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Book ; Thesis: Immune responses against aldehyde modified extracellular matrix in atherosclerosis

Dunér, Pontus

(Doctoral dissertation series ; 2009, 86)

2009

Author's details	Pontus Dunér
Series title	Doctoral dissertation series ; 2009, 86 Doctoral dissertation series / Blekinge Institute of Technology
Collection	Doctoral dissertation series / Blekinge Institute of Technology
Language	German
Size	113 S. : Ill., graph. Darst.
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Lund, Univ., Diss., 2009
Note	Zsfassung in schwed. Sprache
HBZ-ID	HT016222626
ISBN	978-91-86253-74-5 ; 91-86253-74-3
Database	Catalogue ZB MED Medicine, Health

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Article: COVID-19 and Possible Pharmacological Preventive Options.

Duner, Pontus / Salehi, Albert

Journal of clinical medicine research

2020 Volume 12, Issue 12, Page(s) 758–772

Abstract: The dreadful fear of the coronavirus disease 2019 (COVID-19), which is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with the deadly consequences, requires rapid development of pharmacological cures. The ... ...

Abstract	The dreadful fear of the coronavirus disease 2019 (COVID-19), which is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with the deadly consequences, requires rapid development of pharmacological cures. The objective of this review is to speculate about possible pharmacological options, already available today to prevent or treat the COVID-19 in the early stage of its outbreak. A literature search across PubMed and internet was conducted. A number of studies dealing with COVID-19 were identified. The data elucidated that increased pro-inflammatory and decreased anti-inflammatory cytokines in combination with hypoxia, thromboembolism and pneumonia are involved in the pathogenesis of SARS-CoV-2 infection. Although many drugs has been tested in monotherapy regimen with varying outcome or without desirable effect, there is still hope for better results by simultaneously targeting the virus itself and its symptoms. Theoretically, a mixture of at least two available antiviral drugs in combination with other anti-pathogenic and immune system-enhancing drugs or combination of antiviral drugs with convalescent plasma seems likely to have much better effect than the monotherapy regimen of either of these drugs.
Language	English
Publishing date	2020-12-18
Publishing country	Canada
Document type	Journal Article ; Review
ZDB-ID	2548987-2
ISSN	1918-3011 ; 1918-3003
ISSN (online)	1918-3011
ISSN	1918-3003
DOI	10.14740/jocmr4383
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Article ; Online: Ablation of GPR56 Causes β-Cell Dysfunction by ATP Loss through Mistargeting of Mitochondrial VDAC1 to the Plasma Membrane.

Mohammad Al-Amily, Israa / Sjögren, Marie / Duner, Pontus / Tariq, Mohammad / Wollheim, Claes B / Salehi, Albert

Biomolecules

2023 Volume 13, Issue 3

Abstract: The activation of G Protein-Coupled Receptor 56 (GPR56), also referred to as Adhesion G-Protein-Coupled Ceceptor G1 (ADGRG1), by Collagen Type III (Coll III) prompts cell growth, proliferation, and survival, among other attributes. We investigated the ... ...

Abstract	The activation of G Protein-Coupled Receptor 56 (GPR56), also referred to as Adhesion G-Protein-Coupled Ceceptor G1 (ADGRG1), by Collagen Type III (Coll III) prompts cell growth, proliferation, and survival, among other attributes. We investigated the signaling cascades mediating this functional effect in relation to the mitochondrial outer membrane voltage-dependent anion Channel-1 (VDAC1) expression in pancreatic β-cells. GPR56KD attenuated the Coll III-induced suppression of P70S6K, JNK, AKT, NFκB, STAT3, and STAT5 phosphorylation/activity in INS-1 cells cultured at 20 mM glucose (glucotoxicity) for 72 h. GPR56-KD also increased Chrebp, Txnip, and Vdac1 while decreasing Vdac2 mRNA expression. In GPR56-KD islet β-cells, Vdac1 was co-localized with SNAP-25, demonstrating its plasma membrane translocation. This resulted in ATP loss, reduced cAMP production and impaired glucose-stimulated insulin secretion (GSIS) in INS-1 and human EndoC βH1 cells. The latter defects were reversed by an acute inhibition of VDAC1 with an antibody or the VDAC1 inhibitor VBIT-4. We demonstrate that Coll III potentiates GSIS by increasing cAMP and preserving β-cell functionality under glucotoxic conditions in a GPR56-dependent manner by attenuating the inflammatory response. These results emphasize GPR56 and VDAC1 as drug targets in conditions with impaired β-cell function.
MeSH term(s)	Humans ; Adenosine Triphosphate/metabolism ; Cell Membrane/metabolism ; Collagen Type III/metabolism ; Glucose/pharmacology ; Glucose/metabolism ; Islets of Langerhans/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Voltage-Dependent Anion Channel 1/genetics ; Voltage-Dependent Anion Channel 1/metabolism
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE) ; Collagen Type III ; Glucose (IY9XDZ35W2) ; Receptors, G-Protein-Coupled ; VDAC1 protein, human ; Voltage-Dependent Anion Channel 1 (EC 1.6.-) ; ADGRG1 protein, human
Language	English
Publishing date	2023-03-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13030557
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Article ; Online: The functional impact of G protein-coupled receptor 142 (Gpr142) on pancreatic β-cell in rodent.

