-
Je něco špatně v tomto záznamu ?
Multiplex Protein Biomarker Profiling in Patients with Familial Hypercholesterolemia
D. Dlouha, M. Blaha, E. Rohlova, JA. Hubacek, V. Lanska, J. Visek, V. Blaha
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Free Medical Journals
od 2010
PubMed Central
od 2010
Europe PubMed Central
od 2010
ProQuest Central
od 2010-03-01
Open Access Digital Library
od 2010-01-01
Open Access Digital Library
od 2010-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2010
PubMed
34680994
DOI
10.3390/genes12101599
Knihovny.cz E-zdroje
- MeSH
- anticholesteremika terapeutické užití MeSH
- biologické markery krev MeSH
- cholesterol krev metabolismus MeSH
- dospělí MeSH
- hyperlipoproteinemie typ II krev farmakoterapie genetika patologie MeSH
- kardiovaskulární nemoci krev farmakoterapie genetika patologie MeSH
- krevní proteiny klasifikace genetika izolace a purifikace MeSH
- lidé středního věku MeSH
- lidé MeSH
- senioři MeSH
- zánět krev genetika metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Familial hypercholesterolemia (FH), is an autosomal dominant disorder caused by mutations in the LDLR, APOB, PCSK9, and APOE genes and is characterized by high plasma levels of total and low-density lipoprotein (LDL) cholesterol. Our study aimed to analyze the influences of two different therapies on a wide spectrum of plasma protein biomarkers of cardiovascular diseases. Plasma from FH patients under hypolipidemic therapy (N = 18; men = 8, age 55.4 ± 13.1 years) and patients under combined long-term LDL apheresis/hypolipidemic therapy (N = 14; men = 7; age 58.0 ± 13.6 years) were analyzed in our study. We measured a profile of 184 cardiovascular disease (CVD) associated proteins using a proximity extension assay (PEA). Hypolipidemic therapy significantly (all p < 0.01) influenced 10 plasma proteins (TM, DKK1, CCL3, CD4, PDGF subunit B, AGRP, IL18, THPO, and LOX1 decreased; ST2 increased). Under combined apheresis/hypolipidemic treatment, 18 plasma proteins (LDLR, PCSK9, MMP-3, GDF2, CTRC, SORT1, VEGFD, IL27, CCL24, and KIM1 decreased; OPN, COL1A1, KLK6, IL4RA, PLC, TNFR1, GLO1, and PTX3 increased) were significantly affected (all p < 0.006). Hypolipidemic treatment mainly affected biomarkers involved in vascular endothelial maintenance. Combined therapy influenced proteins that participate in cholesterol metabolism and inflammation.
1st Faculty of Medicine Charles University 128 00 Prague Czech Republic
Laboratory of Gene Expression Institute of Biotechnology CAS BIOCEV 252 50 Vestec Czech Republic
Statistical Unit Institute for Clinical and Experimental Medicine 140 21 Prague Czech Republic
Citace poskytuje Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc22012097
- 003
- CZ-PrNML
- 005
- 20220506130839.0
- 007
- ta
- 008
- 220425s2021 sz f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.3390/genes12101599 $2 doi
- 035 __
- $a (PubMed)34680994
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a sz
- 100 1_
- $a Dlouha, Dana $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Videnska 1958/9, 140 21 Prague, Czech Republic $1 https://orcid.org/0000000171671336
- 245 10
- $a Multiplex Protein Biomarker Profiling in Patients with Familial Hypercholesterolemia / $c D. Dlouha, M. Blaha, E. Rohlova, JA. Hubacek, V. Lanska, J. Visek, V. Blaha
- 520 9_
- $a Familial hypercholesterolemia (FH), is an autosomal dominant disorder caused by mutations in the LDLR, APOB, PCSK9, and APOE genes and is characterized by high plasma levels of total and low-density lipoprotein (LDL) cholesterol. Our study aimed to analyze the influences of two different therapies on a wide spectrum of plasma protein biomarkers of cardiovascular diseases. Plasma from FH $a Familial hypercholesterolemia FH is an autosomal dominant disorder caused by mutations in the LDLR APOB PCSK9 and APOE genes and is characterized by high plasma levels of total and low density lipoprotein LDL cholesterol Our study aimed to analyze the influences of two different therapies on a wide spectrum of plasma protein biomarkers of cardiovascular diseases Plasma from FH