner. CCR1 and CCR2 mRNA expression began to increase from 6 h after a 100 nM 9-CRA treatment and reached a maximal level at 12 h. Surface expression of CCRs was monitored by flow cytometry. CCR1 and CCR2 surface expression increased in 9-CRA-treated THP-1 cells, but not in untreated cells. Calcium mobilization and chemotactic activity were determined to examine the effect of 9-CRA on cell movement. The intracellular Ca2+ concentration and the chemotactic activity increased in 9-CRA-treated cells in response to the CCR1-dependent chemokines Lkn-1, MIP-1α, and RANTES, and the CCR2-specific chemokine MCP-1. Increased surface expression of CCR1 and the Ca2+ influx due to 9-CRA were confirmed in peripheral blood monocytes. Taken together, 9-CRA increases the expression levels of mRNA and protein of both CCR1 and CCR2, and the cell migration ability in THP-1 cells and peripheral blood monocytes, indicating that 9-CRA may regulate inflammatory processes through an increased response to CCR1- and CCR2-dependent chemokines.
AB - 9-cis Retinoic acid (9-CRA) is a lipophilic molecule that binds to the retinoid X receptor (RXR). Although retinoic acid (RA) has been known to regulate neutrophil differentiation, a specific role for 9-CRA in chemokine-mediated cellular processes remains obscure. We investigated the effects of 9-CRA on expression of CC chemokine receptors (CCRs) in human monocytic THP-1 cells and peripheral blood monocytes. RNase protection assay was performed to examine the mRNA levels of CCRs in 9-CRA-treated THP-1 cells. mRNA expression of CCR1 and CCR2 was induced in both a dose and time dependent manner. CCR1 and CCR2 mRNA expression began to increase from 6 h after a 100 nM 9-CRA treatment and reached a maximal level at 12 h. Surface expression of CCRs was monitored by flow cytometry. CCR1 and CCR2 surface expression increased in 9-CRA-treated THP-1 cells, but not in untreated cells. Calcium mobilization and chemotactic activity were determined to examine the effect of 9-CRA on cell movement. The intracellular Ca2+ concentration and the chemotactic activity increased in 9-CRA-treated cells in response to the CCR1-dependent chemokines Lkn-1, MIP-1α, and RANTES, and the CCR2-specific chemokine MCP-1. Increased surface expression of CCR1 and the Ca2+ influx due to 9-CRA were confirmed in peripheral blood monocytes. Taken together, 9-CRA increases the expression levels of mRNA and protein of both CCR1 and CCR2, and the cell migration ability in THP-1 cells and peripheral blood monocytes, indicating that 9-CRA may regulate inflammatory processes through an increased response to CCR1- and CCR2-dependent chemokines.
KW - Chemokine
KW - Chemokine receptor
KW - Chemotaxis
KW - Inflammation
KW - Monocyte
KW - Retinoic acid
UR - http://www.scopus.com/inward/record.url?scp=3242669722&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3242669722&partnerID=8YFLogxK
U2 - 10.1016/j.bcp.2004.03.041
DO - 10.1016/j.bcp.2004.03.041
M3 - Article
VL - 68
SP - 611
EP - 620
JO - Biochemical Pharmacology
JF - Biochemical Pharmacology
SN - 0006-2952
IS - 4
ER -