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We have recently isolated a kininogen and another high molecular mass cysteine proteinase inhibitor from the skin of Atlantic salmon [6].. In the tryptic mass map, we also detected pepti

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Purification and characterization of novel kininogens from spotted wolffish and Atlantic cod

Anne Ylo¨nen1, Jari Helin1, Jarl Bøgwald2, Anu Jaakola1, Ari Rinne3and Nisse Kalkkinen1

1

Institute of Biotechnology, Protein Chemistry Laboratory, University of Helsinki, Finland,2Norwegian College of Fishery Science, University of Tromsø, Norway,3Institute of Medical Biology, University of Tromsø, Norway

Kininogens are multifunctional proteins found so far mainly

in mammals They carry vasoactive kinins as well as

parti-cipate in defense, blood coagulation and the acute phase

response In this study, novel kininogens were isolated from

Atlantic cod (Gadus morhua L.) and spotted wolffish

(Anarhichas minor) by papain-affinity chromatography The

molecular mass of cod kininogen determined by

MALDI-TOF mass spectrometry to be 51.0 kDa and it had pI values

of 3.6, 3.9 and 4.4 The molecular mass of wolffish kininogen

was 45.8 kDa and it had pI values of 4.1, 4.3, 4.35 and 4.4

Partial amino-acid sequences determined from both

kinin-ogens showed clear homology with previously determined kininogen sequences Both kininogens were found to inhibit cysteine proteinases like papain and ficin but they had no effect on trypsin, a serine proteinase Wolffish kininogen carried a2,3-sialylated biantennary and triantennary N-gly-cans with extensive sialic acid O-acetylation Cod kininogen carried similar glycan structures but about 1/3 of its glycans carried sulfate at their N-acetylglucosamine units

Keywords: Atlantic cod; spotted wolffish; kininogen; N-gly-cosylation; O-acetylation

Kininogens are large molecular mass (50–114 kDa) cysteine

proteinase inhibitors belonging to class 3 of the cystatin

superfamily They are single-chain proteins composed of an

N-terminal heavy chain, the bradykinin moiety and a

C-terminal light chain The heavy chain and light chain are

interlinked by disulfide bridges Kininogens are further

classified into high molecular mass and low molecular mass

kininogens bearing identical heavy chains but the length and

the amino-acid sequence of the light chain varies A

vasoactive peptide, bradykinin, is released from kininogens

by kallikreins [1]

In addition to carrying bradykinin, kininogens have

many other biological functions They participate in

intrin-sic blood coagulation and in acute phase reactions as well as

inhibit cysteine proteinases [2]

Kininogens have been characterized from many

mam-mals including human, bovine, rat [1], and recently whale

[3] In addition, there are reports on bradykinins in fish

including steelhead trout [4] and Atlantic cod [5] We have

recently isolated a kininogen and another high molecular

mass cysteine proteinase inhibitor from the skin of Atlantic

salmon [6] To our knowledge, no other kininogen from fish

has been described so far

Here, we describe the purification of kininogens from the

skin of spotted wolffish (Anarhichas minor) and A tlantic

cod (Gadus morhua L.) These novel kininogens were

characterized by determining their molecular mases, partial amino-acid sequences, glycan structures, isoelectric points,

as well as their inhibitory activities

M A T E R I A L S A N D M E T H O D S

Fish skin samples The starting material for the purifications were the skin of spotted wolffish (Anarhichas minor) and Atlantic cod (Gadus morhua L.) weighing 2–3 kg The skin (1 kg) was homo-genized in 1 L of 10 mMTris/HCl pH 7.4, 10 mMEDTA, 0.25M sucrose, 0.1 mM phenylmethanesulfonyl fluoride,

5 mM benzamidine and 15 mM sodium azide The homo-genate was centrifuged at 6000 g for 30 min at 4C, and the supernatant was collected To further clarify the superna-tant, it was ultracentrifuged at 100 000 g for 2 h at 4C The clear extract was collected underneath the floating fat Purification and characterization of inhibitors

The inhibitors from skin extracts were purified as described [6] After ultracentrifugation the clarified skin extract was subjected to papain-affinity chromatography, gel filtration, anion-exchange chromatography and reversed-phase chro-matography

