schliessen

Filtern

 

Bibliotheken

Expression of matrix metalloproteinases and their inhibitors during hepatic tissue repair in the rat

Matrix metalloproteinases (MMPs) and their specific inhibitors (TIMPs) are thought to play an essential role in liver injury associated with tissue remodeling. However, their distinct expression profile in different liver repair models still remains to be established. Hepatic expression of collagena... Full description

Journal Title: Histochemistry and cell biology 2000-06, Vol.113 (6), p.443-453
Main Author: Knittel, T
Other Authors: Mehde, M , Grundmann, A , Saile, B , Scharf, J G , Ramadori, G
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Germany: Springer Nature B.V
ID: ISSN: 0948-6143
Link: https://www.ncbi.nlm.nih.gov/pubmed/10933221
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: cdi_pubmed_primary_10933221
title: Expression of matrix metalloproteinases and their inhibitors during hepatic tissue repair in the rat
format: Article
creator:
  • Knittel, T
  • Mehde, M
  • Grundmann, A
  • Saile, B
  • Scharf, J G
  • Ramadori, G
subjects:
  • Acute Disease
  • Animals
  • Blotting, Northern
  • Carbon tetrachloride
  • CCL4 protein
  • Collagen
  • Collagenase
  • Collagenase 3
  • Collagenases - analysis
  • Collagenases - genetics
  • Fibrinolysis
  • Fibrosis
  • Gelatinase A
  • Gene Expression Regulation, Enzymologic - physiology
  • Hepatectomy
  • Hepatitis, Animal - metabolism
  • Immunohistochemistry
  • Inflammation
  • Interstitial collagenase
  • Liver
  • Liver - enzymology
  • Liver - surgery
  • Liver Cirrhosis - metabolism
  • Liver Regeneration - physiology
  • Matrix metalloproteinase
  • Matrix Metalloproteinase 1 - analysis
  • Matrix Metalloproteinase 1 - genetics
  • Matrix Metalloproteinase 10
  • Matrix Metalloproteinase 13
  • Matrix Metalloproteinase 2 - analysis
  • Matrix Metalloproteinase 2 - genetics
  • Matrix Metalloproteinase 3 - analysis
  • Matrix Metalloproteinase 3 - genetics
  • Matrix Metalloproteinase 9 - analysis
  • Matrix Metalloproteinase 9 - genetics
  • Metalloendopeptidases - analysis
  • Metalloendopeptidases - genetics
  • Polymerase chain reaction
  • Rats
  • Rats, Wistar
  • Reverse transcription
  • RNA, Messenger - analysis
  • Stromelysin
  • Stromelysin 1
  • Tissue inhibitor of metalloproteinase 1
  • Tissue Inhibitor of Metalloproteinase-1 - analysis
  • Tissue Inhibitor of Metalloproteinase-1 - genetics
  • Tissue Inhibitor of Metalloproteinase-2 - analysis
  • Tissue Inhibitor of Metalloproteinase-2 - genetics
  • Transforming growth factor-b1
  • Tumor necrosis factor-α
ispartof: Histochemistry and cell biology, 2000-06, Vol.113 (6), p.443-453
description: Matrix metalloproteinases (MMPs) and their specific inhibitors (TIMPs) are thought to play an essential role in liver injury associated with tissue remodeling. However, their distinct expression profile in different liver repair models still remains to be established. Hepatic expression of collagenase (MMP-13), gelatinases A and B (MMP-2, -9), stromelysin-1 and -2 (MMP-3, -10), membrane-type MMP-1 (MMP-14), and TIMP-1 and -2 was studied following single and repeated CCl4-mediated injury and after partial hepatectomy. Expression was analyzed by reverse transcription-PCR (RT-PCR), northern blot analysis, zymography, and immunohistochemistry. Following a single toxic liver injury, MMPs and TIMPs were induced in a distinct time frame in that expression of most MMPs was induced during the early phase of liver injury, was maximal during the inflammatory reaction, and was diminished in the recovery phase. In contrast, TIMP and MMP-2 steady state mRNA levels remained constant in the early phase, were strongly induced during tissue inflammation, and remained increased until the recovery phase. Interestingly, hepatic TNF-alpha expression paralleled the MMP induction profile, while the increase of TGF-beta1 expression mapped to the increase of TIMPs. Chronic liver injury was accompanied by an increase in the steady state mRNA levels of MMP-2 and TIMPs, while other MMPs remained more or less unchanged or were diminished. Partial hepatectomy was followed by a dramatic increase of MMP-14 and to a lesser extent also of TIMP-1 expression; other MMPs and TIMPs were not significantly induced. Liver injury is accompanied by profound changes in hepatic MMP/TIMP expression, the latter being critically dependent on the type of injury. Single toxic injury resulting in complete restoration was characterized by a sequential induction of MMPs and TIMPs suggesting initial matrix breakdown and matrix restoration thereafter. Chronic liver injury leading to fibrosis displays overall diminished matrix degradation mainly through TIMP induction, while liver regeneration induced by partial hepatectomy caused an induction of MMP-14 and TIMP-1 only, which might be unrelated to matrix turnover but connected to pericellular fibrinolysis or fibrolysis required for hepatocellular replication.
