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Article ; Online: Cardiomyocytes, sphingolipids and cardio myotoxicity.

Levin, Malin C / Andersson, Linda / Borén, Jan

2023 Volume 34, Issue 4, Page(s) 180–188

Abstract: Purpose of review: Sphingolipids are structurally diverse membrane lipids localized in lipid bilayers. Sphingolipids are not only important structural components of cellular membranes, but they are also important regulators of cellular trafficking and ... ...

Abstract	Purpose of review: Sphingolipids are structurally diverse membrane lipids localized in lipid bilayers. Sphingolipids are not only important structural components of cellular membranes, but they are also important regulators of cellular trafficking and signal transduction and are implicated in several diseases. Here, we review the latest insights into sphingolipids and their role in cardiac function and cardiometabolic disease. Recent findings: The underlying mechanisms linking sphingolipids to cardiac dysfunction are still not fully clarified. Sphingolipids, and in particular ceramides, have emerged as important players in lipotoxicity, mediating inflammation, impaired insulin signalling and apoptosis. In addition, recent findings highlight the importance of glycosphingolipid homeostasis in cardiomyocyte membranes, where they are required to maintain β-adrenergic signalling and contractile capacity to preserve normal heart function. Thus, glycosphingolipid homeostasis in cardiac membranes characterizes a novel mechanism linking sphingolipids to cardiac disease. Summary: Modulation of cardiac sphingolipids may represent a promising therapeutic approach. Sustained investigation of the link between sphingolipids and cardiomyocyte function is therefore needed and we hope that this review may inspire researchers to further elucidate the action of these lipids.
MeSH term(s)	Humans ; Myocytes, Cardiac ; Sphingolipids ; Myotoxicity ; Ceramides ; Membrane Lipids
Chemical Substances	Sphingolipids ; Ceramides ; Membrane Lipids
Language	English
Publishing date	2023-04-24
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1045394-5
ISSN	1473-6535 ; 0957-9672
ISSN (online)	1473-6535
ISSN	0957-9672
DOI	10.1097/MOL.0000000000000829
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Zs.A 3010: Show issues

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Article: Role of Perilipins in Oxidative Stress-Implications for Cardiovascular Disease.

Cinato, Mathieu / Andersson, Linda / Miljanovic, Azra / Laudette, Marion / Kunduzova, Oksana / Borén, Jan / Levin, Malin C

Antioxidants (Basel, Switzerland)

2024 Volume 13, Issue 2

Abstract: Oxidative stress is the imbalance between the production of reactive oxygen species (ROS) and antioxidants in a cell. In the heart, oxidative stress may deteriorate calcium handling, cause arrhythmia, and enhance maladaptive cardiac remodeling by the ... ...

Abstract	Oxidative stress is the imbalance between the production of reactive oxygen species (ROS) and antioxidants in a cell. In the heart, oxidative stress may deteriorate calcium handling, cause arrhythmia, and enhance maladaptive cardiac remodeling by the induction of hypertrophic and apoptotic signaling pathways. Consequently, dysregulated ROS production and oxidative stress have been implicated in numerous cardiac diseases, including heart failure, cardiac ischemia-reperfusion injury, cardiac hypertrophy, and diabetic cardiomyopathy. Lipid droplets (LDs) are conserved intracellular organelles that enable the safe and stable storage of neutral lipids within the cytosol. LDs are coated with proteins, perilipins (Plins) being one of the most abundant. In this review, we will discuss the interplay between oxidative stress and Plins. Indeed, LDs and Plins are increasingly being recognized for playing a critical role beyond energy metabolism and lipid handling. Numerous reports suggest that an essential purpose of LD biogenesis is to alleviate cellular stress, such as oxidative stress. Given the yet unmet suitability of ROS as targets for the intervention of cardiovascular disease, the endogenous antioxidant capacity of Plins may be beneficial.
Language	English
Publishing date	2024-02-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox13020209
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Article ; Online: pH-Dependent Protonation of Histidine Residues Is Critical for Electrostatic Binding of Low-Density Lipoproteins to Human Coronary Arteries.

