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Next Article 
Blood, Vol. 94 No. 3 (August 1), 1999:
pp. 837-844
Serial Analysis of Gene Expression in Human Monocytes and Macrophages
By
Shin-ichi Hashimoto,
Takuji Suzuki,
Hong-Yan Dong,
Nobuyuki Yamazaki, and
Kouji Matsushima
From the Department of Molecular Preventive Medicine and CREST,
School of Medicine, The University of Tokyo, Tokyo, Japan.
 |
ABSTRACT |
Monocytes/macrophages serve as sentinels involved in chronic
inflammation and the eradication of various pathogens. To define molecularly the differentiation of blood monocytes into macrophages, we
conducted serial analysis of gene expression (SAGE) in human blood
monocytes/macrophages induced by granulocyte-macrophage colony-stimulating factor (GM-CSF) or M-CSF. SAGE analysis of 57,560, 57,463, and 55,856 tags from monocytes, GM-CSF-, and M-CSF-induced macrophages, respectively, allowed identification of 35,037 different transcripts. Interestingly, the genes with the highest expression during differentiation from monocytes into macrophages were genes involved in lipid metabolism. Both CSF-induced macrophages expressed similar sets of genes except for several genes such as monocyte-derived chemokine (MDC), legumain, prostaglandin D synthetase, and lysosomal sialoglycoprotein. The identification of specific gene expression in
human monocytes, GM-CSF-, or M-CSF-induced macrophages provides novel
methods to define macrophage subsets and the maturation and activation
stage of cells of macrophage lineage and, possibly, to diagnose
diseases in which macrophages play a major role. This study represents
the first extensive serial analysis of gene expression for any type of
human hematopoietic cells.
© 1999 by The American Society of Hematology.
| |
INTRODUCTION |
MONOCYTES AND macrophages originate from
multipotent progenitor cells in bone marrow and play a pivotal role in
host defense to pathogens, wound healing, angiogenesis, and various types of chronic inflammation, eg, granulomatous reaction, fibrosis, and atherosclerosis. Under normal steady-state conditions, monocytes migrate randomly to various organs and body cavities where they differentiate into macrophages.1-3 During inflammation or a
local infection with pathogens, chemotactic cytokines (chemokines), and
various peptide and nonpeptide mediators of inflammation are generated
locally and stimulate monocytes to migrate into the site where they
differentiate into macrophages. Macrophages in various tissues and body
cavities vary in their morphology and function and have been given
different names, eg, Kupffer cells in the liver, pulmonary and alveolar
macrophages in the lung, and microglial cells in the central nervous
system. However, the relationship between blood monocytes and various
tissue macrophages remains unclear.
Monocytes and macrophages have several characteristics in common such
as Fc receptors,  2 integrins, phagocytosis of foreign particles,
and production of proinflammatory cytokines. However, these cells have
never been molecularly defined, and the processes of differentiation
and formation of functional subsets of macrophages are not yet understood.
Here we have applied the recently developed serial analysis of gene
expression (SAGE) method to allow quantitative analysis of a large
number of transcripts in human monocytes and macrophages. SAGE has been
shown to provide a means for the quantitative cataloging and comparison
of expressed genes in various physiological, developmental, and
pathological states.4-7 The SAGE technology is based on the following principles: (1) short sequence tags (9 to 11 bp) are generated from the mRNA population of interest; (2) these tags, derived
from a defined location in a transcript, contain sufficient information
to positively identify a transcript; (3) many transcript tags can be
linked together to form long serial molecules and the multiple tags can
be sequenced simultaneously. The expression pattern of any population
of transcripts can be quantitatively evaluated by determining the
abundance of individual tags and identifying the gene corresponding to
each tag.
SAGE libraries were generated from highly purified human blood
monocytes, monocyte-derived macrophages differentiated by
granulocyte-macrophage colony-stimulating factor (GM-CSF) and
monocyte-derived macrophages differentiated by M-CSF. It has been well
established that GM-CSF and M-CSF independently induce the
proliferation and differentiation of monocytes into distinct subsets of
macrophages with different morphology and function,8-11
providing a model of macrophage heterogeneity in different tissue microenvironments.
| |
MATERIALS AND METHODS |
Preparation of cells.
Peripheral blood mononuclear cells (PBMC) were isolated from venous
blood drawn from normal healthy volunteers in Tokyo Metropolitan Red
Cross Blood Center. Briefly, PBMC were isolated by centrifugation on a
Ficoll-Metrizoate density gradient (density [d] 1.077, Lymphoprep; Nycomed, Oslo, Norway) and suspended in RPMI 1640 medium
containing 7.5% FCS (heat-inactivated fetal calf serum; GIBCO,
Gaithersburg, MD), 100 µg/mL streptomycin, and 100 U/mL penicillin.