language: eng
source:
identifier: ISSN: 0948-6143
fulltext: no_fulltext
issn:
  • 0948-6143
  • 1432-119X
url: Link


@attributes
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
RANK2.2818274
LOCALfalse
PrimoNMBib
record
control
sourceidproquest_cross
recordidTN_cdi_pubmed_primary_10933221
sourceformatXML
sourcesystemPC
sourcerecordid2407501943
originalsourceidFETCH-LOGICAL-c264t-cad9db94271b7bcf90dccf7d3f71b72cf6889d7c5db6a58cc278cba4be6bc73c0
addsrcrecordideNpVkMtLAzEQxoMotlaPXiXgeXWSzW42Ryn1AQUvCt6WvNamdB8mWaj_vVnbg85lmI_ffDN8CF0TuCMA_D4AMFJBKlLACZoTltOMEPFxiuYgWJWVSZmhixC2EyIoPUczAiLPKSVzZFb7wdsQXN_hvsGtjN7tcWuj3O36wffRuk4GG7DsDI4b6zx23cYpF3sfsBm96z7xxg4yOo2jC2G02Kfxl5sWsJfxEp01chfs1bEv0Pvj6m35nK1fn16WD-tM05LFTEsjjBKMcqK40o0Ao3XDTd5MAtVNWVXCcF0YVcqi0prySivJlC2V5rmGBbo9-KbHv0YbYr3tR9-lkzVlwAsgguWJyg6U9n0I3jb14F0r_XdNoJ4yrf9lmvibo-uoWmv-0IcQ4QdFfHP-
sourcetypeAggregation Database
isCDItrue
recordtypearticle
pqid2407501943
display
typearticle
titleExpression of matrix metalloproteinases and their inhibitors during hepatic tissue repair in the rat
creatorKnittel, T ; Mehde, M ; Grundmann, A ; Saile, B ; Scharf, J G ; Ramadori, G
creatorcontribKnittel, T ; Mehde, M ; Grundmann, A ; Saile, B ; Scharf, J G ; Ramadori, G
descriptionMatrix metalloproteinases (MMPs) and their specific inhibitors (TIMPs) are thought to play an essential role in liver injury associated with tissue remodeling. However, their distinct expression profile in different liver repair models still remains to be established. Hepatic expression of collagenase (MMP-13), gelatinases A and B (MMP-2, -9), stromelysin-1 and -2 (MMP-3, -10), membrane-type MMP-1 (MMP-14), and TIMP-1 and -2 was studied following single and repeated CCl4-mediated injury and after partial hepatectomy. Expression was analyzed by reverse transcription-PCR (RT-PCR), northern blot analysis, zymography, and immunohistochemistry. Following a single toxic liver injury, MMPs and TIMPs were induced in a distinct time frame in that expression of most MMPs was induced during the early phase of liver injury, was maximal during the inflammatory reaction, and was diminished in the recovery phase. In contrast, TIMP and MMP-2 steady state mRNA levels remained constant in the early phase, were strongly induced during tissue inflammation, and remained increased until the recovery phase. Interestingly, hepatic TNF-alpha expression paralleled the MMP induction profile, while the increase of TGF-beta1 expression mapped to the increase of TIMPs. Chronic liver injury was accompanied by an increase in the steady state mRNA levels of MMP-2 and TIMPs, while other MMPs remained more or less unchanged or were diminished. Partial hepatectomy was followed by a dramatic increase of MMP-14 and to a lesser extent also of TIMP-1 expression; other MMPs and TIMPs were not significantly induced. Liver injury is accompanied by profound changes in hepatic MMP/TIMP expression, the latter being critically dependent on the type of injury. Single toxic injury resulting in complete restoration was characterized by a sequential induction of MMPs and TIMPs suggesting initial matrix breakdown and matrix restoration thereafter. Chronic liver injury leading to fibrosis displays overall diminished matrix degradation mainly through TIMP induction, while liver regeneration induced by partial hepatectomy caused an induction of MMP-14 and TIMP-1 only, which might be unrelated to matrix turnover but connected to pericellular fibrinolysis or fibrolysis required for hepatocellular replication.