Glise, Lars / Rutberg, Mikael / Håversen, Liliana / Levin, Malin C / Levin, Max / Jeppsson, Anders / Borén, Jan / Fogelstrand, Per

Arteriosclerosis, thrombosis, and vascular biology

2022 Volume 42, Issue 8, Page(s) 1037–1047

Abstract: Background: The initiating step in atherogenesis is the electrostatic binding of LDL (low-density lipoprotein) to proteoglycan glycosaminoglycans in the arterial intima. However, although proteoglycans are widespread throughout the intima of most ... ...

Abstract	Background: The initiating step in atherogenesis is the electrostatic binding of LDL (low-density lipoprotein) to proteoglycan glycosaminoglycans in the arterial intima. However, although proteoglycans are widespread throughout the intima of most coronary artery segments, LDL is not evenly distributed, indicating that LDL retention is not merely dependent on the presence of proteoglycans. We aim to identify factors that promote the interaction between LDL and the vessel wall of human coronary arteries. Methods: We developed an ex vivo model to investigate binding of labeled human LDL to human coronary artery sections without the interference of cellular processes. Results: By staining consecutive sections of human coronary arteries, we found strong staining of sulfated glycosaminoglycans throughout the arterial intima, whereas endogenous LDL deposits were focally distributed. Ex vivo binding of LDL was uniform at all intimal areas with sulfated glycosaminoglycans. However, lowering the pH from 7.4 to 6.5 triggered a 35-fold increase in LDL binding. The pH-dependent binding was abolished by pretreating LDL with diethyl-pyrocarbonate, which blocks the protonation of histidine residues, or cyclohexanedione, which inhibits the positive charge of site B on LDL. Thus, both histidine protonation and site B are required for strong electrostatic LDL binding to the intima. Conclusions: This study identifies histidine protonation as an important component for electrostatic LDL binding to human coronary arteries. Our findings show that the local pH will have a profound impact on LDL's affinity for sulfated glycosaminoglycans, which may influence the retention and accumulation pattern of LDL in the arterial vasculature.
MeSH term(s)	Coronary Vessels/metabolism ; Glycosaminoglycans/metabolism ; Histidine ; Humans ; Hydrogen-Ion Concentration ; Lipoproteins, LDL/metabolism ; Proteoglycans/metabolism ; Static Electricity
Chemical Substances	Glycosaminoglycans ; Lipoproteins, LDL ; Proteoglycans ; Histidine (4QD397987E)
Language	English
Publishing date	2022-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.122.317868
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Zs.A 1705: Show issues

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Article ; Online: The extracellular matrix protein MAGP1 is a key regulator of adipose tissue remodeling during obesity.

Levin, Malin C / Borén, Jan

Diabetes

2014 Volume 63, Issue 6, Page(s) 1858–1859

MeSH term(s)	Adipocytes/metabolism ; Adipose Tissue/metabolism ; Animals ; Contractile Proteins/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Extracellular Matrix Proteins/metabolism ; Male ; Obesity/metabolism ; Transforming Growth Factor beta/metabolism
Chemical Substances	Contractile Proteins ; Extracellular Matrix Proteins ; Transforming Growth Factor beta ; microfibrillar protein
Language	English
Publishing date	2014-06
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db14-0331
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Uh III Zs.175: Show issues

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Article ; Online: Cardiac Plin5 interacts with SERCA2 and promotes calcium handling and cardiomyocyte contractility.

Cinato, Mathieu / Mardani, Ismena / Miljanovic, Azra / Drevinge, Christina / Laudette, Marion / Bollano, Entela / Henricsson, Marcus / Tolö, Johan / Bauza Thorbrügge, Marcos / Levin, Max / Lindbom, Malin / Arif, Muhammad / Pacher, Pal / Andersson, Linda / Olofsson, Charlotta S / Borén, Jan / Levin, Malin C

Life science alliance

2023 Volume 6, Issue 4

Abstract: The adult heart develops hypertrophy to reduce ventricular wall stress and maintain cardiac function in response to an increased workload. Although pathological hypertrophy generally progresses to heart failure, physiological hypertrophy may be ... ...