Mass spectrometry Matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry was performed on a BiflexTM time-of-flight instrument (Bruker Daltonik, Bremen, Germany) equipped with a nitrogen laser operating

at 337 nm Proteins were analysed in sinapic acid (Fluka Chemie AG, Buchs, Switzerland), as described previously [6] Glycans were analysed using 2,4,6-trihydroxyacetophe-none (Fluka) or 2,5-dihydroxybenzoic acid (Aldrich,

Correspondence to A Ylo¨nen, Protein Chemistry Laboratory,

Institute of Biotechnology, PO Box 56 (Viikinkaari 9), FIN-00014

University of Helsinki, Finland.

Fax: + 358 9191 59416, Tel.: + 358 9191 59414,

E-mail: anne.ylonen@helsinki.fi

Enzymes: papain (EC 3.4.22.2); ficin (EC 3.4.22.3); trypsin

(EC 3.4.21.4); glutamyl endopeptidase GluC (EC 3.4.21.19).

(Received 5 December 2001, revised 2 April 2002, accepted

10 April 2002)

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Steinheim, Germany) as the matrix as described previously

[7] Peptides were analysed using

a-cyano-4-hydroxycin-namic acid matrix (Aldrich) as described previously [7]

Capillary isoelectric focusing

Capillary isoelectric focusing was performed by using a

BioFocus 3000 Capillary Electrophoresis System

(Bio-Rad, Richmond, CA, USA) Focusing was performed in

Bio-Lyte Ampholyte (pH 3–10, Bio-Rad), in an eCAP

neutral capillary (50 lm· 50 cm, Beckman Instruments,

Fullerton, CA, USA) according to the manufacturer’s

instructions BioMark CIEF markers (pI values 5.3, 6.4,

7.4, 8.4 and 10.4, Bio-Rad) were used for internal

calibra-tion

SDS/PAGE and electroblotting

The proteins were separated by SDS/PAGE in a 12%

polyacrylamide (w/v) gel [8] and stained with silver [9] For

N-terminal sequencing, the SDS/PAGE separated proteins

were subjected to electroblotting on a poly(vinylidene

difluoride) membrane (ProBlott, PerkinElmer, Applied

Biosystems, CA, USA) in 10 mM

3-(cyclohexylamino)pro-pane-1-sulfonic acid (pH 11)/10% (v/v) methanol with a

constant potential of 50 V for 120 min [10] After staining

with Coomassie Brilliant Blue (0.1% in 1% acetic acid/40%

methanol) and destaining (50% methanol) the protein

bands were cut out and loaded on the sequencer

Alkylation, enzymatic digestion and peptide separation

For in-gel digestion, the proteins were separated by SDS/

PAGE and stained with Coomassie Brilliant Blue (0.1% in

0.5% acetic acid/30% methanol) and destained (30%

methanol) The excised protein bands were alkylated with

iodoacetamide and digested with trypsin as described

previously [11] For in-solution digestion, the purified

proteins from reversed-phase chromatography were

alkyl-ated with 4-vinylpyridine and enzymatically digested with

trypsin [6] or endoproteinase GluC For endoproteinase,

GluC digestion a 30-lg sample of alkylated protein was

dissolved in 50 lL of 50 mM ammonium acetate, pH 4.3

and digested with 0.5 lg of endoproteinase GluC by

incubation at 37C overnight Generated peptides were

separated by reversed-phase chromatography

Sequence analysis

Protein N-terminal sequencing and internal peptide

sequen-cing were performed with a Procise 494Asequencer

(PerkinElmer Applied Biosystems Division)

Inhibition assay

After each chromatographic step the inhibitory activity of

collected fractions was determined using papain as the

enzyme in the assay [6] The same assay was used to

determine inhibitory activites of purified proteins against

papain, ficin and trypsin with BANA (Na-benzoyl-DL

-arginine-2-naphtylamide, Fluka Chemie AG) as a substrate

Positive controls were leupeptin for papain and ficin and

phenylmethanesulfonylfluoride for trypsin

Glycan isolation Samples ( 30 lg) of wolffish kininogen and cod kininogen were subjected to enzymatic N-glycan removal with N-glycosidase F The dry protein sample was dissolved in