This medium contained less than 3 pg of lipopolysaccharide (LPS) per mL
as assessed by a Limulus amebocyte lysate test. PBMC were incubated with anti-CD14 monoclonal antibody (MoAb) coated with microbeads, and
monocytes were isolated by passing the PBMC through a magnetic cell
separation system (MACS; Miltenyi Biotec, Bergish Gladbach, Germany)
with a type VR column. These cell suspensions were then aliquoted into plastic tissue culture plates and incubated for 30 minutes at 37°C, 5% CO2 to obtain the highly purified
cells. More than 99% of the cells were judged to be monocytes by
morphology, positive staining for CD14 (LeuM3; Becton Dickinson, San
Jose, CA) in a flow cytometric analysis and nonspecific esterase staining.
SAGE protocol.
mRNAs of monocytes and macrophages were purified from a mixture of
total RNA from at least six donors. Monocytes were incubated with M-CSF
(100 ng/mL; Morinaga Milk Industry Co, Ltd, Tokyo, Japan) or GM-CSF
(500 U/mL; Kirin Brewery Co, Ltd, Tokyo, Japan) in RPMI 1640 containing
7.5% FCS in 5% CO2 at 37°C for 7 days. Total RNA from
these cells was isolated by direct lysis in RNAzol B (TEL-TEST, Inc,
Friendswood, TX). Poly(A)+ RNA were isolated using the FastTrac mRNA
purification kit (Invitrogen, San Diego, CA) according to the
manufacturer's instructions. A schematic diagram of the SAGE
technique4-7 (by Vogelstein et al) is accessible on SAGE
Home Page via the Internet (http://www.sagenet.org/). SAGE libraries
were generated using 2.5 µg poly(A)+ RNA and were converted to cDNA
with a BRL synthesis kit (GIBCO-BRL, Gaithersburg, MD) following the
manufacturer's protocol, with the inclusion of primer
biotin-5'-T18-3'. The cDNA was cleaved with the restriction enzyme NlaIII, and the 3'-terminal cDNA fragments were
bound to streptavidin-coated magnetic beads (Dynal, Oslo, Norway).
After capture of 3' cDNA fragments, the bound cDNA was divided
into two pools, and one of the following linkers containing recognition sites for BsmF1 was ligated to each pool: linker 1, 5'-TTTGGATTTGCTGGTGCAGTACAACTAGGCTTAATAGGGACATG-3', 5'-TCCCTATTAAGCCTAGTTGTACTGCACCAGCAAATCC[Amino mod.
C7]-3', linker 2, 5'-TTTCTGCTCGAATTCAAGCTTCTAACGATGTACGGGGACATG-3',
5'-TCCCCGTACATCGTTAGAAGCTTGAATTCGAGCAG[amino mod. C7]. Because
BsmF1 cleaves 14 bp away from its recognition site and the
NlaIII site overlaps the BsmF1 site by 1 bp, a 15-bp SAGE tag was released with BsmF1. SAGE tag overhangs were
filled in with Klenow, and tags from the two pools were combined and ligated to each other. The ligation product was diluted and then amplified with polymerase chain reaction (PCR) for 26 cycles with 5'-GGATTTGCTGGTGCAGTACA-3' and
5'-CTGCTCGAATTCAAGCTTCT-3' as primers. The PCR product
was analyzed by polyacrylamide gel electrophoresis (PAGE), and the PCR
product containing two tags ligated tail to tail (ditag) was excised.
The PCR product was then cleaved with NlaIII, and the band
containing the ditags was excised and self-ligated. After ligation, the
concatenated products were separated by PAGE and products between 400 bp and 900 bp were excised. These products were cloned into the
SphI site of pZero-1 (Invitrogen). Colonies were screened for
inserts by PCR, with M13 forward and M13 reverse sequences located
outside the cloning site as primers. PCR products containing
inserts of greater than 400 bp were sequenced with the TaqFS
Dyeterminater kit and analyzed using a 96 lanes-377 ABI
automated sequencer (Perkin-Elmer, Branchburg, NJ).
SAGE was performed on mRNA from human monocytes, GM-CSF-, and
M-CSF-induced macrophages. Sequence files were analyzed by means of
the SAGE program group and DNAsis softwear (Takara, Osaka, Japan).
After correcting for sequencing mistakes, a total of 170,879 tags
representing 57,560, 57,463, and 55,856 from human monocytes, GM-CSF-,
and M-CSF-induced macrophages, respectively, were analyzed.