Abstract	The adult heart develops hypertrophy to reduce ventricular wall stress and maintain cardiac function in response to an increased workload. Although pathological hypertrophy generally progresses to heart failure, physiological hypertrophy may be cardioprotective. Cardiac-specific overexpression of the lipid-droplet protein perilipin 5 (Plin5) promotes cardiac hypertrophy, but it is unclear whether this response is beneficial. We analyzed RNA-sequencing data from human left ventricle and showed that cardiac
MeSH term(s)	Animals ; Humans ; Mice ; Calcium/metabolism ; Cardiomegaly/genetics ; Heart Failure ; Myocytes, Cardiac/metabolism ; Perilipin-5/metabolism ; Calcium Signaling ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Perilipin-5 ; Plin5 protein, mouse ; Atp2a2 protein, mouse (EC 7.2.2.10) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8)
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202201690
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Article ; Online: Castration of Male Mice Induces Metabolic Remodeling of the Heart.

Svedlund Eriksson, Elin / Johansson, Inger / Mårtensson, Anna K F / Lantero Rodriguez, Marta / Schilperoort, Maaike / Kroon, Jan / Kooijman, Sander / Omerovic, Elmir / Andersson, Linda / Levin, Malin C / Rensen, Patrick C N / Tivesten, Åsa

Journal of the Endocrine Society

2022 Volume 6, Issue 11, Page(s) bvac132

Abstract: Androgen deprivation therapy of prostate cancer, which suppresses serum testosterone to castrate levels, is associated with increased risk of heart failure. Here we tested the hypothesis that castration alters cardiac energy substrate uptake, which is ... ...

Abstract	Androgen deprivation therapy of prostate cancer, which suppresses serum testosterone to castrate levels, is associated with increased risk of heart failure. Here we tested the hypothesis that castration alters cardiac energy substrate uptake, which is tightly coupled to the regulation of cardiac structure and function. Short-term (3-4 weeks) surgical castration of male mice reduced the relative heart weight. While castration did not affect cardiac function in unstressed conditions, we observed reductions in heart rate, stroke volume, cardiac output, and cardiac index during pharmacological stress with dobutamine in castrated vs sham-operated mice. Experiments using radiolabeled lipoproteins and glucose showed that castration shifted energy substrate uptake in the heart from lipids toward glucose, while testosterone replacement had the opposite effect. There was increased expression of fetal genes in the heart of castrated mice, including a strong increase in messenger RNA and protein levels of β-myosin heavy chain (MHC), the fetal isoform of MHC. In conclusion, castration of male mice induces metabolic remodeling and expression of the fetal gene program in the heart, in association with a reduced cardiac performance during pharmacological stress. These findings may be relevant for the selection of treatment strategies for heart failure in the setting of testosterone deficiency.
Language	English
Publishing date	2022-09-01
Publishing country	United States
Document type	Journal Article
ISSN	2472-1972
ISSN (online)	2472-1972
DOI	10.1210/jendso/bvac132
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Article ; Online: Lipid profiling of human diabetic myocardium reveals differences in triglyceride fatty acyl chain length and degree of saturation.

Björnson, Elias / Östlund, Ylva / Ståhlman, Marcus / Adiels, Martin / Omerovic, Elmir / Jeppsson, Anders / Borén, Jan / Levin, Malin C

International journal of cardiology

2020 Volume 320, Page(s) 106–111

Abstract: Background: Type 2 diabetes is a major health problem in the world, and is strongly associated with impaired cardiac function and increased mortality. The causal relationship between type 2 diabetes and impaired cardiac function is still incompletely ... ...

Abstract	Background: Type 2 diabetes is a major health problem in the world, and is strongly associated with impaired cardiac function and increased mortality. The causal relationship between type 2 diabetes and impaired cardiac function is still incompletely understood but changes in the cardiac lipid metabolism are believed to be a contributing factor. The objective of this study was to determine the lipid profile in human myocardial biopsies collected in vivo from patients with type 2 diabetes and compare to non-diabetic controls. Method: We conducted full lipidomics analyses, using mass spectrometry, of 85 right atrial biopsies obtained from diabetic and non-diabetic patients undergoing elective cardiac surgery. The patients were characterized clinically and serum was analyzed for lipids and biochemical markers. Results: The groups did not differ in BMI and in circulating triglycerides. We demonstrate that type 2 diabetes is associated with alterations in the cardiac lipidome. Interestingly, the absolute amount of lipids is not altered in the diabetic myocardium. However, triglycerides with longer fatty acyl chains are more abundant and there is a higher degree of unsaturated fatty acid chains in triglycerides in diabetic myocardium. Conclusions: Our study reveals that type 2 diabetes is a relatively strong determinant of the human cardiac lipidome (compared to other clinical variables). Although the total lipid content in the diabetic myocardium is not increased, the lipid composition is markedly affected.
MeSH term(s)	Diabetes Mellitus, Type 2/metabolism ; Heart ; Humans ; Lipid Metabolism ; Myocardium/metabolism ; Triglycerides/metabolism
Chemical Substances	Triglycerides
Language	English
Publishing date	2020-07-30
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	779519-1
ISSN	1874-1754 ; 0167-5273
ISSN (online)	1874-1754
ISSN	0167-5273
DOI	10.1016/j.ijcard.2020.07.017
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Zs.A 1673: Show issues