100 lL of 20 mM sodium phosphate buffer containing 0.1% SDS and 1% b-octylglucoside, and 2 U of N-glycosidase-F (Roche Biochemicals, Switzerland) were added After 48 h incubation at 37C, the reaction mixture was diluted with 4 vol of water, and the de-N-glycosylated protein was adsorbed to poly(vinylidene difluoride) mem-brane by centrifugation in a ProSpinTMsample preparation cartridge (PerkinElmer Applied Biosystems Division) The N-glycans were collected from the poly(vinylidene difluo-ride) flow-through, and were further purified by passing through a BondElut C18 extraction cartridge (Varian SPP, Harbor City, CA, USA) and by gel filtration chromato-graphy as described previously [12] No separation of the individual N-glycan components was attempted prior to mass spectrometric analyses

The poly(vinylidene difluoride) membrane carrying the de-N-glycosylated protein was subjected to b-elimination to liberate potential O-glycosidically linked glycans The membrane was incubated in 150 lL of 1M NaBH4 in 0.1MNaOH for 48 h at 37C, and the liberated oligosac-charide alditols were recovered as described previously [12] O-Glycan fractions were subjected to permethylation [13] prior to MALDI-TOF MS analysis

Removal of O-acetyl groups The isolated N-glycans were saponified as described previ-ously [14]

Glycosidase digestions Digestions with Newcastle disease virus (NDV) neuramini-dase and Streptococcus pneumoniae b1,4-galactosineuramini-dase (Oxford Glycosciences, Abingdon, UK) were carried out

as described previously [14] Digestion with jack bean b-galactosidase (Glyko, Novato, CA, USA) was carried out

in 10 lL of 100 mMsodium citrate, pH 4.5, at 37C An aliquot of 1.5 lL was removed after 16 h of digestion, drop-dialysed against water and analysed by MALDI-TOF MS Phosphatase treatment

Dry N-glycan samples were dissolved in 50 mMammonium bicarbonate, and 1 U of calf intestinal alkaline phosphatase (New England Biolabs, Beverly, MA, USA) was added Synthetic phosphorylated peptides were used as positive controls After a 2-h incubation at 37C the solution was passed through a POROS R3 (PerSeptive Biosystems, Framingham MA, USA) tip, and a sample of the flow-through carrying the glycans was drop-dialysed and analysed by MALDI-TOF MS

R E S U L T S

Isolation of cysteine proteinase inhibitors The first step in cysteine proteinase inhibitor isolation from the cod skin extract was affinity chromatography on

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immobilized papain Cysteine proteinase inhibitors bound

into papain matrix were eluted and the fractions showing

over 70% inhibitory activity in the inhibition assay were

pooled, concentrated and further purified by gel filtration

The fractions from gel filtration exhibiting inhibitory

activity were subjected to anion-exchange chromatography,

yielding a single major protein peak expressing inhibitory

activity This fraction was further subjected to

reversed-phase chromatography and the protein obtained was

analysed by SDS/PAGE and MALDI-TOF spectrometry

(Fig 1) In SDS/PAGE, the inhibitor from cod skin

migrated at a position corresponding to 78 kDa, whereas

MALDI-TOF mass spectrometry gave a molecular mass of

51.0 kDa Apparently, the glycans on this inhibitor result in

the slower migration in SDS/PAGE than expected Some

purified cod inhibitor samples carried also a very faint

60-kDa band as analysed by SDS/PAGE The relationship

between the major 78 kDa and minor 60 kDa gel bands

were investigated by in-gel digestion and peptide mass

fingerprinting All peptide signals present in the

MALDI-TOF mass maps from the 60 kDa band were also present in

the mass map from the 78-kDa band, suggesting that the

60-kDa band represents a fragment of the 78-kDa band

Similar related forms were detected also in salmon

kinino-gen [6]