Reverse transcriptase (RT)-PCR.
Total RNA (200 ng) was prepared by use of RNAzol B. The RNA was
reverse-transcribed in 50 µL of 10 mmol/L Tris-HCl (pH 8.3), 6.5 mmol/L MgCl2, 50 mmol/L KCl, 10 mmol/L dithiothreitol, 1 mmol/L of each dNTP, 2 µmol/L random hexamer, and 2.4 U/µL of Moloney murine leukemia virus reverse transcriptase for 1 hour at 42°C. Complementary DNA (cDNA), corresponding to 40 ng of
total RNA, was boiled for 3 minutes and quenched on ice before
amplification by PCR. The conditions for PCR were as follows: in a
50-µL reaction, 15 µmol/L of each primer, 125 µmol/L each of
deoxyguanosine triphosphate (dGTP), deoxyadenosine triphosphate (dATP),
deoxycytidine triphosphate (dCTP), and deoxythymidine
triphosphate (dTTP) (Toyobo, Osaka, Japan), 50 mmol/L KCl, 10 mmol/L
Tris-HCl, pH 8.3, 1.5 mmol/L MgCl2, and AmplyTaq
(Perkin-Elmer). Primers used were as follows. Legumain: sense
5'-CAGTGATCGTGGCAGGTTCA-3', antisense
5'-TTGCCGGATCCTATACCCTTC-3', GOS2: sense
5'-AAGATGGTGAAGCTGTACGTGC-3', antisense
5'-TGGATGCTTGTGGTAGGTCAGT-3', Thymosin beta 10: sense
5'-TGGCAGACAAACCAGACATGG-3', antisense 5'-ATTTGGCAGTCCGATTGGG-3', GA733-1: sense
5'-AACAACAGGAAACCTGACTGGG-3', antisense
5'-CAGTAAGGGCAAGCTGAGGAAT-3', MDC: sense
5'-ACCGGATCAGTTCAGAAACCA-3', antisense
5'-ACTTCTTTGCCGTCCCCTTT-3'. Reaction mixtures were
incubated in a Perkin-Elmer DNA Thermal cycler for 30 cycles
(denaturation for 60 seconds at 94°C, annealing for 60 seconds at
58°C, extension for 120 seconds at 72°C).
Statistical analysis.
Statistical significance between samples was calculated as described
previously.12
| |
RESULTS |
The morphology of freshly isolated GM-CSF- and M-CSF-induced
macrophages.
Figure 1 shows the morphology of GM-CSF-
and M-CSF-induced macrophages. GM-CSF-induced macrophages were round,
whereas M-CSF-induced macrophages were spindle-like. The distinct
morphology of these cells has been described
elsewhere.13,14
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| Fig 1.
Photographs of normal human blood monocytes, GM-CSF- and
M-CSF-induced macrophages. Monocytes were cultured in RPMI 1640 medium
plus 7.5% FCS in the presence of (A) rhGM-CSF (500 U/mL) or (B)
rhM-CSF (100 ng/mL) for 7 days.
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|
SAGE tag abundance expression in monocytes, GM-CSF-, and
M-CSF-induced macrophages.
A total of 170,879 tags, including 57,560, 57,463, and 55,856 tags from
monocytes, GM-CSF-, and M-CSF-induced macrophages, respectively,
allowed identification of 35,037 different transcripts. Tables 1 and 2
show the top 30 transcripts in monocytes, GM-CSF-, and M-CSF-induced
macrophages. The most expressed genes in human monocytes
were identified as MRP-14, with expression frequency of 1.87%,
followed by ferritin H-chain and elongation factor  subunit (Table
1). In contrast, the most expressed genes in GM-CSF- and
M-CSF-induced macrophages were identified as ferritin L-chain (abundance, 2.69%) and apolipoprotein C-1 (2.21%), respectively. High
expression of many genes encoding cytoskeleton proteins, lipid
metabolism-related proteins, mitochondrial proteins, proteases, and
iron regulation proteins was observed (Table 2).
Comparison of expression patterns in monocytes, GM-CSF- and
M-CSF-induced macrophages.
Comparison of the expressed genes among monocytes, GM-CSF-, and
M-CSF-induced macrophages showed that the expression levels of most of
the transcripts (more than 20,000 transcripts) in these cells were
similar (Fig 2). However, the expression
profiles also showed 354 and 314 transcripts of GM-CSF- and
M-CSF-induced macrophages, respectively, which were different from
those of monocytes (P < .01). Expression levels of 201 of 354 and 157 of 314 genes were decreased in GM-CSF- and M-CSF-induced
macrophages as compared with those in monocytes. Conversely, 153 and
157 transcripts were expressed at higher levels in the GM-CSF- and
M-CSF-induced macrophages, respectively, than in monocytes.