identifier
0ISSN: 0948-6143
1EISSN: 1432-119X
2DOI: 10.1007/s004180000150
3PMID: 10933221
languageeng
publisherGermany: Springer Nature B.V
subjectAcute Disease ; Animals ; Blotting, Northern ; Carbon tetrachloride ; CCL4 protein ; Collagen ; Collagenase ; Collagenase 3 ; Collagenases - analysis ; Collagenases - genetics ; Fibrinolysis ; Fibrosis ; Gelatinase A ; Gene Expression Regulation, Enzymologic - physiology ; Hepatectomy ; Hepatitis, Animal - metabolism ; Immunohistochemistry ; Inflammation ; Interstitial collagenase ; Liver ; Liver - enzymology ; Liver - surgery ; Liver Cirrhosis - metabolism ; Liver Regeneration - physiology ; Matrix metalloproteinase ; Matrix Metalloproteinase 1 - analysis ; Matrix Metalloproteinase 1 - genetics ; Matrix Metalloproteinase 10 ; Matrix Metalloproteinase 13 ; Matrix Metalloproteinase 2 - analysis ; Matrix Metalloproteinase 2 - genetics ; Matrix Metalloproteinase 3 - analysis ; Matrix Metalloproteinase 3 - genetics ; Matrix Metalloproteinase 9 - analysis ; Matrix Metalloproteinase 9 - genetics ; Metalloendopeptidases - analysis ; Metalloendopeptidases - genetics ; Polymerase chain reaction ; Rats ; Rats, Wistar ; Reverse transcription ; RNA, Messenger - analysis ; Stromelysin ; Stromelysin 1 ; Tissue inhibitor of metalloproteinase 1 ; Tissue Inhibitor of Metalloproteinase-1 - analysis ; Tissue Inhibitor of Metalloproteinase-1 - genetics ; Tissue Inhibitor of Metalloproteinase-2 - analysis ; Tissue Inhibitor of Metalloproteinase-2 - genetics ; Transforming growth factor-b1 ; Tumor necrosis factor-α
ispartofHistochemistry and cell biology, 2000-06, Vol.113 (6), p.443-453
rightsSpringer-Verlag 2000.