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Article ; Online: Cardiomyocyte-specific PCSK9 deficiency compromises mitochondrial bioenergetics and heart function.

Cardiovascular research

2023 Volume 119, Issue 7, Page(s) 1537–1552

Abstract: Aims: Pro-protein convertase subtilisin-kexin type 9 (PCSK9), which is expressed mainly in the liver and at low levels in the heart, regulates cholesterol levels by directing low-density lipoprotein receptors to degradation. Studies to determine the ... ...

Abstract	Aims: Pro-protein convertase subtilisin-kexin type 9 (PCSK9), which is expressed mainly in the liver and at low levels in the heart, regulates cholesterol levels by directing low-density lipoprotein receptors to degradation. Studies to determine the role of PCSK9 in the heart are complicated by the close link between cardiac function and systemic lipid metabolism. Here, we sought to elucidate the function of PCSK9 specifically in the heart by generating and analysing mice with cardiomyocyte-specific Pcsk9 deficiency (CM-Pcsk9-/- mice) and by silencing Pcsk9 acutely in a cell culture model of adult cardiomyocyte-like cells. Methods and results: Mice with cardiomyocyte-specific deletion of Pcsk9 had reduced contractile capacity, impaired cardiac function, and left ventricular dilatation at 28 weeks of age and died prematurely. Transcriptomic analyses revealed alterations of signalling pathways linked to cardiomyopathy and energy metabolism in hearts from CM-Pcsk9-/- mice vs. wild-type littermates. In agreement, levels of genes and proteins involved in mitochondrial metabolism were reduced in CM-Pcsk9-/- hearts. By using a Seahorse flux analyser, we showed that mitochondrial but not glycolytic function was impaired in cardiomyocytes from CM-Pcsk9-/- mice. We further showed that assembly and activity of electron transport chain (ETC) complexes were altered in isolated mitochondria from CM-Pcsk9-/- mice. Circulating lipid levels were unchanged in CM-Pcsk9-/- mice, but the lipid composition of mitochondrial membranes was altered. In addition, cardiomyocytes from CM-Pcsk9-/- mice had an increased number of mitochondria-endoplasmic reticulum contacts and alterations in the morphology of cristae, the physical location of the ETC complexes. We also showed that acute Pcsk9 silencing in adult cardiomyocyte-like cells reduced the activity of ETC complexes and impaired mitochondrial metabolism. Conclusion: PCSK9, despite its low expression in cardiomyocytes, contributes to cardiac metabolic function, and PCSK9 deficiency in cardiomyocytes is linked to cardiomyopathy, impaired heart function, and compromised energy production.
MeSH term(s)	Animals ; Mice ; Energy Metabolism ; Lipids ; Mitochondria/metabolism ; Myocytes, Cardiac/metabolism ; Proprotein Convertase 9/genetics ; Proprotein Convertase 9/metabolism ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; Subtilisin/metabolism
Chemical Substances	Lipids ; PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-) ; Receptors, LDL ; Subtilisin (EC 3.4.21.62) ; Pcsk9 protein, mouse (EC 3.4.21.-)
Language	English
Publishing date	2023-03-07
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/cvad041
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Zs.A 565: Show issues

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Article ; Online: Testosterone reduces metabolic brown fat activity in male mice.

