Glycosaminoglycan metabolism of HL-60 cells during differentiation induction by tetradecanoylphorbol-13-acetate

Sharon D Luikart; James L. Sackrison

doi:10.1016/0145-2126(86)90053-6

Glycosaminoglycan metabolism of HL-60 cells during differentiation induction by tetradecanoylphorbol-13-acetate

Sharon D Luikart
, James L. Sackrison

Medicine - Veteran's Administration Medical Center

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

5 Scopus citations

Abstract

Many biochemical responses to phorbol ester differentiation inducers have been reported, including alterations in synthesis of specific gene products such as glycoproteins. Stage-specific glycosaminoglycan changes have previously been associated with the differentiation process, including a dramatic reduction in cellular chondroitin 4-sulfate during human myeloid leukemia cell maturation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). We have demonstrated that treatment of HL-60 human promyelocytic leukemia cells with 4-methyl-umbelliferyl-β-d-xyloside increases precursor incorporation into glycosaminoglycans linked to β-d-xyloside, rather than core protein, eliminating the need for core protein and xylosyl-transferase. Therefore, these β-d-xyloside-treated cells were used to study the decreased glycosaminoglycan production during TPA-induced HL-60 differentiation. Exposure of these pretreated HL-60 cells to TPA, which induces macrophage-like maturation, resulted in a 70% reduction of incorporation of [³⁵S]sulfate into cell-associated glycosaminoglycans. Thus, even in HL-60 cells in which glycosaminoglycan production is maximally stimulated by β-d-xyloside, TPA is a strong inhibitor of free glycosaminoglycan chain production, and this biochemical effect is associated with other features of leukocyte maturation.

Original language	English (US)
Pages (from-to)	1083-1090
Number of pages	8
Journal	Leukemia research
Volume	10
Issue number	9
DOIs	https://doi.org/10.1016/0145-2126(86)90053-6
State	Published - 1986

Bibliographical note

Funding Information:
SYN'I'ItESIS of glycosaminoglycans has been correlated with discrete maturational stages of development in several embryonic systems [1-6], as well as in normal [7, 8] and leukemic [9] leukocytes. A dramatic decrease in cellular glycosaminoglycans appears to be associated with the induction of a mature phenotype by TPA or dimethyl sulfoxide in human myeloid leukemia cells [9]. Decreased glycosaminoglycan levels in mature compared to immature myeloid cells concur with the findings of Olsson [10] using freshly isolated peripheral blood leukocytes from leukemia patients and autoradio- * This investigation was supported, in part, by PHS Grant CA-38972. awarded by the National Cancer Institute, DHHS, Grant CH-39973 from the American Cancer Society, a Minnesota Medical Foundation Grant, the Coleman Leukemia Research Fund. and the Masonic Memorial Hospital Fund, Inc. S.D.L. is a Leukemia Society of America Special Fellow and an American Cancer Society Junior Faculty Clinical Fellow (JFCF 782). Abbreviations: TPA. 12-O-terta decanoylphorbol-13-acetate DPM. disintegrations per minute. Correspondence to: Dr. Sharon D. Luikart, Box 325 Mayo Memorial Building. University of Minncsota Hospitals, 420 Dclawarc Strcct S.E., Minncapolis. MN 55455, U.S.A.

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SDG 3 Good Health and Well-being

Keywords

Glycosaminoglycans
HL-60 human promyelocytic leukemia cells
leukemic cell differentiation
phorbol esters
proteoglycans

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10.1016/0145-2126(86)90053-6

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title = "Glycosaminoglycan metabolism of HL-60 cells during differentiation induction by tetradecanoylphorbol-13-acetate",

abstract = "Many biochemical responses to phorbol ester differentiation inducers have been reported, including alterations in synthesis of specific gene products such as glycoproteins. Stage-specific glycosaminoglycan changes have previously been associated with the differentiation process, including a dramatic reduction in cellular chondroitin 4-sulfate during human myeloid leukemia cell maturation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). We have demonstrated that treatment of HL-60 human promyelocytic leukemia cells with 4-methyl-umbelliferyl-β-d-xyloside increases precursor incorporation into glycosaminoglycans linked to β-d-xyloside, rather than core protein, eliminating the need for core protein and xylosyl-transferase. Therefore, these β-d-xyloside-treated cells were used to study the decreased glycosaminoglycan production during TPA-induced HL-60 differentiation. Exposure of these pretreated HL-60 cells to TPA, which induces macrophage-like maturation, resulted in a 70\% reduction of incorporation of [35S]sulfate into cell-associated glycosaminoglycans. Thus, even in HL-60 cells in which glycosaminoglycan production is maximally stimulated by β-d-xyloside, TPA is a strong inhibitor of free glycosaminoglycan chain production, and this biochemical effect is associated with other features of leukocyte maturation.",

keywords = "Glycosaminoglycans, HL-60 human promyelocytic leukemia cells, leukemic cell differentiation, phorbol esters, proteoglycans",