lds50peer_reviewed
links
openurl$$Topenurl_article
thumbnail$$Usyndetics_thumb_exl
backlink$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10933221$$D View this record in MEDLINE/PubMed
search
creatorcontrib
0Knittel, T
1Mehde, M
2Grundmann, A
3Saile, B
4Scharf, J G
5Ramadori, G
title
0Expression of matrix metalloproteinases and their inhibitors during hepatic tissue repair in the rat
1Histochemistry and cell biology
addtitleHistochem Cell Biol
descriptionMatrix metalloproteinases (MMPs) and their specific inhibitors (TIMPs) are thought to play an essential role in liver injury associated with tissue remodeling. However, their distinct expression profile in different liver repair models still remains to be established. Hepatic expression of collagenase (MMP-13), gelatinases A and B (MMP-2, -9), stromelysin-1 and -2 (MMP-3, -10), membrane-type MMP-1 (MMP-14), and TIMP-1 and -2 was studied following single and repeated CCl4-mediated injury and after partial hepatectomy. Expression was analyzed by reverse transcription-PCR (RT-PCR), northern blot analysis, zymography, and immunohistochemistry. Following a single toxic liver injury, MMPs and TIMPs were induced in a distinct time frame in that expression of most MMPs was induced during the early phase of liver injury, was maximal during the inflammatory reaction, and was diminished in the recovery phase. In contrast, TIMP and MMP-2 steady state mRNA levels remained constant in the early phase, were strongly induced during tissue inflammation, and remained increased until the recovery phase. Interestingly, hepatic TNF-alpha expression paralleled the MMP induction profile, while the increase of TGF-beta1 expression mapped to the increase of TIMPs. Chronic liver injury was accompanied by an increase in the steady state mRNA levels of MMP-2 and TIMPs, while other MMPs remained more or less unchanged or were diminished. Partial hepatectomy was followed by a dramatic increase of MMP-14 and to a lesser extent also of TIMP-1 expression; other MMPs and TIMPs were not significantly induced. Liver injury is accompanied by profound changes in hepatic MMP/TIMP expression, the latter being critically dependent on the type of injury. Single toxic injury resulting in complete restoration was characterized by a sequential induction of MMPs and TIMPs suggesting initial matrix breakdown and matrix restoration thereafter. Chronic liver injury leading to fibrosis displays overall diminished matrix degradation mainly through TIMP induction, while liver regeneration induced by partial hepatectomy caused an induction of MMP-14 and TIMP-1 only, which might be unrelated to matrix turnover but connected to pericellular fibrinolysis or fibrolysis required for hepatocellular replication.
subject
0Acute Disease
1Animals
2Blotting, Northern
3Carbon tetrachloride
4CCL4 protein
5Collagen
6Collagenase
7Collagenase 3
8Collagenases - analysis
9Collagenases - genetics
10Fibrinolysis
11Fibrosis
12Gelatinase A
13Gene Expression Regulation, Enzymologic - physiology
14Hepatectomy
15Hepatitis, Animal - metabolism
16Immunohistochemistry
17Inflammation
18Interstitial collagenase
19Liver
20Liver - enzymology
21Liver - surgery
22Liver Cirrhosis - metabolism
23Liver Regeneration - physiology
24Matrix metalloproteinase
25Matrix Metalloproteinase 1 - analysis
26Matrix Metalloproteinase 1 - genetics
27Matrix Metalloproteinase 10
28Matrix Metalloproteinase 13
29Matrix Metalloproteinase 2 - analysis
30Matrix Metalloproteinase 2 - genetics
31Matrix Metalloproteinase 3 - analysis
32Matrix Metalloproteinase 3 - genetics
33Matrix Metalloproteinase 9 - analysis
34Matrix Metalloproteinase 9 - genetics
35Metalloendopeptidases - analysis
36Metalloendopeptidases - genetics
37Polymerase chain reaction
38Rats
39Rats, Wistar
40Reverse transcription
41RNA, Messenger - analysis
42Stromelysin
43Stromelysin 1
44Tissue inhibitor of metalloproteinase 1
45Tissue Inhibitor of Metalloproteinase-1 - analysis
46Tissue Inhibitor of Metalloproteinase-1 - genetics
47Tissue Inhibitor of Metalloproteinase-2 - analysis
48Tissue Inhibitor of Metalloproteinase-2 - genetics
49Transforming growth factor-b1
50Tumor necrosis factor-α
issn
00948-6143
11432-119X
fulltextfalse
rsrctypearticle
creationdate2000
recordtypearticle
recordideNpVkMtLAzEQxoMotlaPXiXgeXWSzW42Ryn1AQUvCt6WvNamdB8mWaj_vVnbg85lmI_ffDN8CF0TuCMA_D4AMFJBKlLACZoTltOMEPFxiuYgWJWVSZmhixC2EyIoPUczAiLPKSVzZFb7wdsQXN_hvsGtjN7tcWuj3O36wffRuk4GG7DsDI4b6zx23cYpF3sfsBm96z7xxg4yOo2jC2G02Kfxl5sWsJfxEp01chfs1bEv0Pvj6m35nK1fn16WD-tM05LFTEsjjBKMcqK40o0Ao3XDTd5MAtVNWVXCcF0YVcqi0prySivJlC2V5rmGBbo9-KbHv0YbYr3tR9-lkzVlwAsgguWJyg6U9n0I3jb14F0r_XdNoJ4yrf9lmvibo-uoWmv-0IcQ4QdFfHP-
startdate200006
enddate200006
creator
0Knittel, T
1Mehde, M
2Grundmann, A
3Saile, B
4Scharf, J G
5Ramadori, G
generalSpringer Nature B.V
scope
0CGR
1CUY
2CVF
3ECM
4EIF
5NPM
6AAYXX
7CITATION
83V.