Lantero Rodriguez, Marta / Schilperoort, Maaike / Johansson, Inger / Svedlund Eriksson, Elin / Palsdottir, Vilborg / Kroon, Jan / Henricsson, Marcus / Kooijman, Sander / Ericson, Mia / Borén, Jan / Ohlsson, Claes / Jansson, John-Olov / Levin, Malin C / Rensen, Patrick C N / Tivesten, Åsa

The Journal of endocrinology

2021 Volume 251, Issue 1, Page(s) 83–96

Abstract: Brown adipose tissue (BAT) burns substantial amounts of mainly lipids to produce heat. Some studies indicate that BAT activity and core body temperature are lower in males than females. Here we investigated the role of testosterone and its receptor (the ... ...

Abstract	Brown adipose tissue (BAT) burns substantial amounts of mainly lipids to produce heat. Some studies indicate that BAT activity and core body temperature are lower in males than females. Here we investigated the role of testosterone and its receptor (the androgen receptor; AR) in metabolic BAT activity in male mice. Castration, which renders mice testosterone deficient, slightly promoted the expression of thermogenic markers in BAT, decreased BAT lipid content, and increased basal lipolysis in isolated brown adipocytes. Further, castration increased the core body temperature. Triglyceride-derived fatty acid uptake, a proxy for metabolic BAT activity in vivo, was strongly increased in BAT from castrated mice (4.5-fold increase vs sham-castrated mice) and testosterone replacement reversed the castration-induced increase in metabolic BAT activity. BAT-specific AR deficiency did not mimic the castration effects in vivo and AR agonist treatment did not diminish the activity of cultured brown adipocytes in vitro, suggesting that androgens do not modulate BAT activity via a direct, AR-mediated pathway. In conclusion, testosterone is a negative regulator of metabolic BAT activity in male mice. Our findings provide new insight into the metabolic actions of testosterone.
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Animals ; Male ; Mice ; Mice, Inbred C57BL ; Norepinephrine/metabolism ; Orchiectomy ; Receptors, Androgen/deficiency ; Testosterone/deficiency
Chemical Substances	Receptors, Androgen ; Testosterone (3XMK78S47O) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2021-09-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3028-4
ISSN	1479-6805 ; 0022-0795
ISSN (online)	1479-6805
ISSN	0022-0795
DOI	10.1530/JOE-20-0263
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Article ; Online: Intussusceptive Angiogenesis in Human Metastatic Malignant Melanoma.

Pandita, Ankur / Ekstrand, Matias / Bjursten, Sara / Zhao, Zhiyuan / Fogelstrand, Per / Le Gal, Kristell / Ny, Lars / Bergo, Martin O / Karlsson, Joakim / Nilsson, Jonas A / Akyürek, Levent M / Levin, Malin C / Borén, Jan / Ewald, Andrew J / Mostov, Keith E / Levin, Max

The American journal of pathology

2021 Volume 191, Issue 11, Page(s) 2023–2038

Abstract: Angiogenesis supplies oxygen and nutrients to growing tumors. Inhibiting angiogenesis may stop tumor growth, but vascular endothelial growth factor inhibitors have limited effect in most tumors. This limited effect may be explained by an additional, less ...

Abstract	Angiogenesis supplies oxygen and nutrients to growing tumors. Inhibiting angiogenesis may stop tumor growth, but vascular endothelial growth factor inhibitors have limited effect in most tumors. This limited effect may be explained by an additional, less vascular endothelial growth factor-driven form of angiogenesis known as intussusceptive angiogenesis. The importance of intussusceptive angiogenesis in human tumors is not known. Epifluorescence and confocal microscopy was used to visualize intravascular pillars, the hallmark structure of intussusceptive angiogenesis, in tumors. Human malignant melanoma metastases, patient-derived melanoma xenografts in mice (PDX), and genetically engineered v-raf murine sarcoma viral oncogene homolog B1 (BRAF)-induced, phosphatase and TENsin homolog deleted on chromosome 10 (PTEN)-deficient (BPT) mice (Braf
MeSH term(s)	Aged ; Aged, 80 and over ; Animals ; Female ; Heterografts ; Humans ; Male ; Matrix Metalloproteinase 9/metabolism ; Melanoma/metabolism ; Melanoma/pathology ; Mice ; Middle Aged ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; Melanoma, Cutaneous Malignant
Chemical Substances	Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2021-08-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2021.07.009
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