Al-Amily, Israa Mohammad / Dunér, Pontus / Groop, Leif / Salehi, Albert

Pflugers Archiv : European journal of physiology

2019 Volume 471, Issue 4, Page(s) 633–645

Abstract: We have recently shown that the G protein-coupled receptor 142 (GPR142) is expressed in both rodent and human pancreatic β-cells. Herein, we investigated the cellular distribution of GPR142 within islets and the effects of selective agonists of GPR142 on ...

Abstract	We have recently shown that the G protein-coupled receptor 142 (GPR142) is expressed in both rodent and human pancreatic β-cells. Herein, we investigated the cellular distribution of GPR142 within islets and the effects of selective agonists of GPR142 on glucose-stimulated insulin secretion (GSIS) in the mouse islets and INS-1832/13 cells. Double-immunostaining revealed that GPR142 immunoreactivity in islets mainly occurs in insulin-positive cells. Potentiation of GSIS by GPR142 activation was accompanied by increased cAMP content in INS-1832/13 cells. PKA/Epac inhibition markedly suppressed the effect of GPR142 activation on insulin release. Gpr142 knockdown (Gpr142-KD) in islets was accompanied by elevated release of MCP-1, IFNγ, and TNFα during culture period and abolished the modulatory effect of GPR142 activation on the GSIS. Gpr142-KD had no effect on Ffar1, Ffar2, or Ffar3 mRNA while reducing Gpr56 and increasing Tlr5 and Tlr7 mRNA expression. Gpr142-KD was associated with an increased expression of Chrebp, Txnip, RhoA, and mitochondrial Vdac1 concomitant with a reduced Pdx1, Pax6, and mitochondrial Vdac2 mRNA levels. Long-term exposure of INS-1832/13 cells to hyperglycemia reduced Gpr142 and Vdac2 while increased Chrebp, Txnip, and Vdac1 mRNA expression. GPR142 agonists or Bt
MeSH term(s)	Animals ; Cell Survival/physiology ; Cyclic AMP/metabolism ; Female ; Glucose/metabolism ; Insulin/metabolism ; Insulin Secretion/physiology ; Insulin-Secreting Cells/metabolism ; Islets of Langerhans/metabolism ; Mice ; Mice, Inbred C57BL ; Receptors, G-Protein-Coupled/metabolism ; Rodentia/metabolism ; Signal Transduction/physiology
Chemical Substances	GPR142 protein, mouse ; Insulin ; Receptors, G-Protein-Coupled ; Cyclic AMP (E0399OZS9N) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-02-15
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-019-02262-7
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Article ; Online: Transforming growth factor-β2 is associated with atherosclerotic plaque stability and lower risk for cardiovascular events.

Edsfeldt, Andreas / Singh, Pratibha / Matthes, Frank / Tengryd, Christoffer / Cavalera, Michele / Bengtsson, Eva / Dunér, Pontus / Volkov, Petr / Karadimou, Glykeria / Gisterå, Anton / Orho-Melander, Marju / Nilsson, Jan / Sun, Jiangming / Gonçalves, Isabel

Cardiovascular research

2023 Volume 119, Issue 11, Page(s) 2061–2073

Abstract: Aims: Transforming growth factor-beta (TGF-β) exists in three isoforms TGF-β1, -β2, and -β3. TGF-β1 has been suggested to be important for maintaining plaque stability, yet the role of TGF-β2 and -β3 in atherosclerosis remains to be investigated.This ... ...