In the tryptic mass map, we also detected peptide masses

which were tentatively identified as fish bradykinin (m/z

1065.59) peptide as well as fish Arg-bradykinin (m/z

1221.72), previously detected also from salmon kininogen

tryptic digest These results were verified by peptide

(Table 1)] Accordingly, this cysteine proteinase inhibitor

was named cod kininogen Several isoelectric forms (pI

values 3.6, 3.9 and 4.4) of this kininogen were detected by

capillary isoelectric focusing, which may be partly ascribed

to heterogeneous glycosylation The yield of reversed-phase

purified cod kininogen from 200 mL of cod skin extract was

 800 lg

Acysteine proteinase inhibitor was isolated from wolffish skin extract as above The wolffish inhibitor purified by reversed-phase chromatography still exhibited two bands in SDS/PAGE, 67 and 42 kDa (Fig 1) In MALDI-TOF MS, this fraction only shows one clear signal at 45.8 kDa (Fig 1), probably representing the 67-kDa band that stains poorly in gels Similar behaviour was observed for salmon kininogen [6], and it is possible that the poor staining may be partly the result of extensive glycosylation Both bands of the wolffish inhibitor were investigated by in-gel digestion and mass mapping As above, the peptide patterns obtained were similar, and both included signals appropriate for the fish bradykinin and Arg-bradykinin sequences Peptide sequencing verified these observations and therefore the cysteine proteinase inhibitor of wolffish skin was named wolffish kininogen Several forms of the protein with different isoelectric points were again observed (pI values 4.1, 4.3, 4.35, 4.4) The yield of reversed phase purified wolffish kininogen was  850 lg from 200 mL of skin extract

We have previously isolated two high molecular mass cysteine proteinase inhibitors from the skin of Atlantic salmon, a kininogen and a 42-kDa protein named salarin [6] An identical experimental approach was used in the present study, but interestingly no salarin type inhibitor was detected in the skin of wolffish or cod

Inhibition studies The inhibitory activity of cod and wolffish kininogen was measured with samples purified by reversed phase chroma-tography Both kininogens were found to inhibit papain and ficin (cysteine proteinases) but neither of them had any effect on trypsin (a serine proteinase) Their specific activities against papain were calculated from inhibition curves (Fig 2) and were found to be 940 UÆmg)1for cod kininogen and 6200 UÆmg)1for wolffish kininogen (units are defined

Fig 1 SDS/PAGE visualized by silver staining of purified cod kininogen and wolf fish kininogen, and MALDI-TOF mass spectra of kininogens purified by reversed-phase chramotography.

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as lg of papain inhibited per mg of inhibitor, data not

shown) The inhibitory activity of cod kininogen and

wolffish kininogen has also been investigated with different

cathepsins isolated from cod, wolffish and salmon

(E Weber, Institute of Physiological Chemistry,

Martin-Luther-University, Halle-Wittenberg, Germany, personal

communication) These experiments suggest that these

kininogens inhibit specifically cathepsin L but not cathepsin

B or cathepsin H

Determination of partial amino-acid sequences N-Terminal sequencing of the kininogens was only success-ful from the 42-kDa band of wolffish kininogen (XLVQPGVLI…, Table 1) The major bands of both kininogens and also the 60-kDa band of cod kininogen were found to be N-terminally blocked Peptides were generated from both kininogens by digesting the alkylated proteins with trypsin or endoproteinase GluC The peptides were separated by reversed phase chromatography and selected peptides were subjected to sequence analysis Afew overlapping sequences from trypsin and endoproteinase GluC digested peptides were obtained and the results from sequencing are shown in Tables 1 Both cod and wolffish kininogens carried the fish bradykinin peptide RPPGWSPLR that we have previously shown to be present

in Atlantic salmon kininogen [6] The fish bradykinin peptide has also been found previously from enzyme-treated plasma of Atlantic cod [5] and steelhead trout [4] Most of the determined peptide sequences could be aligned with the heavy chain of human kininogen (Fig 3), verifying the identity of these novel kininogens The highly conserved cystatin sequence QVVAG was also found among the cod sequences The complete primary structures of cod kinino-gen and wolffish kininokinino-gen will be revealed by molecular cloning, which also enables more detailed homology and phylogenetic comparisons

Glycosylation studies The difference between the apparent Mrin SDS/PAGE and that analysed by MALDI-TOF MS implied that both kininogens are glycosylated To release potential N-glycans

Fig 2 Inhibition of papain (0.625 mg) by different amounts of cod

kininogen and wolffish kininogen.