97QP
107RV
117TK
127X7
137XB
1488A
1588E
168AO
178C1
188FE
198FH
208FI
218FJ
228FK
23ABUWG
24AZQEC
25BBNVY
26BENPR
27BHPHI
28DWQXO
29FYUFA
30GHDGH
31GNUQQ
32HCIFZ
33K9.
34KB0
35LK8
36M0S
37M1P
38M7P
39NAPCQ
40PQEST
41PQQKQ
42PQUKI
43PRINS
sort
creationdate200006
titleExpression of matrix metalloproteinases and their inhibitors during hepatic tissue repair in the rat
authorKnittel, T ; Mehde, M ; Grundmann, A ; Saile, B ; Scharf, J G ; Ramadori, G
facets
frbrtype5
frbrgroupidcdi_FETCH-LOGICAL-c264t-cad9db94271b7bcf90dccf7d3f71b72cf6889d7c5db6a58cc278cba4be6bc73c0
rsrctypearticles
prefilterarticles
languageeng
creationdate2000
topic
0Acute Disease
1Animals
2Blotting, Northern
3Carbon tetrachloride
4CCL4 protein
5Collagen
6Collagenase
7Collagenase 3
8Collagenases - analysis
9Collagenases - genetics
10Fibrinolysis
11Fibrosis
12Gelatinase A
13Gene Expression Regulation, Enzymologic - physiology
14Hepatectomy
15Hepatitis, Animal - metabolism
16Immunohistochemistry
17Inflammation
18Interstitial collagenase
19Liver
20Liver - enzymology
21Liver - surgery
22Liver Cirrhosis - metabolism
23Liver Regeneration - physiology
24Matrix metalloproteinase
25Matrix Metalloproteinase 1 - analysis
26Matrix Metalloproteinase 1 - genetics
27Matrix Metalloproteinase 10
28Matrix Metalloproteinase 13
29Matrix Metalloproteinase 2 - analysis
30Matrix Metalloproteinase 2 - genetics
31Matrix Metalloproteinase 3 - analysis
32Matrix Metalloproteinase 3 - genetics
33Matrix Metalloproteinase 9 - analysis
34Matrix Metalloproteinase 9 - genetics
35Metalloendopeptidases - analysis
36Metalloendopeptidases - genetics
37Polymerase chain reaction
38Rats
39Rats, Wistar
40Reverse transcription
41RNA, Messenger - analysis
42Stromelysin
43Stromelysin 1
44Tissue inhibitor of metalloproteinase 1
45Tissue Inhibitor of Metalloproteinase-1 - analysis
46Tissue Inhibitor of Metalloproteinase-1 - genetics
47Tissue Inhibitor of Metalloproteinase-2 - analysis
48Tissue Inhibitor of Metalloproteinase-2 - genetics
49Transforming growth factor-b1
50Tumor necrosis factor-α
toplevelpeer_reviewed
creatorcontrib
0Knittel, T
1Mehde, M
2Grundmann, A
3Saile, B
4Scharf, J G
5Ramadori, G
collection
0Medline
1MEDLINE
2MEDLINE (Ovid)
3MEDLINE
4MEDLINE
5PubMed
6CrossRef
7ProQuest Central (Corporate)
8Calcium & Calcified Tissue Abstracts
9Nursing & Allied Health Database
10Neurosciences Abstracts
11Health & Medical Collection
12ProQuest Central (purchase pre-March 2016)
13Biology Database (Alumni Edition)
14Medical Database (Alumni Edition)
15ProQuest Pharma Collection
16Public Health Database
17ProQuest SciTech Collection
18ProQuest Natural Science Collection
19Hospital Premium Collection
20Hospital Premium Collection (Alumni Edition)
21ProQuest Central (Alumni) (purchase pre-March 2016)
22ProQuest Central (Alumni Edition)
23ProQuest Central Essentials
24Biological Science Collection
25ProQuest Central
26Natural Science Collection
27ProQuest Central Korea
28Health Research Premium Collection
29Health Research Premium Collection (Alumni)
30ProQuest Central Student
31SciTech Premium Collection
32ProQuest Health & Medical Complete (Alumni)
33Nursing & Allied Health Database (Alumni Edition)