Abstract	Aims: Transforming growth factor-beta (TGF-β) exists in three isoforms TGF-β1, -β2, and -β3. TGF-β1 has been suggested to be important for maintaining plaque stability, yet the role of TGF-β2 and -β3 in atherosclerosis remains to be investigated.This study explores the association of the three isoforms of TGF-β with plaque stability in the human atherosclerotic disease. Methods and results: TGF-β1, -β2, and -β3 proteins were quantified in 223 human carotid plaques by immunoassays. Indications for the endarterectomy were: symptomatic carotid plaque with stenosis >70% or without symptoms and >80% stenosis. Plaque mRNA levels were assessed by RNA sequencing. Plaque components and extracellular matrix were measured histologically and biochemically. Matrix metalloproteinases and monocyte chemoattractant protein-1 (MCP-1) was measured with immunoassays. The effect of TGF-β2 on inflammation and protease activity was investigated in vitro using THP-1 and RAW264.7 macrophages. Patients were followed longitudinally for cardiovascular (CV) events.TGF-β2 was the most abundant isoform and was increased at both protein and mRNA levels in asymptomatic plaques. TGF-β2 was the main determinant separating asymptomatic plaques in an Orthogonal Projections to Latent Structures Discriminant Analysis. TGF-β2 correlated positively to features of plaque stability and inversely to markers of plaque vulnerability. TGF-β2 was the only isoform inversely correlated to the matrix-degrading matrix metalloproteinase-9 and inflammation in the plaque tissue. In vitro, TGF-β2 pre-treatment reduced MCP-1 gene and protein levels as well as matrix metalloproteinase-9 gene levels and activity. Patients with plaques with high TGF-β2 levels had a lower risk to suffer from future CV events. Conclusions: TGF-β2 is the most abundant TGF-β isoform in human plaques and may maintain plaque stability by decreasing inflammation and matrix degradation.
MeSH term(s)	Humans ; Transforming Growth Factor beta2/genetics ; Transforming Growth Factor beta1 ; Matrix Metalloproteinase 9/genetics ; Plaque, Atherosclerotic ; Constriction, Pathologic ; Transforming Growth Factor beta/metabolism ; Protein Isoforms ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Inflammation/genetics ; Transforming Growth Factors ; Cardiovascular Diseases
Chemical Substances	Transforming Growth Factor beta2 ; Transforming Growth Factor beta1 ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Transforming Growth Factor beta ; Protein Isoforms ; RNA, Messenger ; Transforming Growth Factors (76057-06-2)
Language	English
Publishing date	2023-05-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvad079
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Article ; Online: Inhibitory effect of UDP-glucose on cAMP generation and insulin secretion.

Parandeh, Fariborz / Amisten, Stefan / Verma, Gaurav / Mohammed Al-Amily, Israa / Dunér, Pontus / Salehi, Albert

The Journal of biological chemistry

2020 Volume 295, Issue 45, Page(s) 15245–15252

Abstract: Type-2 diabetes (T2D) is a global disease caused by the inability of pancreatic β-cells to secrete adequate insulin. However, the molecular mechanisms underlying the failure of β-cells to respond to glucose in T2D remains unknown. Here, we investigated ... ...