Table 1 Peptide sequences determined from cod kininogen (A) and wolffish kininogen (B) X ¼ amino acid not detected N ¼ glycosylated asparagine according to Edman degradation and mass spectrometry.

A

4 R R P P G W S P L Ra,b

7 Q V V A G L Ra

B

10 F N E R L S T G H Ka

11 F P L S V S I S K a

a Peptide aligned with human kininogen b Contains fish bradykinin sequence c N-Terminus of fragment d Glycopeptide.

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for structural characterization, samples of the kininogens

were subjected to N-glycan liberation by N-glycosidase F

The released glycans were isolated by gel filtration and

N-glycan pools were analysed by MALDI-TOF MS The

spectrum of cod kininogen N-glycans is shown in Fig 4A,

revealing an extremely heterogeneous pattern Two major

clusters of ions are observed, and within both clusters

adducts of +42 or +80 Da can be revealed We have

recently identified from salmon kininogen N-glycans very

high levels of sialic acid O-acetylation [14], and it is probable

that the +42 Da adducts in the cod kininogen N-glycans

represent this modification as well This is supported by the

higher number of acetyl (Ac) groups in those glycans that

carry more sialic acid residues The +80 Da adduct could

be either phosphorylation or sulfation As will be described

below, the ions carrying the +80 Da adduct were stable

against alkaline phosphatase treatment, establishing the

presence of sulfate (SO3) groups The assignments are

therefore as follows (all [M-H]– ions): m/z 1932.3 and

1973.6, monosialylated biantennary glycans with 0 and 1

acetyl groups, respectively The signal at m/z 2012.8 is

assigned as a monosialylated biantennary glycan with one

sulfate (SO3), while the ion at m/z 2053.5 carries one acetyl

and one sulfate group Disialylated biantennary glycans are

found at m/z 2222.8, 2264.8 (+1 Ac), 2306.8 (+2 Ac),

2344.9 (+1 Ac, +1 SO3), and 2387.2 (+2 Ac, +1 SO3)

Disialylated triantennary species are found at m/z 2588.5,

2630.4 (+1 Ac), 2672.2 (+ 2 Ac), 2710.8 (+ 1 Ac, +1

SO3), 2752.9 (+ 2 Ac, +1 SO3), and finally, trisialylated

biantennary glycans at m/z 2879.3, 2921.4 (+1 Ac), 2963.4

(+2 Ac), 3005.4 (+3 Ac), 3044.1 (+2 Ac, +1 SO3) and

3086.1 (+3 Ac, +1 SO3)

Short alkaline hydrolysis (saponification) of the

N-glycans yielded glycans devoid of additional acetyl

groups, an indication that these were O-acetyl substituents

[15] The MALDI-TOF spectrum of the de-O-acetylated

glycans reveals the sulfated species very clearly at m/z 2302.8

and m/z 2960.0, representing the monosulfated disialylated

biantennary and trisialylated triantennary species,

respect-ively (Fig 4B) Sulfated species are observed also for the monosialylated biantennary and disialylated triantennary species, at m/z 2012.2 and m/z 2667.6, respectively

To obtain additional data on the glycan structures alkaline phosphatase and exoglycosidase digestions were performed for the de-O-acetylated species First, the desial-ylated glycans were treated with alkaline phosphatase No removal of the +80 Da adducts could be observed under conditions where full dephosphorylation of both phosphor-ylated glycans and peptides is consistently obtained, thus verifying the adduct’s nature as sulfation (not shown) The glycans were then subjected to Newcastle disease virus (NDV) sialidase treatment, which liberates a2,3-linked but not a2,6-linked sialic acids, and practically complete desialylation was observed (Fig 4C) The small signal at m/

z2394.0 may represent desialylated tetraantennary glycans The sulfate group remained in the oligosaccharide part, although at a reduced intensity It should be noted that the sulfated glycans are now observed as +102 Da adducts, exhibiting [M-H + 2Na]+ions The reduced signal of the sulfated species is probably due to fragmentation in the MALDI-TOF MS analysis, where partial sulfate loss (but not loss of phosphate) is in our experience invariably observed in the positive ion reflector mode The more gentle negative ion mode cannot be used here, as neutral carbo-hydrates do not ionize in the negative ion mode

