Bax inhibitor-1 down-regulation in the progression of chronic liver diseases
BACKGROUND: Bax inhibitor-1 (BI-1) is an evolutionary conserved endoplasmic reticulum protein that, when overexpressed in mammalian cells, suppresses the apoptosis induced by Bax, a pro-apoptotic member of the Bcl-2 family. The aims of this study were: (1) to clarify the role of intrinsic anti- and pro-apoptotic mediators, evaluating Bax and BI-1 mRNA and protein expressions in liver tissues from patients with different degrees of liver damage; (2) to determine whether HCV and HBV infections modulate said expression.
METHODS: We examined 62 patients: 39 with chronic hepatitis (CH) (31 HCV-related and 8 HBV-related); 7 with cirrhosis (6 HCV-related and 1 HBV-related); 13 with hepatocellular carcinoma (HCC) [7 in viral cirrhosis (6 HCV- and 1 HBV-related), 6 in non-viral cirrhosis]; and 3 controls. Bax and BI-1 mRNAs were quantified by real-time PCR, and BI-1 protein expression by Western blot.
RESULTS: CH tissues expressed significantly higher BI-1 mRNA levels than cirrhotic tissues surrounding HCC (P < 0.0001) or HCC (P < 0.0001). Significantly higher Bax transcripts were observed in HCV-genotype-1-related than in HCV-genotype-3-related CH (P = 0.033). A positive correlation emerged between BI-1 and Bax transcripts in CH tissues, even when HCV-related CH and HCV-genotype-1-related CH were considered alone (P = 0.0007, P = 0.0005 and P = 0.0017, respectively).
CONCLUSIONS: BI-1 expression is down-regulated as liver damage progresses. The high BI-1 mRNAs levels observed in early liver disease may protect virus-infected cells against apoptosis, while their progressive downregulation may facilitate hepatocellular carcinogenesis. HCV genotype seems to have a relevant role in Bax transcript expression.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2010 |
---|---|
Erschienen: |
2010 |
Enthalten in: |
Zur Gesamtaufnahme - volume:10 |
---|---|
Enthalten in: |
BMC gastroenterology - 10(2010) vom: 01. Apr., Seite 35 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Kotsafti, Andromachi [VerfasserIn] |
---|
Links: |
---|
Themen: |
63231-63-0 |
---|
Anmerkungen: |
Date Completed 15.07.2010 Date Revised 20.10.2021 published: Electronic Citation Status MEDLINE |
---|
doi: |
10.1186/1471-230X-10-35 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM197039448 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM197039448 | ||
003 | DE-627 | ||
005 | 20231223205731.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231223s2010 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1186/1471-230X-10-35 |2 doi | |
028 | 5 | 2 | |a pubmed24n0657.xml |
035 | |a (DE-627)NLM197039448 | ||
035 | |a (NLM)20359348 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Kotsafti, Andromachi |e verfasserin |4 aut | |
245 | 1 | 0 | |a Bax inhibitor-1 down-regulation in the progression of chronic liver diseases |
264 | 1 | |c 2010 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 15.07.2010 | ||
500 | |a Date Revised 20.10.2021 | ||
500 | |a published: Electronic | ||
500 | |a Citation Status MEDLINE | ||
520 | |a BACKGROUND: Bax inhibitor-1 (BI-1) is an evolutionary conserved endoplasmic reticulum protein that, when overexpressed in mammalian cells, suppresses the apoptosis induced by Bax, a pro-apoptotic member of the Bcl-2 family. The aims of this study were: (1) to clarify the role of intrinsic anti- and pro-apoptotic mediators, evaluating Bax and BI-1 mRNA and protein expressions in liver tissues from patients with different degrees of liver damage; (2) to determine whether HCV and HBV infections modulate said expression | ||
520 | |a METHODS: We examined 62 patients: 39 with chronic hepatitis (CH) (31 HCV-related and 8 HBV-related); 7 with cirrhosis (6 HCV-related and 1 HBV-related); 13 with hepatocellular carcinoma (HCC) [7 in viral cirrhosis (6 HCV- and 1 HBV-related), 6 in non-viral cirrhosis]; and 3 controls. Bax and BI-1 mRNAs were quantified by real-time PCR, and BI-1 protein expression by Western blot | ||
520 | |a RESULTS: CH tissues expressed significantly higher BI-1 mRNA levels than cirrhotic tissues surrounding HCC (P < 0.0001) or HCC (P < 0.0001). Significantly higher Bax transcripts were observed in HCV-genotype-1-related than in HCV-genotype-3-related CH (P = 0.033). A positive correlation emerged between BI-1 and Bax transcripts in CH tissues, even when HCV-related CH and HCV-genotype-1-related CH were considered alone (P = 0.0007, P = 0.0005 and P = 0.0017, respectively) | ||
520 | |a CONCLUSIONS: BI-1 expression is down-regulated as liver damage progresses. The high BI-1 mRNAs levels observed in early liver disease may protect virus-infected cells against apoptosis, while their progressive downregulation may facilitate hepatocellular carcinogenesis. HCV genotype seems to have a relevant role in Bax transcript expression | ||
650 | 4 | |a Comparative Study | |
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 7 | |a Apoptosis Regulatory Proteins |2 NLM | |
650 | 7 | |a Membrane Proteins |2 NLM | |
650 | 7 | |a TMBIM6 protein, human |2 NLM | |
650 | 7 | |a RNA |2 NLM | |
650 | 7 | |a 63231-63-0 |2 NLM | |
700 | 1 | |a Farinati, Fabio |e verfasserin |4 aut | |
700 | 1 | |a Cardin, Romilda |e verfasserin |4 aut | |
700 | 1 | |a Burra, Patrizia |e verfasserin |4 aut | |
700 | 1 | |a Bortolami, Marina |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t BMC gastroenterology |d 2001 |g 10(2010) vom: 01. Apr., Seite 35 |w (DE-627)NLM110904761 |x 1471-230X |7 nnns |
773 | 1 | 8 | |g volume:10 |g year:2010 |g day:01 |g month:04 |g pages:35 |
856 | 4 | 0 | |u http://dx.doi.org/10.1186/1471-230X-10-35 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 10 |j 2010 |b 01 |c 04 |h 35 |