Abstract	Type-2 diabetes (T2D) is a global disease caused by the inability of pancreatic β-cells to secrete adequate insulin. However, the molecular mechanisms underlying the failure of β-cells to respond to glucose in T2D remains unknown. Here, we investigated the relative contribution of UDP-glucose (UDP-G), a P2Y14-specific agonist, in the regulation of insulin release using human isolated pancreatic islets and INS-1 cells. P2Y14 was expressed in both human and rodent pancreatic β-cells. Dose-dependent activation of P2Y14 by UDP-G suppressed glucose-stimulated insulin secretion (GSIS) and knockdown of P2Y14 abolished the UDP-G effect. 12-h pretreatment of human islets with pertussis-toxin (PTX) improved GSIS and prevented the inhibitory effect of UDP-G on GSIS. UDP-G on GSIS suppression was associated with suppression of cAMP in INS-1 cells. UDP-G decreased the reductive capacity of nondiabetic human islets cultured at 5 mm glucose for 72 h and exacerbated the negative effect of 20 mm glucose on the cell viability during culture period. T2D donor islets displayed a lower reductive capacity when cultured at 5 mm glucose for 72 h that was further decreased in the presence of 20 mm glucose and UDP-G. Presence of a nonmetabolizable cAMP analog during culture period counteracted the effect of glucose and UDP-G. Islet cultures at 20 mm glucose increased apoptosis, which was further amplified when UDP-G was present. UDP-G modulated glucose-induced proliferation of INS-1 cells. The data provide intriguing evidence for P2Y14 and UDP-G's role in the regulation of pancreatic β-cell function.
MeSH term(s)	Animals ; Cyclic AMP/biosynthesis ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Female ; Humans ; Insulin Secretion/drug effects ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Pertussis Toxin/pharmacology ; Rats ; Tumor Cells, Cultured ; Uridine Diphosphate Glucose/antagonists & inhibitors ; Uridine Diphosphate Glucose/metabolism
Chemical Substances	Cyclic AMP (E0399OZS9N) ; Pertussis Toxin (EC 2.4.2.31) ; Uridine Diphosphate Glucose (V50K1D7P4Y)
Language	English
Publishing date	2020-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA120.012929
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Article ; Online: Antibodies against apoB100 peptide 210 inhibit atherosclerosis in apoE

Dunér, Pontus / Mattisson, Ingrid Yao / Fogelstrand, Per / Glise, Lars / Ruiz, Stacey / Farina, Christopher / Borén, Jan / Nilsson, Jan / Bengtsson, Eva

Scientific reports

2021 Volume 11, Issue 1, Page(s) 9022

Abstract: Atherosclerotic plaques are characterized by an accumulation and subsequent oxidation of LDL, resulting in adaptive immune responses against formed or exposed neoepitopes of the LDL particle. Autoantibodies against native p210, the 3136-3155 amino acid ... ...

Abstract	Atherosclerotic plaques are characterized by an accumulation and subsequent oxidation of LDL, resulting in adaptive immune responses against formed or exposed neoepitopes of the LDL particle. Autoantibodies against native p210, the 3136-3155 amino acid sequence of the LDL protein apolipoprotein B-100 (apoB100) are common in humans and have been associated with less severe atherosclerosis and decreased risk for cardiovascular events in clinical studies. However, whether apoB100 native p210 autoantibodies play a functional role in atherosclerosis is not known. In the present study we immunized apoE
MeSH term(s)	Animals ; Apolipoprotein B-100/antagonists & inhibitors ; Apolipoprotein B-100/genetics ; Apolipoprotein B-100/immunology ; Atherosclerosis/immunology ; Atherosclerosis/prevention & control ; Autoantibodies/immunology ; Female ; Fusion Proteins, bcr-abl/immunology ; Immunoglobulin G/metabolism ; Lipoproteins, LDL/metabolism ; Malaria Vaccines/immunology ; Malondialdehyde/analogs & derivatives ; Malondialdehyde/metabolism ; Mice ; Peptide Fragments/immunology
Chemical Substances	Apob protein, mouse ; Apolipoprotein B-100 ; Autoantibodies ; Immunoglobulin G ; Lipoproteins, LDL ; Malaria Vaccines ; PADRE 45 ; Peptide Fragments ; malondialdehyde-low density lipoprotein, mouse ; Malondialdehyde (4Y8F71G49Q) ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2021-04-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-88430-1
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Article ; Online: ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions.

Mantani, Polyxeni T / Dunér, Pontus / Ljungcrantz, Irena / Nilsson, Jan / Björkbacka, Harry / Fredrikson, Gunilla Nordin

BMC immunology

2019 Volume 20, Issue 1, Page(s) 47

Abstract: Background: Expansion of type 2 innate lymphoid cells (ILC2s) in hypercholesterolaemic mice protects against atherosclerosis while different ILC2 subsets have been described (natural, inflammatory) based on their suppression of tumorigenicity 2 (ST2) ... ...