34ProQuest Biological Science Collection
35Health & Medical Collection (Alumni Edition)
36Medical Database
37Biological Science Database
38Nursing & Allied Health Premium
39ProQuest One Academic Eastern Edition
40ProQuest One Academic
41ProQuest One Academic UKI Edition
42ProQuest Central China
jtitleHistochemistry and cell biology
delivery
delcategoryRemote Search Resource
fulltextno_fulltext
addata
au
0Knittel, T
1Mehde, M
2Grundmann, A
3Saile, B
4Scharf, J G
5Ramadori, G
formatjournal
genrearticle
ristypeJOUR
atitleExpression of matrix metalloproteinases and their inhibitors during hepatic tissue repair in the rat
jtitleHistochemistry and cell biology
addtitleHistochem Cell Biol
date2000-06
risdate2000
volume113
issue6
spage443
epage453
pages443-453
issn0948-6143
eissn1432-119X
abstractMatrix metalloproteinases (MMPs) and their specific inhibitors (TIMPs) are thought to play an essential role in liver injury associated with tissue remodeling. However, their distinct expression profile in different liver repair models still remains to be established. Hepatic expression of collagenase (MMP-13), gelatinases A and B (MMP-2, -9), stromelysin-1 and -2 (MMP-3, -10), membrane-type MMP-1 (MMP-14), and TIMP-1 and -2 was studied following single and repeated CCl4-mediated injury and after partial hepatectomy. Expression was analyzed by reverse transcription-PCR (RT-PCR), northern blot analysis, zymography, and immunohistochemistry. Following a single toxic liver injury, MMPs and TIMPs were induced in a distinct time frame in that expression of most MMPs was induced during the early phase of liver injury, was maximal during the inflammatory reaction, and was diminished in the recovery phase. In contrast, TIMP and MMP-2 steady state mRNA levels remained constant in the early phase, were strongly induced during tissue inflammation, and remained increased until the recovery phase. Interestingly, hepatic TNF-alpha expression paralleled the MMP induction profile, while the increase of TGF-beta1 expression mapped to the increase of TIMPs. Chronic liver injury was accompanied by an increase in the steady state mRNA levels of MMP-2 and TIMPs, while other MMPs remained more or less unchanged or were diminished. Partial hepatectomy was followed by a dramatic increase of MMP-14 and to a lesser extent also of TIMP-1 expression; other MMPs and TIMPs were not significantly induced. Liver injury is accompanied by profound changes in hepatic MMP/TIMP expression, the latter being critically dependent on the type of injury. Single toxic injury resulting in complete restoration was characterized by a sequential induction of MMPs and TIMPs suggesting initial matrix breakdown and matrix restoration thereafter. Chronic liver injury leading to fibrosis displays overall diminished matrix degradation mainly through TIMP induction, while liver regeneration induced by partial hepatectomy caused an induction of MMP-14 and TIMP-1 only, which might be unrelated to matrix turnover but connected to pericellular fibrinolysis or fibrolysis required for hepatocellular replication.
copGermany
pubSpringer Nature B.V
pmid10933221
doi10.1007/s004180000150