The desialylated glycans were further subjected to digestion with S pneumoniae b-galactosidase Under the conditions used, this enzyme liberates b1,4-linked galactose units only The MALDI-TOF spectrum of the digested glycans shows a complete removal of galactose units from the nonsulfated biantennary (m/z 1663.7 to m/z 1339.5) and triantennary (m/z 2028.9 to m/z 1542.7) species (Fig 4D) One galactose unit in the sulfated glycans was resistant to the enzyme, as revealed by the signals at m/z 1603.6 (biantennary) and m/z 1806.8 (triantennary) This is as expected, as S pneumoniae b-galactosidase is not able to hydrolyze galactose from Galb1–4GlcNAc-R type struc-tures where either Gal or GlcNA c is sulfated [16] However,

Fig 3 Alignment of peptides from cod

kininogen (COD KIN) and wolf fish kininogen

(WF KIN) with heavy chain of human

kininogen (KNH-HUM, P01042) sequence.

Identical amino acids are shaded.

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b-galactosidase from jack beans is inhibited by sulfate on

the Gal unit only, and as shown in Fig 4E, even the last

galactose unit is removed by the latter enzyme (m/z 1603.6

to m/z 1441.4 and m/z 1806.8 to m/z 1644.5) This indicates

that the sulfate is linked to the GlcNAc residue

Altogether, the cod kininogen carries biantennary and

triantennary N-glycans that are terminated by a2,3-linked

sialic acids, a high number of which are O-acetylated About

1/3 of the glycans carry sulfate at N-acetylglucosamine units

of their Neu5Aca2,3Galb1,4GlcNAc antennae

The isolated N-glycans of the wolffish kininogen exhib-ited a complicated pattern in MALDI-TOF MS (Fig 4F), with two major clusters of ions Adducts of +42 Da are again evident in the spectrum, implying extensive O-acetylation of sialic acids The signals were tentatively identified as follows (all [M-H]– ions): monosialylated biantennary glycans, m/z 1932.2 and 1974.3 (+1 Ac) Disialylated biantennary, m/z 2223.1, 2265.1 (+1 Ac), 2307.0 (+2 Ac), 2349.3 (+3 Ac) and 2391.2 (+4 Ac) Disialylated triantennary, m/z 2588.7, 2630.5 (+1 Ac),

Fig 4 MALDI-TOF spectra of kininogen N-glycans (A) Intact cod kininogen N-glycans, and the cod kininogen N-glycans after successive incubations (B) in 0.1 M NaOH (saponification) (C) with NDV sialidase (D) with S pneumoniae b-galactosidase and (E) jack bean b-galactosidase (F) Intact wolffish N-glycans, and after successive incubations (G) in 0.1 M NaOH (H) with NDV sialidase and (I) with S pneumoniae b-galactosidase.The proposed glycan structures are shown: j, GlcNA c; s, mannose; h, galactose; r, N-acetylneuraminic acid; circled S, sulfate The spectra shown in A, B, F and G were recorded in linear negative ion mode, signals are [M-H]–ions, and average mass values are shown The spectra of C, D, E, H, and I were obtained in reflector positive ion mode, signals are [M + Na] + ions with monoisotopic mass values.

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2673.1 (+2 Ac), 2714.8 (+3 Ac) Finally, trisialylated