Abstract	Background: Expansion of type 2 innate lymphoid cells (ILC2s) in hypercholesterolaemic mice protects against atherosclerosis while different ILC2 subsets have been described (natural, inflammatory) based on their suppression of tumorigenicity 2 (ST2) and killer-cell lectin like receptor G1 (KLRG1) expression. The aim of the current study is to characterize the interleukin 25 (IL25)-induced splenic ILC2 population (Lin Results: Immunomagnetically enriched, FACS-sorted ILC2s from the spleens of IL-25 treated apoE Conclusions: With the current data we designate the IL25-induced ILC2 population to decrease the lipid content of atherosclerotic lesions in apoE
MeSH term(s)	Adoptive Transfer ; Animals ; Apolipoproteins E/deficiency ; Atherosclerosis/etiology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Biomarkers ; Cytokines/metabolism ; Disease Models, Animal ; Immunity, Innate ; Immunophenotyping ; Lipids/blood ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Mice ; Mice, Knockout
Chemical Substances	Apolipoproteins E ; Biomarkers ; Cytokines ; Lipids
Language	English
Publishing date	2019-12-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1471-2172
ISSN (online)	1471-2172
DOI	10.1186/s12865-019-0330-z
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Article ; Online: Antibodies against apoB100 peptide 210 inhibit atherosclerosis in apoE-/- mice

Pontus Dunér / Ingrid Yao Mattisson / Per Fogelstrand / Lars Glise / Stacey Ruiz / Christopher Farina / Jan Borén / Jan Nilsson / Eva Bengtsson

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 10

Abstract: Abstract Atherosclerotic plaques are characterized by an accumulation and subsequent oxidation of LDL, resulting in adaptive immune responses against formed or exposed neoepitopes of the LDL particle. Autoantibodies against native p210, the 3136–3155 ... ...

Abstract	Abstract Atherosclerotic plaques are characterized by an accumulation and subsequent oxidation of LDL, resulting in adaptive immune responses against formed or exposed neoepitopes of the LDL particle. Autoantibodies against native p210, the 3136–3155 amino acid sequence of the LDL protein apolipoprotein B-100 (apoB100) are common in humans and have been associated with less severe atherosclerosis and decreased risk for cardiovascular events in clinical studies. However, whether apoB100 native p210 autoantibodies play a functional role in atherosclerosis is not known. In the present study we immunized apoE-/- mice with p210-PADRE peptide to induce an antibody response against native p210. We also injected mice with murine monoclonal IgG against native p210. Control groups were immunized with PADRE peptide alone or with control murine monoclonal IgG. Immunization with p210-PADRE induced an IgG1 antibody response against p210 that was associated with reduced atherosclerotic plaque formation in the aorta and reduced MDA-LDL content in the lesions. Treatment with monoclonal p210 IgG produced a similar reduction in atherosclerosis as immunization with p210-PADRE. Our findings support an atheroprotective role of antibodies against the apoB100 native p210 and suggest that vaccines that induce the expression of native p210 IgG represent a potential therapeutic strategy for lowering cardiovascular risk.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Associations of Interleukin-5 With Plaque Development and Cardiovascular Events.

Knutsson, Anki / Björkbacka, Harry / Dunér, Pontus / Engström, Gunnar / Binder, Christoph J / Nilsson, Anna Hultgårdh / Nilsson, Jan

JACC. Basic to translational science

2019 Volume 4, Issue 8, Page(s) 891–902

Abstract: Experimental studies have suggested an atheroprotective role of interleukin (IL)-5 through the stimulation of natural immunoglobulin M antibody expression. In the present study we show that there are no associations between baseline levels of IL-5 and ... ...

Abstract	Experimental studies have suggested an atheroprotective role of interleukin (IL)-5 through the stimulation of natural immunoglobulin M antibody expression. In the present study we show that there are no associations between baseline levels of IL-5 and risk for development of coronary events or stroke during a 15.7 ± 6.3 years follow-up of 696 subjects randomly sampled from the Malmö Diet and Cancer study. However, presence of a plaque at the carotid bifurcation was associated with lower IL-5 and IL-5 deficiency resulted in increased plaque development at sites of oscillatory blood flow in
Language	English
Publishing date	2019-11-06
Publishing country	United States
Document type	Journal Article
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2019.07.002
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