patients u $a Familial hypercholesterolemia (FH), is an autosomal dominant disorder caused by mutations in the LDLR, APOB, PCSK9, and APOE genes and is characterized by high plasma levels of total and low-density lipoprotein (LDL) cholesterol. Our study aimed to analyze the influences of two different therapies on a wide spectrum of plasma protein biomarkers of cardiovascular diseases. Plasma from FH patients under hypolipidemic therapy (N = 18; men = 8, age 55.4 ± 13.1 years) and patients under combined long-term LDL apheresis/hypolipidemic therapy (N = 14; men = 7; age 58.0 ± 13.6 years) were analyzed in our study. We measured a profile of 184 cardiovascular disease (CVD) associated proteins using a proximity extension assay (PEA). Hypolipidemic therapy significantly (all p < 0.01) influenced 10 plasma proteins (TM, DKK1, CCL3, CD4, PDGF subunit B, AGRP, IL18, THPO, and LOX1 decreased; ST2 increased). Under combined apheresis/hypolipidemic treatment, 18 plasma proteins (LDLR, PCSK9, MMP-3, GDF2, CTRC, SORT1, VEGFD, IL27, CCL24, and KIM1 decreased; OPN, COL1A1, KLK6, IL4RA, PLC, TNFR1, GLO1, and PTX3 increased) were significantly affected (all p < 0.006). Hypolipidemic treatment mainly affected biomarkers involved in vascular endothelial maintenance. Combined therapy influenced proteins that participate in cholesterol metabolism and inflammation.
- 650 _2
- $a dospělí $7 D000328
- 650 _2
- $a senioři $7 D000368
- 650 _2
- $a anticholesteremika $x terapeutické užití $7 D000924
- 650 _2
- $a biologické markery $x krev $7 D015415
- 650 _2
- $a krevní proteiny $x klasifikace $x genetika $x izolace a purifikace $7 D001798
- 650 _2
- $a kardiovaskulární nemoci $x krev $x farmakoterapie $x genetika $x patologie $7 D002318
- 650 _2
- $a cholesterol $x krev $x metabolismus $7 D002784
- 650 _2
- $a ženské pohlaví $7 D005260
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a hyperlipoproteinemie typ II $x krev $x farmakoterapie $x genetika $x patologie $7 D006938
- 650 _2
- $a zánět $x krev $x genetika $x metabolismus $7 D007249
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a lidé středního věku $7 D008875
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Blaha, Milan $u 4th Department of Internal Medicine-Hematology, Faculty of Medicine in Hradec Králové, University Hospital Hradec Králové and Charles University, 500 05 Hradec Králové, Czech Republic
- 700 1_
- $a Rohlova, Eva $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Videnska 1958/9, 140 21 Prague, Czech Republic $u Laboratory of Gene Expression, Institute of Biotechnology CAS, BIOCEV, 252 50 Vestec, Czech Republic $u Department of Anthropology and Human Genetics, Faculty of Science, Charles University, 120 00 Prague, Czech Republic
- 700 1_
- $a Hubacek, Jaroslav A $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Videnska 1958/9, 140 21 Prague, Czech Republic $u First Faculty of Medicine, Charles University, 128 00 Prague, Czech Republic $1 https://orcid.org/0000000165371353
- 700 1_
- $a Lanska, Vera $u Statistical Unit, Institute for Clinical and Experimental Medicine, 140 21 Prague, Czech Republic
- 700 1_
- $a Visek, Jakub $u 3rd Department of Internal Medicine-Metabolism and Gerontology, Faculty of Medicine in Hradec Králové, University Hospital Hradec Králové and Charles University, 500 05 Hradec Králové, Czech Republic
- 700 1_
- $a Blaha, Vladimir $u 3rd Department of Internal Medicine-Metabolism and Gerontology, Faculty of Medicine in Hradec Králové, University Hospital Hradec Králové and Charles University, 500 05 Hradec Králové, Czech Republic $1 https://orcid.org/0000000180889919 $7 xx0002944
- 773 0_
- $w MED00174652 $t Genes $x 2073-4425 $g Roč. 12, č. 10 (2021)
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/34680994 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y p $z 0
- 990 __
- $a 20220425 $b ABA008
- 991 __
- $a 20220506130832 $b ABA008
- 999 __
- $a ok $b bmc $g 1789616 $s 1163298
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2021 $b 12 $c 10 $e 20211012 $i 2073-4425 $m Genes $n Genes $x MED00174652
- LZP __
- $a Pubmed-20220425