author = "Luikart, \{Sharon D\} and Sackrison, \{James L.\}",

note = "Funding Information: SYN'I'ItESIS of glycosaminoglycans has been correlated with discrete maturational stages of development in several embryonic systems [1-6], as well as in normal [7, 8] and leukemic [9] leukocytes. A dramatic decrease in cellular glycosaminoglycans appears to be associated with the induction of a mature phenotype by TPA or dimethyl sulfoxide in human myeloid leukemia cells [9]. Decreased glycosaminoglycan levels in mature compared to immature myeloid cells concur with the findings of Olsson [10] using freshly isolated peripheral blood leukocytes from leukemia patients and autoradio- * This investigation was supported, in part, by PHS Grant CA-38972. awarded by the National Cancer Institute, DHHS, Grant CH-39973 from the American Cancer Society, a Minnesota Medical Foundation Grant, the Coleman Leukemia Research Fund. and the Masonic Memorial Hospital Fund, Inc. S.D.L. is a Leukemia Society of America Special Fellow and an American Cancer Society Junior Faculty Clinical Fellow (JFCF 782). Abbreviations: TPA. 12-O-terta decanoylphorbol-13-acetate DPM. disintegrations per minute. Correspondence to: Dr. Sharon D. Luikart, Box 325 Mayo Memorial Building. University of Minncsota Hospitals, 420 Dclawarc Strcct S.E., Minncapolis. MN 55455, U.S.A.",

year = "1986",

doi = "10.1016/0145-2126(86)90053-6",

language = "English (US)",

volume = "10",

pages = "1083--1090",

journal = "Leukemia research",

issn = "0145-2126",

publisher = "Elsevier Ltd",

number = "9",

}

TY - JOUR

T1 - Glycosaminoglycan metabolism of HL-60 cells during differentiation induction by tetradecanoylphorbol-13-acetate

AU - Luikart, Sharon D

AU - Sackrison, James L.

N1 - Funding Information: SYN'I'ItESIS of glycosaminoglycans has been correlated with discrete maturational stages of development in several embryonic systems [1-6], as well as in normal [7, 8] and leukemic [9] leukocytes. A dramatic decrease in cellular glycosaminoglycans appears to be associated with the induction of a mature phenotype by TPA or dimethyl sulfoxide in human myeloid leukemia cells [9]. Decreased glycosaminoglycan levels in mature compared to immature myeloid cells concur with the findings of Olsson [10] using freshly isolated peripheral blood leukocytes from leukemia patients and autoradio- * This investigation was supported, in part, by PHS Grant CA-38972. awarded by the National Cancer Institute, DHHS, Grant CH-39973 from the American Cancer Society, a Minnesota Medical Foundation Grant, the Coleman Leukemia Research Fund. and the Masonic Memorial Hospital Fund, Inc. S.D.L. is a Leukemia Society of America Special Fellow and an American Cancer Society Junior Faculty Clinical Fellow (JFCF 782). Abbreviations: TPA. 12-O-terta decanoylphorbol-13-acetate DPM. disintegrations per minute. Correspondence to: Dr. Sharon D. Luikart, Box 325 Mayo Memorial Building. University of Minncsota Hospitals, 420 Dclawarc Strcct S.E., Minncapolis. MN 55455, U.S.A.

PY - 1986

Y1 - 1986

N2 - Many biochemical responses to phorbol ester differentiation inducers have been reported, including alterations in synthesis of specific gene products such as glycoproteins. Stage-specific glycosaminoglycan changes have previously been associated with the differentiation process, including a dramatic reduction in cellular chondroitin 4-sulfate during human myeloid leukemia cell maturation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). We have demonstrated that treatment of HL-60 human promyelocytic leukemia cells with 4-methyl-umbelliferyl-β-d-xyloside increases precursor incorporation into glycosaminoglycans linked to β-d-xyloside, rather than core protein, eliminating the need for core protein and xylosyl-transferase. Therefore, these β-d-xyloside-treated cells were used to study the decreased glycosaminoglycan production during TPA-induced HL-60 differentiation. Exposure of these pretreated HL-60 cells to TPA, which induces macrophage-like maturation, resulted in a 70% reduction of incorporation of [35S]sulfate into cell-associated glycosaminoglycans. Thus, even in HL-60 cells in which glycosaminoglycan production is maximally stimulated by β-d-xyloside, TPA is a strong inhibitor of free glycosaminoglycan chain production, and this biochemical effect is associated with other features of leukocyte maturation.

AB - Many biochemical responses to phorbol ester differentiation inducers have been reported, including alterations in synthesis of specific gene products such as glycoproteins. Stage-specific glycosaminoglycan changes have previously been associated with the differentiation process, including a dramatic reduction in cellular chondroitin 4-sulfate during human myeloid leukemia cell maturation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). We have demonstrated that treatment of HL-60 human promyelocytic leukemia cells with 4-methyl-umbelliferyl-β-d-xyloside increases precursor incorporation into glycosaminoglycans linked to β-d-xyloside, rather than core protein, eliminating the need for core protein and xylosyl-transferase. Therefore, these β-d-xyloside-treated cells were used to study the decreased glycosaminoglycan production during TPA-induced HL-60 differentiation. Exposure of these pretreated HL-60 cells to TPA, which induces macrophage-like maturation, resulted in a 70% reduction of incorporation of [35S]sulfate into cell-associated glycosaminoglycans. Thus, even in HL-60 cells in which glycosaminoglycan production is maximally stimulated by β-d-xyloside, TPA is a strong inhibitor of free glycosaminoglycan chain production, and this biochemical effect is associated with other features of leukocyte maturation.

KW - Glycosaminoglycans

KW - HL-60 human promyelocytic leukemia cells

KW - leukemic cell differentiation

KW - phorbol esters

KW - proteoglycans

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DO - 10.1016/0145-2126(86)90053-6

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AN - SCOPUS:0022922255

SN - 0145-2126

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EP - 1090

JO - Leukemia research

JF - Leukemia research

IS - 9

ER -

Glycosaminoglycan metabolism of HL-60 cells during differentiation induction by tetradecanoylphorbol-13-acetate

Abstract

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