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| Fig 2.
Comparison of gene expression frequency in monocytes,
GM-CSF-, or M-CSF-induced macrophages. A semilogarithmic plot shows
116 and 73 tags that were decreased more than 10 times in GM-CSF- or
M-CSF-induced macrophages, respectively, compared with monocytes,
whereas 118 and 137 tags increased more than 10 times in GM-CSF- or
M-CSF-induced macrophages, respectively, compared with monocytes.
Moreover, 21 tags increased more than 10 times in GM-CSF-induced
macrophages compared with M-CSF-induced macrophages; 34 tags increased
more than 10 times in M-CSF-induced macrophages compared with
GM-CSF-induced macrophages; 57,560, 57,463, and 55,856 tags derived
from monocytes, GM-CSF-, or M-CSF-induced macrophages, respectively,
were used for this analysis. The relative expression of each transcript
was determined by dividing the number of tags observed in monocytes or
both macrophages, as indicated. To avoid division by 0, we used a tag
value of 1 for any tag that was not detectable in one sample. These
ratios are plotted on the abscissa. The number of genes comprising each
ratio is plotted on the ordinate.
|
|
Genes expressed in GM-CSF- versus M-CSF-induced macrophages were more
similar to each other than they were to genes expressed in monocytes.
The 117 transcribed genes of GM-CSF- and M-CSF-induced macrophages
were expressed at significantly different levels (P < .01).
Of the 117 transcribed genes, 57 were expressed at an increased level
in GM-CSF-induced macrophages compared with M-CSF-induced macrophages, and 60 of the 117 transcribed genes were expressed at a
higher level in M-CSF-induced macrophages compared with
GM-CSF-induced macrophages.
Next, differently expressed genes were searched through the
GenBank data base to identify the individual genes.
Table 3 shows the top 30 increased
transcripts in GM-CSF-induced macrophages. Most of the increased
transcripts in GM-CSF-induced macrophages were identical to those in
M-CSF-induced macrophages. For example, tag frequency of hc-gp39 was 0 in monocytes, whereas it increased to 288 and 182 in GM-CSF-induced
macrophages and M-CSF-induced macrophages, respectively. Gene
expression of apolipoprotein C-1 in monocytes also increased from 6 to
1,515 and 1,261 in GM-CSF- and M-CSF-induced macrophages,
respectively. Increase of the expression of several genes identified
here, such as hc-gp39, osteopontin,15 gelsolin,16 apolipoprotein E,17
CD9,18 chitotriosidase,19 and cellular retinoic
acid binding protein20 have been reported previously.
Table 4 shows the top 30 transcripts
decreased in GM-CSF-induced macrophages compared with monocytes. The
decreased transcripts in GM-CSF-induced macrophages also showed a
similar tendency in M-CSF-induced macrophages. The decrease in
expression of MRP-8, MRP-14,21 and ficolin22
genes has been described. The greatest decrease in mRNAs was identified
for complement proteins; ficolin and properdin, DNA-binding protein;
GOS3, GOS2, tristetraprolin,23 and core promoter element
binding protein (CPBP). Furthermore, we investigated the difference in
gene expression between GM-CSF- and M-CSF-induced macrophages
(Table 5). Highly expressed genes in
GM-CSF-induced macrophages, MDC, GA733-1, and osteonectin were not
expressed in M-CSF-induced macrophages. On the other hand, M-CSF-induced macrophages expressed legumain, an asparaginyl
endopeptidase,24 lysosomal sialoglycoprotein at a high
level compared with GM-CSF-induced macrophages.
RT-PCR of genes represented in the SAGE analysis.
Although we obtained blood from a minimum of six healthy volunteers to
find the average in gene expression, there could be differences in the
gene expression between individual donor-derived cells. To address this
question, we arbitrarily selected four differently expressed genes and
evaluated them in three donor-derived samples by RT-PCR
(Fig 3). The expression of each transcript
was compared with SAGE data. GOS2 was highly expressed in monocytes; monocytes 42: GM-M (GM-CSF-induced macrophages) 0:
M-M (M-CSF-induced macrophages) 2, MDC was highly expressed in
GM-M; monocytes 0: GM-M 117: M-M 8, GA733-1 was highly
expressed in GM-M; monocytes 0: GM-M 15: M-M 0, thymosin beta
10 was expressed in all cell types; monocytes 214: GM-M 246: M-M
266, legumain was highly expressed in M-M; monocytes 0: GM-M 2:
M-M 34. These results confirm our SAGE data for monocytes, GM-M,
and M-M and establish the general expression profile of the
identified genes.