triantennary, m/z 2879.8, 2921.5 (+1 Ac), 2963.8 (+2 Ac),

3005.6 (+3 Ac), 3047.7 (+4 Ac), 3089.7 (+5 Ac), 3131.3

(+6 Ac), 3173.7 (+7 Ac) No signals corresponding to

sulfated glycans were observed in these N-glycans

The MALDI-TOF spectrum of the saponified wolffish

N-glycans was much simpler, exhibiting signals assignable

to sialylated biantennary and triantennary glycans

(Fig 4G) Treatment of the de-O-acetylated glycans with

NDV sialidase resulted in complete removal of the sialic

acid residues (Fig 4H), indicating that the sialic acids were

a2,3-linked Digestion of the desialylated glycans with

S pneumoniaeb-galactosidase abolished all terminal

galac-tose residues (Fig 4I), showing that these were b1,4-linked

To summarize, wolffish kininogen carried a2,3-sialylated

biantennary and triantennary N-glycans, with extensive

sialic acid O-acetylation

Also O-glycosidic glycans were recovered from wolffish

kininogen The permethylated O-glycan pool was analysed

by MALDI-TOF MS, and the spectrum revealed one major

[M + Na]+signal at m/z 1256.63 (not shown) The mass is

appropriate for the composition (Neu5Ac)2(Hex)1

-(HexNAc-ol)1, suggesting that wolffish kininogen carries

disialylated core type-1 O-glycans similar to those

previ-ously identified from salmon kininogen [14]

The exact natures of the O-acetylated and sulfated

residues is beyond the scope of the present study

Prelim-inary LC-MS/MS analysis of wolffish kininogen sialic

acids as 1,2-diamino-4,5-methylenedioxybenzene derivatives

revealed 7-, 8-, and 9-O-acetylation, but no 4-O-acetylation

of Neu5Ac This suggests a similar type of O-acetylation as

that recently found in Atlantic salmon glycoproteins [14]

D I S C U S S I O N

The present study describes the identification of two novel

kininogens from Atlantic cod (Gadus morhua L.) and

spotted wolffish (Anarhichas minor) The characteristic

bradykinin sequence RPPGWSPLR was demonstrated in

both cod and wolffish kininogens In addition, the highly

conserved cystatin peptide QVVAG, which is found in

domains 2 and 3 for mammalian kininogens [1], was present

in cod kininogen We have previously characterized a

kininogen from Atlantic salmon (Salmo salar L.) as well [6]

In both of these studies, we have used a method that catches

large molecular cysteine proteinase inhibitors with

papain-affinity chromatography

Kininogens have many biochemically defined properties;

they are substrates for kallikreins and release vasoactive

peptide bradykinin Furthermore, they act like cystatins

inhibiting cysteine proteinases Cod and wolffish kininogens

and previously isolated salmon kininogen all possess these

properties Kininogen seems to be very conserved both in

structure and its effects

We recently characterized the glycosylation of kininogen

isolated from Atlantic salmon (Salmo salar L.), which was

shown to carry extensively O-acetylated sialic acids as

terminal elements on biantennary N-glycans [14] This

structural feature is conserved in the kininogens of cod and

spotted wolffish, as shown in the present study In addition,

sulfated N-acetylglucosamine residues were observed in the

antennae of cod kininogen N-glycans, but not in kininogens

from salmon or spotted wolffish The biological relevance of

O-acetylation or sulfation in the kininogens remains to be established It is known that, in general, sialic acid O-acetylation protects glycans from enzymatic degradation,

as many sialidases are inhibited by this modification [17]

It is noticeable that Atlantic salmon also carried another high molecular mass (42.7 kDa) cysteine proteinase inhib-itor, named salarin [6] The present study shows no evidence for the existence of this type of protein in Atlantic cod or spotted wolffish Recently, we isolated from another salmo-nid species, Arctic charr (Salvelinus alpinus), a 42-kDa papain-inhibiting protein with an N-terminus identical with that of salarin It is therefore possible that salarin type proteins are typical only to salmonids, and the more evolved fish species analysed in the present study have lost this protein in evolution Alternatively, salarin-type proteins may have lost their cysteine proteinase inhibitory activity and thus cannot be isolated by papain affinity chromatography

A C K N O W L E D G E M E N T S

We wish to thank Dr Mikko Ja¨rvinen for critical review of this manuscript The study has been carried out with financial support from the Commission of the European Communities, Agriculture and Fisheries (FAIR) specific RTD programme, CT97-3508, Fish cysteine proteinase inhibitors and infectious diseases It does not necessarily reflect its views and in no way anticipates the Commision’s future policy

in this area This study was also partly supported by a grant from the Academy of Finland (grant no 46692 to J H.).

R E F E R E N C E S

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