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| Fig 3.
RT-PCR analysis of genes expressed differently in
monocytes, M-CSF-, and GM-CSF-induced macrophages. RT-PCR was
performed on total RNA isolated from 1, human monocytes; 2, GM-CSF-induced macrophages; 3, M-CSF-induced macrophages. A, B, and C
indicate different donors.
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| |
DISCUSSION |
Heterogeneity within the mononuclear phagocyte system may be due to the
microenvironment and local differences in the production of growth
factors, such as GM-CSF and M-CSF. It is generally accepted that
alveolar macrophages are derived from peripheral blood monocytes, and
GM-CSF is a pivotal factor for the development of alveolar macrophages
in lung.25 On the other hand, M-CSF also is crucial for
some tissue macrophages because M-CSF-deficient mice have diminished
or absent tissue macrophages in kidney, spleen, liver, and
bone.26 To investigate more precisely the changes in gene expression during differentiation of the monocyte/macrophage lineage, we performed a SAGE in human blood monocytes and macrophages induced by
GM-CSF or M-CSF.
A technology that identifies differentially expressed genes can provide
an important tool for cell biology. Several methods, such as Northern
blotting, RT-PCR, differential display, and subtraction have been
useful in such studies. However, these technologies can analyze only
limited numbers of genes, and quantitative analysis of the
transcription of individual genes is difficult. SAGE allows for both
the quantitative and simultaneous analysis of large numbers of
transcripts (10,000 to 50,000 expressed genes). Thus, we chose to use
SAGE for this purpose. SAGE analysis of 57,560, 57,463, and 55,856 tags
from monocytes, GM-CSF-, and M-CSF-induced macrophages, respectively,
allowed identification of 35,037 different transcripts. Interestingly,
in macrophages, high expression of the genes encoding proteins in lipid
metabolism (such as apolipoprotein E, osteopontin, CD9, sterol
27-hydroxylase,27 and lisosomal acid lipase28) were observed. These results suggest that alteration of lipid metabolism system in mononuclear phagocytes is associated with their
differentiation, and that these changes may contribute to atherosclerosis.
The difference in gene expression between GM-CSF- and M-CSF-induced
macrophages showed that a highly expressed gene in GM-CSF-induced macrophages, MDC, was not expressed in M-CSF-induced macrophages. MDC
is a novel chemokine, which selectively attracts CCR4-positive Th2-type
lymphocytes.29-31 Therefore, GM-CSF-induced macrophages could have a role in Th2 dominated immune diseases. On the other hand,
M-CSF-induced macrophages expressed legumain, an asparaginyl endopeptidase,24 at a high level. However, the significance of selective high expression of legumain in M-CSF-induced macrophages remains to be examined. The hydrolysis of asparaginyl bond is prominent
in the processing of lysosomal hydrolases such as cathepsin B, H, and
D.32 Moreover, macrophages highly express cathepsin D mRNA
(Table 2). Therefore, the high expression of legumain mRNA in
M-CSF-induced macrophages may have a functional role in M-CSF-induced macrophages.
In conclusion, identification of the genes selectively expressed in
human blood monocytes, GM-CSF-, and M-CSF-induced macrophages should
provide useful information in defining the ontogeny, development, and
function of cells in the monocyte and macrophage lineage. Furthermore,
many of the novel genes identified as selectively expressed in
monocytes, GM-CSF-, and M-CSF-induced macrophages should provide
important clues to further studies of macrophage biology and, in
combination with newly developed DNA microarrayer systems, may
eventually be useful for the diagnosis of human diseases or the
monitoring of their treatments.
| |
ACKNOWLEDGMENT |
We are very grateful to Drs V. Velculescu, L. Zhang, W. Zhou, B. Vogelstein, and K. Kinzler for their help in SAGE analysis and also to
Dr C. Vestergaard for reviewing the manuscript.
| |
FOOTNOTES |
Submitted October 29, 1998; accepted February 26, 1999.
The publication costs of this
article were defrayed in part by
page charge payment. This article
must therefore be hereby marked
"advertisement"
in accordance with 18 U.S.C. section
1734 solely to indicate this fact.
Address reprint requests to Kouji Matsushima, MD, PhD, Department of
Molecular Preventive Medicine, School of Medicine, University of Tokyo,
7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan; e-mail:
koujim{at}m.u-tokyo.ac.jp.
| |
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TOP
ABSTRACT
INTRODUCTION